What is a Dermatologist?
Dermatology (from Greek derma, “skin”) is a branch of medicine dealing with the skin and its appendages (hair, nails, sweat glands etc). A medical doctor who specializes in dermatology is a dermatologist.
Scope of the field
Dermatologists are physicians (medical doctors) specializing in the diagnosis and treatment of diseases and tumors of the skin and its appendages. There are medical and surgical sides to the specialty. Dermatologic surgeons practice skin cancer surgery (including Mohs’ micrographic surgery), laser surgery, photodynamic therapy (PDT) and cosmetic procedures using botulinum toxin (‘Botox’), soft tissue fillers, sclerotherapy and liposuction. Dermatopathologists interpret tissue under the microscope (histopathology). Pediatric dermatologists specialize in the diagnoses and treatment of skin disease in children. Immunodermatologists specialize in the diagnosis and management of skin diseases driven by an altered immune system including blistering (bullous) diseases like pemphigus. In addition, there are a wide range of congenital syndromes managed by dermatologists.
Residency training program in North America
A minimum of 8 years of college and post graduate training is required to become a dermatologist in the United States and Canada. This includes graduation from a 4-year college, a 4-year medical school followed by a year of post graduate training in medicine, surgery or pediatrics (called an internship) after which a physician may apply for admission to graduate dermatology residency training. Dermatology residencies are among the most competitive in terms of admission. Following the successful completion of formal residency training in dermatology (3 years) the physician is qualified to take certifying board examinations (written) by the American Board of Dermatology or the American Osteopathic College of Dermatology. Once board certified, dermatologists become Diplomates of the American Board of Dermatology or the American Osteopathic College of Dermatology AOCD. They are then eligible to apply for fellowship status in the American Academy of Dermatology. Some dermatologists undertake advanced subspecialty training in programs known as fellowships after completion of their residency training. These fellowships are either one or two years in duration. Fellowships in dermatology include pediatric dermatology, surgical dermatology including Mohs micrographic surgery, dermatopathology (pathology of skin diseases) and dermatological immunology.
How Dermatologists Were Selected
Consumers’ Research Council of America has compiled a list of Dermatologists throughout the United States by utilizing a point value system. This method uses a point value for criteria that we deemed valuable in determining top health care professionals.
The criteria that was used and assessed a point value is as follows:
Each year the Dermatologist has been in practice
Education and Continuing Education
Membership in Professional Medical Associations
Completing an approved residency program and
Simply put, Dermatologists that have accumulated a certain amount of points qualified for the list. This does not mean that doctors that did not accumulate enough points are not good Dermatologists; they merely did not qualify for this list because of the points needed for qualification.
Similar studies have been done with other professions using a survey system. This type of study would ask fellow professionals whom they would recommend. We found this method to be more of a popularity contest. For instance, professionals who work in a large office have much more of a chance of being mentioned as opposed to a professional who has a small private practice. In addition, many professionals have a financial arrangement for back-and-forth referrals. For these reasons, we developed the point value system.
Since this is a subjective call, there is no study that is 100% accurate. As with any profession, there will be some degree of variance in opinion. If you survey 100 patients of a particular Dermatologist on their level of satisfaction, you will undoubtedly hear that some are very satisfied, some moderately satisfied and some dissatisfied. This is really quite normal.
We feel that a point value system takes out the personal and emotional factor and deals with factual criteria. We have made certain assumptions. For example, we feel that more years in practice is better than less years in practice; more education is better than less education, being board certified is better than not being certified, etc.
The Top Dermatologist list that we have compiled is current as of a certain date and other doctors may have qualified since that date. Nonetheless, we feel that the list of top Dermatologists is a good starting point for you to find a qualified health care specialist.
No fees, donations, sponsorships or advertising are accepted from any individuals, professionals, corporations or associations. This policy is strictly adhered to, ensuring an unbiased selection.
Choosing a Dermatologist
Choosing a Dermatologist is an important decision. Thus, our goal is to assist you in making that decision.
First of all, when selecting a Dermatologist, you may want to begin your search several different ways:
|Ask family, friends, neighbors and/or co-workers.|
|Contact your local Chamber of Commerce or Better Business Bureau for reputable physicians that specialize in the area of medicine that you have a need for.|
|Contact your city, county or state medical agencies for names of qualified Dermatologists. Contact and ask for referrals from medical associations. Many are listed in this publication.|
|Ask your family doctor. They are in constant contact with all kinds of health care professionals and will be able to provide you with recommendations.|
|We recommend that you interview the Dermatologist and ask the following:
How long have you been in practice?
Is your staff friendly and accommodating?
What are the procedures if we need a doctor in the middle of the night or on a weekend?
Do you have an associate that covers for you when you are not available?
Do you have more than one office and if so, how is your time divided between offices?
What kind of continuing education do you utilize?
Do you accept phone calls during office hours?
How do you stay current on the latest drug prescriptions available and medical testaments?
What types of insurance coverage do you accept?
How do you handle billing? Do you require payment at the time of visit?
Discuss your family medical history and particular problems you are concerned about.
After you have consulted a few Dermatologists you should have a good idea which one you felt most comfortable with and whom best answered your questions.
The skin is the largest organ of the body and obviously the most visible. Although many skin diseases are isolated, some are manifestations of internal disease. Hence, a dermatologist is schooled in aspects of surgery, rheumatology (many rheumatic diseases can feature skin symptoms and signs), immunology, neurology (the “neurocuteaneous syndromes”, such as neurofibromatosis and tuberous sclerosis), infectious diseases and endocrinology. The study of genetics is also becoming increasingly important.
Venereology and Phlebology
Venereology, the subspecialty that diagnoses and treats sexually transmitted diseases, and phlebology, the specialty that deals with problems of the superficial venous system, are both part of a dermatologist’s expertise.
Cosmetic dermatology has long been an important part of the field, and dermatologists have been the primary innovators in this area. In the 1900’s dermatologists employed Dermabrasion to improve acne scarring and fat microtransfer was used to fill in cutaneous defects. More recently, dermatologists have been the driving force behind the development and safe and effective employment of lasers, new dermal filling agents (collagen and hyaluronic acid), botulinum toxin (“Botox”), nonabrasive laser rejuvenation procedures, intense pulsed-light systems, photodynamic therapy, and chemical peeling.
Dermatologic surgery is performed by all dermatologists. Surgery is an integral part of dermatology residency training; thus all dermatologists are well trained in cutaneous surgery. Specialized training through a 1 year Dermatologic surgery fellowship is available upon completion of the dermatology residency, and usually focuses on training in Mohs micrographic surgery. Most Dermatologic surgeons who have a special interest in this field apply for fellowship status in the American Society for Dermatologic Surgery, a professional organization dedicated to supporting and educating these physicians.
Techniques available to a dermatologic surgeon include lasers, traditional scalpel surgery, electrosurgery, cryosurgery, photodynamic therapy, liposuction, Blepharoplasty (cosmetic eyelid surgery), minimally-invasive facelift surgery (e.g., the S-lift), and a variety of topical and injectable agents such as dermal fillers including fat transfer and hyaluronic acid. Some specially trained dermatologic surgeons perform Mohs cancer surgery, which can be an effective method for the treatment of recurrent, indistinct, or difficult skin cancers.
Any mole that is irregular in color or shape should be examined by a dermatologist to determine if it is a malignant melanoma, the most serious and life-threatening form of skin cancer. Following a visual examination and a dermatoscopic exam (an invaluable new instrument that illuminates a mole without reflected light), a dermatologist may biopsy a suspicious mole. If it is malignant, it will be excised in the dermatologist’s office.
The first step of any contact with a physician is the medical history. In order to classify a cutaneous eruption, the dermatologist will ask detailed questions on the duration and temporal pattern of skin problems, itching or pain, relation to food intake, sunlight, over-the-counter creams and clothing. When an underlying disease is suspected, an additional detailed history of related symptoms will be elicited (such as arthritis in a suspected case of lupus erythematosus).
Dermatology has the obvious benefit of having easy access to tissue for diagnosis. Physical examination is generally done under bright light and preferably involves the whole body. At this stage, the doctor may apply Wood’s light, which may aid in diagnosing types of mycosis or demonstrate the extent of pigmented lesions, or use a dermatoscope which enlarges a suspected lesion and visualizes it without reflected light. The dermatoscope is helpful in differentiating a benign naevus from melanoma or a seborrheic Keratosis from a mole. A morphological classification of dermatological lesions is important in the diagnosis of dermatological disorders. Dermatologic diagnosis is often dependent upon pattern recognition of lesions and symptoms.
Culture or Gram staining of suspected infectious lesions may identify a pathogen and help direct therapy.
If the diagnosis is uncertain or a cutaneous malignancy is suspected, the dermatologic surgeon may perform a small punch biopsy (using a local anesthetic) for examination under the microscope by the dermatologist who is a trained dermatopathologist.
The skin is obviously accessible to topical local therapy. Antibiotic creams can help eliminate infections, while inflammatory skin diseases (such as eczema and psoriasis) often respond to steroid creams or topical anthralin. Dermatologists are innovators of new immune enhancing treatments, like topical imiquimod for superficial cancers and injection immunotherapy for warts as discussed below.
Topical medications treat many dermatological diseases, but dermatologists also use oral medications. Antibiotics and immune suppressants or immune enhancing agents (injection immunotherapy or topical imiquimod) for dermatological diseases or tumors. Isotretinoin (“Accutane”) is used for severe cystic acne vulgaris and often produces a life-time remission of this disfiguring disease. Isotretinoin prescribing in the U.S. is now controlled by a cumbersome FDA governmental website called iPLEDGE. Various new modalities of treatment are in the foray, with the advent of laser technology things are quite promising.
Photomedicine involves the use of ultraviolet light, often in combination with oral or topical agents, to treat skin disease (eg. psoriasis or mycosis fungoides).
Surgical intervention by a dermatologic surgeon may be necessary, for example, to treat varicose veins or skin cancer. Varicose veins can be treated with sclerotherapy (injecting an agent that obliterates the vein) or the long-pulsed Nd:YAG laser. Skin cancers can be managed with excision (including Mohs cancer surgery), cryosurgery, x-ray, or with the recent topical immune enhancing agent imiquimod. (See above section on “Dermatologic Surgery” for more details.)
Psychodermatology and Hypnodermatology involve using hypnosis in combination with other pseudo-psychological therapies to treat skin disorders.
Dermatopathology is a subspecialty of anatomical pathology interested in skin diseases. Dermatopathologists work in close association with dermatologists. In fact, many doctors master both specialties. Dermatologists recognize most skin diseases based on their appearance, distribution on the body and behavior with time. Occasionally, these criteria are not enough and a skin biopsy is taken to be examined under the microscope. This microscopic examination reveals the histology of the disease and clarifies the diagnosis. Occasionally, additional testing needs to be performed on skin samples, such as immunofluorescence, electron microscopy or flow cytometry.
One of the greatest challenges of dermatopathology is the high number of different skin diseases. There are an estimated 1500 different rashes and skin tumors, including variants, and not one doctor who has seen them all. Therefore, dermatology and dermatopathology are among the most complex specialties of Medicine.
A licensed dermatopathologist has completed four years of medical school, followed by residency training of three to five years in either dermatology or general pathology. Following that, an additional one to two years of dermatopathology training are completed. In the United States, they are first certified by the American Board of Pathology or dermatology, then obtain subspecialty board certification in dermatopathology. Since 2003, the International Board of Dermatopathology certifies candidates in Europe.
All About Skin
In zootomy and dermatology, skin is an organ of the integumentary system made up of multiple layers of epithelial tissues that guard underlying muscles and organs. As the interface with the surroundings, it plays the most important role in protecting against pathogens. Its other main functions are insulation and temperature regulation, sensation and vitamin D and B synthesis. Skin is considered one of the most important parts of the body.
Skin has pigmentation, or melanin, provided by melanocytes, which absorb some of the potentially dangerous ultraviolet radiation in sunlight. It also contains DNA repair enzymes which help to reverse UV damage, and people who lack the genes for these enzymes suffer high rates of skin cancer. One form predominantly produced by UV light, malignant melanoma, is particularly invasive, causing it to spread quickly, and can often be deadly. Human skin pigmentation varies among populations in a striking manner. This has sometimes led to the classification of people(s) on the basis of skin color.
Mammalian skin often contains hairs, which in sufficient density is called fur. The hair mainly serves to augment the insulation the skin provides, but can also serve as a secondary sexual characteristic or as camouflage. On some animals the skin is very hard and thick, and can be processed to create leather. Reptiles and fish have hard protective scales on their skin for protection, and birds have hard feathers, all made of tough keratins. Amphibian skin is not a strong barrier to passage of chemicals and is often subject to osmosis. A frog sitting in an anesthetic solution will quickly go to sleep.
Damaged skin will try to heal by forming scar tissue, often giving rise to discoloration and depigmentation of the skin.
The skin is often known as “the largest organ of the human body”. This applies to exterior surface, as it covers the body, appearing to have the largest surface area of all the organs. Moreover, it applies to weight, as it weighs more than any single internal organ, accounting for about 15 percent of body weight. For the average adult human, the skin has a surface area of between 1.5-2.0 square meters, most of it is between 2-3 mm thick. The average square inch of skin holds 650 sweat glands, 20 blood vessels, 60,000 melanocytes, and more than a thousand nerve endings.
Epidermis is the outermost layer of the skin. It forms the waterproof, protective wrap over the body’s surface and is made up of stratified squamous epithelium with an underlying basal lamina.
The outermost epidermis consists of stratified squamous epithelium with an underlying connective tissue section, or dermis, and a hypodermis, or basement membrane. The epidermis contains no blood vessels, and cells in the deepest layers are nourished by diffusion from blood capillaries extending to the upper layers of the dermis. The main type of cells which make up the epidermis are keratinocytes, with melanocytes and Langerhans cells also present. The epidermis can be further subdivided into the following strata (beginning with the outermost layer): corneum, lucidum (only in feet), granulosum, spinosum, basale. Cells are formed through mitosis at the basale layer. The daughter cells, (see cell division) move up the strata changing shape and composition as they die due to isolation from their blood source. The cytoplasm is released and the protein keratin is inserted. They eventually reach the corneum and slough off (desquamation). This process is called keratinization and takes place within about 30 days. This keratinized layer of skin is responsible for keeping water in the body and keeping other harmful chemicals and pathogens out, making skin a natural barrier to infection.
Epidermis contains no blood vessels, and is nourished by diffusion from the dermis. The main type of cells which make up the epidermis are keratinocytes, melanocytes, Langerhans cells and Merkels cells.
Epidermis is divided into several layers where cells are formed through mitosis at the innermost layers. They move up the strata changing shape and composition as they differentiate and become filled with keratin. They eventually reach the top layer called stratum corneum and become sloughed off, or desquamated. This process is called keratinization and takes place within weeks. The outermost layer of Epidermis consists of 25 to 30 layers of dead cells.
Epidermis is divided into the following 5 sublayers or strata:
|Stratum germinativum (also called “stratum basale”)|
The dermis is the layer of skin beneath the epidermis that consists of connective tissue and cushions the body from stress and strain. The dermis is tightly connected to the epidermis by a basement membrane. It also harbors many nerve endings that provide the sense of touch and heat. It contains the hair follicles, sweat glands, sebaceous glands, apocrine glands and blood vessels. The blood vessels in the dermis provide nourishment and waste removal to its own cells as well as the Stratum basale of the epidermis.
The dermis is structurally divided into two areas: a superficial area adjacent to the epidermis, called the papillary region, and a deep thicker area known as the reticular region.
The papillary region is composed of loose areolar connective tissue. It is named for its fingerlike projections called papillae, that extend toward the epidermis. The papillae provide the dermis with a “bumpy” surface that interdigitates with the epidermis, strengthening the connection between the two layers of skin.
In the palms, fingers, soles, and toes, the influence of the papillae projecting into the epidermis forms contours in the skin’s surface. These are called friction ridges, because they help the hand or foot to grasp by increasing friction. Friction ridges occur in patterns (see fingerprint) that are genetically determined and are therefore unique to the individual, making it possible to use fingerprints or footprints as a means of identification.
The reticular region lies deep in the papillary region and is usually much thicker. It is composed of dense irregular connective tissue, and receives its name from the dense concentration of collagenous, elastic, and reticular fibers that weave throughout it. These protein fibers give the dermis its properties of strength, extensibility, and elasticity.
The hypodermis is not part of the skin, and lies below the dermis. Its purpose is to attach the skin to underlying bone and muscle as well as supplying it with blood vessels and nerves. It consists of loose connective tissue and elastin. The main cell types are fibroblasts, macrophages and adipocytes (the hypodermis contains 50% of body fat). Fat serves as padding and insulation for the body.
Microorganisms like Staphylococcus epidermidis colonize the skin surface. These microorganisms serve as ecoorgan. The density of skin flora depends on region of the skin. The disinfected skin surface gets recolonized from bacteria residing in the deeper areas of the hair follicle, gut and urogenital openings.
Individuals with ancestors from different parts of the world have highly visible differences in skin pigmentation. Individuals with African ancestry (black people) tend towards darker skin, while those of Northern European descent (white people) have paler skin. Between these extremes are individuals of Asian, South-East Asian, Native American, Middle Eastern, Polynesian and Melanesian descent.
African American skin has more variation in color from one part of the body to another then does the skin of other racial groups. Part of this is the result of the variations in the thickness of the skin or different parts of the body. The thicker the skin the more layers of cell with melanin in them, and the darker the color.
|1.||Protection: an anatomical barrier between the internal and external environment in bodily defense; Langerhans cells in the skin are part of the adaptive immune system|
|2.||Sensation: contains a variety of nerve endings that react to heat, cold, touch, pressure, vibration, and tissue injury; see somatosensory system and touch.|
|3.||Heat regulation: the skin contains a blood supply far greater than its requirements which allows precise control of energy loss by radiation, convection and conduction. Dilated blood vessels increase perfusion and heat loss while constricted vessels greatly reduce cutaneous blood flow and conserve heat. Erector pili muscles are significant in animals.|
|4.||Control of evaporation: the skin provides a relatively dry and impermeable barrier to fluid loss. Loss of this function contributes to the massive fluid loss in burns.|
|5.||Aesthetics and communication: others see our skin and can assess our mood, physical state and attractiveness.|
|6.||Storage and synthesis: acts as a storage center for lipids and water, as well as a means of synthesis of vitamin D and B by action of UV on certain parts of the skin. This synthesis is linked to pigmentation, with darker skin producing more vitamin B than D, and vice versa.|
|7.||Excretion: The concentration of urea is 1/130th that of urine. Excretion by sweating is at most a secondary function to temperature regulation.|
|8.||Absorption: Oxygen, nitrogen and carbon dioxide can diffuse into the epidermis in small amounts, some animals using their skin for their sole respiration organ. In addition, medicine can be administered through the skin, by ointments or by means of adhesive patch, such as the nicotine patch or iontophoresis. The skin is an important site of transport in many other organisms.|
The skin must be regularly cleaned; unless enough care is taken it will become cracked or inflamed. Unclean skin favors the development of pathogenic organisms – the dead cells that continually slough off of the epidermis mix with the secretions of the sweat and sebaceous glands and the dust found on the skin to form a filthy layer on its surface. If not washed away, the slurry of sweat and sebaceous secretions mixed with dirt and dead skin is decomposed by bacterial flora, producing a foul smell. Functions of the skin are disturbed when it is dirty; it becomes more easily damaged, the release of antibacterial compounds decreases and dirty skin is more prone to develop infections. Cosmetics should be used carefully because these may cause allergic reactions. Each season requires suitable clothing in order to facilitate the evaporation of the sweat. Sunlight, water and air play an important role in keeping the skin healthy.
The skin supports its own ecosystems of microorganisms, including yeasts and bacteria, which cannot be removed by any amount of cleaning. Estimates place the number of individual bacteria on the surface of one square inch of human skin at 50 million though this figure varies greatly over the average 20 feet 2 of human skin. Oily surfaces, such as the face, may contain over 500 million bacteria per square inch. Despite these vast quantities, all of the bacteria found on the skin’s surface would fit into a volume the size of a pea. In general the microorganisms keep one another in check and are part of a healthy skin. When the balance is disturbed there may be an overgrowth and infection, such as when antibiotics kill microbes, resulting in an overgrowth of yeast. The skin is continuous with the inner epithelial lining of the body at the orifices, each of which supports its own complement of microbes.
As skin ages, it becomes thinner and more easily damaged. Intensifying this effect is the decreasing ability of skin to heal itself. Skin sagging is caused by the fall in elasticity. Skin also receives less blood flow and lower gland activity.
Common Skin Disorders and Treatments:
Dandruff (also called scurf and historically termed Pityriasis capitis) is due to the excessive shedding of dead skin cells from the scalp. As it is normal for skin cells to die and flake off, a small amount of flaking is normal and in fact quite common. Some people, however, either chronically or as a result of certain triggers, experience an unusually large amount of flaking, which can also be accompanied by redness and irritation. Most cases of dandruff can be easily treated with specialized shampoos.
Excessive flaking can also be a symptom of seborrhoeic dermatitis, psoriasis, fungal infection or excoriation associated with infestation of head lice. Dandruff is a global phenomenon and many people find that dandruff can cause social or self-esteem problems. Treatment can be important for purely social reasons.
As the epidermal layer continually replaces itself, cells are pushed outward where they eventually die and flake off. In most people, these flakes of skin are too small to be visible. However, certain conditions cause cell turnover to be unusually rapid, especially in the scalp. For people with dandruff, skin cells may mature and be shed in 2 – 7 days, as opposed to around a month in people without dandruff. The result is that dead skin cells are shed in large, oily clumps, which appear as white or grayish patches on the scalp and clothes.
Dandruff has been shown to be the result of three required factors: 1) Skin oil commonly referred to as sebum or sebaceous secretions; 2) the metabolic by-products of skin micro-organisms (most specifically Malassezia yeasts); and 3) an individual susceptibility. Rarely dandruff can be a manifestation of an allergic reaction to chemicals in Hair Gels/Sprays,HairOils and sometimes even dandruff medications like Ketoconazole. Common older literature cites the fungus Malassezia furfur (previously known as Pityrosporum ovale) as the cause of dandruff. Whilst this fungus is found naturally on the skin surface of both healthy people and those with dandruff it has recently been shown that a scalp specific fungus Malassezi Globosa is the responsible agent. This fungus metabolizes triglycerides present in sebum by the expression of lipase, resulting in a lipid byproduct oleic acid (OA). Penetration by OA of the top layer of the epidermis, the stratum corneum, results in an inflammatory response which disturbs homeostasis and results in erratic cleavage of straum corneum cells. There is no convincing evidence that food, excessive perspiration or climate have any role in the pathogenesis of dandruff.
There have been many strategies for the control of dandruff. Simply increasing shampooing will remove flakes. However, elimination of the fungus results in dramatic improvement. Regular shampooing with an anti-fungal product will not only treat but prevent recurrence.
Flaking is a symptom of seborrheic dermatitis. Joseph Bark notes that “Redness and itching is actually seborrheic dermatitis, and it frequently occurs around the folds of the nose and the eyebrow areas, not just the scalp.” Dry, thick, well-defined lesions consisting of large, silvery scales may be traced to the less common psoriasis of the scalp.
Seasonal changes, stress, and immuno-suppression seem to affect seborrheic dermatitis. Simple dandruff does not cause hair loss.
|Head & Shoulders® anti-dandruff shampoo containing active ingredient Zinc pyrithione.|
|Nizoral® Shampoo anti-fungal/anti-dandruff shampoo containing active ingredient Ketoconazole.|
|Selsun Blue® anti-dandruff shampoo containing active ingredient Selenium sulfide.|
The antifungal properties of Tea Tree Oil (Melaleuca Oil) have been reported as useful in the treatment of dandruff.
Severe forms of flaking if accompanied by flaking or scaling on other parts of the body, might best be treated by a dermatologist.
|Dandruff is sometimes confused with dried shampoo. This usually occurs when hair isn’t rinsed properly.|
|Dandruff is not an organism like lice; it is just dead skin that accumulates in the scalp.|
|Dandruff is unlikely to be the cause of hair loss.|
Diaper rash (U.S.) or nappy rash (UK), is a generic term applied to skin rashes in the diaper area that are caused by a various skin disorders and/or irritants.
Generic rash or irritant diaper dermatitis (IDD) is characterized by joined patches of erythema and scaling mainly seen on the convex surfaces, with the skin folds spared.
Diaper dermatitis with secondary bacterial or fungal involvement tends to spread to concave surfaces (i.e. skin folds), as well as convex surfaces, and often exhibits a central red, beefy erythema with satellite pustules around the border (Hockenberry, 2003).
Other rashes that often occur in the diaper area include Seborrheic dermatitis and Atopic dermatitis. Both Seborrheic and Atopic dermatitis require individualized treatment and are not the subject of this article.
|Seborrheic dermatitis, typified by oily, thick yellowish scales, is most commonly seen on the scalp (cradle cap) but can also appear in the inguinal folds.|
|Atopic dermatitis, or eczema, is associated with allergic reaction, often hereditary. This class of rashes may appear anywhere on the body and is characterized by intense itchiness.|
Irritant diaper dermatitis develops when skin is exposed to prolonged wetness, increased skin pH caused by urine and feces, and resulting breakdown of the stratum corneum, or outermost layer of the skin. In adults, the stratum corneum is composed of 25 to 30 layers of flattened dead keratinocytes, which are continuously shed and replaced from below. These dead cells are interlay with lipids secreted by the stratum granulosum just underneath, which help to make this layer of the skin a waterproof barrier. The stratum corneum’s function is to reduce water loss, repel water, protect deeper layers of the skin from injury and to repel microbial invasion of the skin (Tortora and Grabowski, 2003). In infants, this layer of the skin is much thinner and more easily disrupted.
Although wetness alone macerates the skin, softening the stratum corneum and greatly increasing susceptibility to friction injury, urine has an additional impact on skin integrity because of its effect on skin pH. While studies show that ammonia alone is only a mild skin irritant, when urea breaks down in the presence of fecal urease it increases skin pH, which in turn promotes the activity of fecal enzymes such as protease and lipase (Atherton, 2004; Wolf, Wolf, Tuzun and Tuzun, 2001). These fecal enzymes increase the skin’s permeability to bile salts and act as irritants in and of themselves.
The interaction between fecal enzyme activity and IDD explains the observation that infant diet and diaper rash are linked, since fecal enzymes are in turn affected by diet. Breast-fed babies, for example, have a lower incidence of diaper rash, possibly because their stools have lower pH and lower enzymatic activity. Diaper rash is also most likely to be diagnosed in infants 8–12 months old, perhaps in response to an increase in eating solid foods and dietary changes around that age that affect fecal composition. Any time an infant’s diet undergoes a significant change (i.e. from breast milk to formula or from milk to solids) there appears to be an increased likelihood of diaper rash.
The link between feces and IDD is also apparent in the observation that infants are more susceptible to developing diaper rash after treatment with antibiotics, which affect the intestinal microflora. Also, there is an increased incidence of diaper rash in infants who have suffered from diarrhea in the previous 48 hours, which may be due to the fact that fecal enzymes such as lipase and protease are more active in feces which have passed rapidly through the gastrointestinal tract.
The significance of secondary infection in IDD remains controversial. Atherton contends that, “Candida albicans can only be isolated from a minority of IDD cases; in many cases this is a reflection of antibiotic therapy. It has also been established that bacterial infection does not play a substantial part in the development of IDD.”
However, there is little argument that once the stratum corneum has been damaged by a combination of physical and chemical factors, the skin is necessarily more vulnerable to secondary infections by bacteria and fungi. In analyzing swab samples at the perianal, inguinal and oral areas of 76 infants, Ferrazzini et al. (2003) found that colonization with Candida albicans was significantly more likely in children with symptomatic diaper rash than without. Staphylococcus aureus was also present more frequently in symptomatic than in healthy infants, but the difference was not statistically significant. A wide variety of other infections has been reported on occasion, including Proteus mirabilis, enterococci and Pseudomonas aeruginosa, but it appears that Candida is the most common opportunistic invader in diaper areas (Ferrazzini et al., 2003; Ward et al., 2000).
Although apparently healthy infants sometimes culture positive for Candida and other organisms without exhibiting any symptoms, there does seem to be a positive correlation between the severity of the diaper rash noted and the likelihood of secondary involvement (Ferrazzini et al., 2003; Gupta & Skinner, 2004; Wolf et al., 2001).
The most effective treatment, although not always the most practical one, is to discontinue use of diapers, allowing the affected skin to air out. Other commonly recommended remedies include oil-based protectants, often using various over-the-counter “diaper creams”, but sometimes people use petroleum jelly and shark liver oil or cod liver oil; zinc oxide based ointments, and, in extreme cases, anti-fungal cremes. Low concentration hydrocortisone creams are also sometimes used to treat the symptoms of diaper rash, although they do little to clear up the rash itself.
Herpes Simplex Virus
Herpes simplex virus 1 and 2 (HSV-1 and HSV-2) are two strains of the Herpes virus family, Herpesviridae, which cause infections in humans. HSV-1 and 2 are also referred to as Human Herpes Virus 1 and 2 (HHV-1 and HHV-2).
After an initial, or primary, infection, HSV establishes latency, during which the virus is present in the cell bodies of nerves which innervate the area of original outbreak. During reactivation, virus is produced in the cell and transported outwardly via the nerve cell’s axon to the skin. The ability of Herpes virus to establish latency leads to the chronic nature of Herpes infection; after the initial infection subsides, Herpes symptoms may periodically recur in the form of outbreaks of herpetic sores near the site of original infection.
Herpes infections are marked by painful, watery blisters in the skin or mucous membranes (such as the mouth or lips) or on the genitals. The blisters resemble those seen in Chickenpox — an infection caused by a third member of the alpha-Herpesviridae subfamily, Varicella Zoster Virus (VZV), also known as Human Herpes Virus 3 (HHV-3). Lesions heal with a crudescent scab, the hallmark of herpetic disease. Herpes is contagious if the carrier is producing and releasing (“shedding”) virus. This is particularly likely during an outbreak, although individuals may shed virus between outbreaks. Although no cure is yet available, treatments exist which reduce the likelihood of viral shedding. An infection on the lips is commonly known as a “cold sore” or “fever blister”; not to be confused with a canker sore, which is not caused by the HSV virus.
HSV is generally transmitted by direct contact of lips or genitals when the sores are present, or just before they appear (known as shedding). In addition, herpes may be transmitted during childbirth, which can be fatal to the infant. The immature immune system of the child is unable to defend against the virus and even if treated, infection can result in brain damage. Transmission occurs while passing through the birth canal and the risk of infection is minimal if there are no symptoms or exposed blisters during delivery. The first outbreak after exposure to HSV is commonly more severe than future outbreaks, as the body has not had a chance to produce antibodies; this first outbreak also carries the risk of developing meningitis.
Treatment is available in the form of antiviral medications such as nucleoside analog, which reduce the duration of symptoms and accelerate healing.
Nucleoside analogs are molecules which possess a similarity to natural nucleosides — the building-blocks of DNA and RNA. Because the replicating virus incorporates these analogs into viral DNA, the genetic material produced contains defects and mutations. As a result, the subsequent generation of virus produced is damaged and reduced in number.
|Oral Prodrug||Drug||Analog of Nucleoside||Nucleoside Family|
(bioavailability: 75% oral)
(trade names: Famvir)
(1.5% oral, IV, locally topical)
(5% oral, IV, locally intraocular)
Treatment should begin at the first symptoms of an outbreak for best results as far as duration and healing; should treatment begin before the lesions appear, it is possible that the outbreak can be averted. Another option is the use of daily suppressive therapy, in which antivirals are taken every day over the course of years. Suppressive therapy reduces frequency of symptoms and recurrence of outbreaks. In addition, suppressive therapy reduces subclinical shedding, lowering the risk of transmission through sexual contact or kissing.
Of these, Ganciclovir is known to have cytotoxic effects on infected cells, while Aciclovir is not known to have this effect.
Fusion inhibitors prevent “fusion” of the viral envelope with the cell membrane. This prevents viral entry to the cell.
One of three key protein structures involved in HSV DNA replication is the Helicase-Primase structure. New research compounds which bind to this megamolecule show remarkable effectiveness against HSV. In particular, BAY 57-1293 has been used to treat infant HSV-2 encephalitis, and has also shown positive results in animals models of HSV infection.
The amino acid lysine has demonstrated the ability to reduce the duration of infection through inhibiting the replication of the HSV. When foods high in lysine are consumed in preference to foods high in arginine, HSV replication may be inhibited; conversely, consuming foods high in arginine may interfere with the therapeutic use of lysine. However, according to the American Social Health Association: “While some studies have suggested that lysine supplements can reduce the frequency of recurrences or healing time, other trials have been unable to replicate those results. Therefore, there is not sufficient information to discern how effective it may be, in addition to what the effective dosages or frequency of L-lysine may be.”
Undecylenic acid (Castor oil derivative) is also proven to have anti-bacterial and anti-viral properties that are effective on viral skin infections such as the herpes simplex virus (HSV).
Butylated Hydroxytoluene (BHT), commonly available as a food preservative, has been shown in in-vitro laboratory studies to inactivate the herpes virus. In-vivo studies in animals confirmed the anti-viral activity of BHT against genital herpes. However BHT has not been clinically tested and approved to treat herpes infections in humans.
Boils or furuncles are skin diseases caused by the inflammation of hair follicles, thus resulting in the localized accumulation of pus and dead tissues. Individual boils can cluster together and form an interconnected network of boils called carbuncles. In severe cases, boils may develop to form abscesses.
The symptoms of boils are red, pus-filled lumps that are tender, warm, and/or painful. A yellow or white point at the center of the lump can be seen when the boil is ready to drain or discharge pus. In a severe infection, multiple boils may develop and the patient may experience fever and swollen lymph nodes. A recurring boil is called chronic furunculosis.
In some people, itching may develop before the lumps begin to develop. Boils are most often found on the back, underarms, shoulders, face, thighs and buttocks. Sometimes boils will emit an unpleasant smell.
Boils are generally caused by an infection of the hair follicles by Staphylococcus aureus or staph, a strain of bacteria that normally lives on the skin surface. It is thought that a tiny cut of the skin allows this bacterium to enter the follicles and cause an infection. This can happen during bathing or while using a razor.
People with immune system disorders, diabetes, poor hygiene or malnutrition (Vitamin A or E deficiency) are particularly susceptible to getting boils. However they may also occur in healthy, hygienic individuals. Hidradenitis suppurativa causes frequent boils. Boils in the armpits can sometimes be caused by anti-perspirant deodorants.
Most boils run their course within 4 to 10 days. For most people, self-care by applying a warm compress or soaking the boil in warm water can help alleviate the pain and hasten draining of the pus (colloquially referred to as “bringing the boil to a head”). Fire cupping can be utilized to facilitate this procedure. Once the boil drains, the area should be washed with antibacterial soap or antibacterial herbs (chickweed poultice) and bandaged well. For recurring cases, sufferers may benefit from diet supplements of Vitamin A and E.
In serious cases, prescription oral antibiotics such as dicloxacillin (Dynapen) or cephalexin (Keflex), or topical antibiotics, are commonly used. For patients allergic to penicillin-based drugs, erythromycin (E-base, Erycin) may also be used.
However, some boils are caused by a superbug known as community-acquired Methicillin-resistant Staphylococcus aureus, or CA-MRSA. Bactrim or other sulfa drugs must be prescribed relatively soon after boil has started to form. MRSA tends to increase the speed of growth of the infection.
Magnesium sulfate paste applied to the affected area can prevent the growth of bacteria and reduce boils by absorbing pus and drying up the lesion.
For most cases, there are no serious complications and a full recovery is expected.
Athlete’s foot, or tinea pedis, is a fungal infection of the skin of the foot, usually between the toes, caused by parasitic fungi.
The body normally hosts a variety of saprotrophic microorganisms, including bacteria and fungi. Some of these are useful to the body. Pathogenic or disease causing organisms or the overgrowth of saprotrophic ones can multiply rapidly and cause infection. Athlete’s foot is a layman’s description of a skin fungal infection. Fungal infections of the skin are called dermatophytosis. Dermatophytes may be spread from other humans (anthropophilic), animals (zoophilic) or may come from the soil (geophilic). Anthropophillic dermatophytes are restricted to human hosts and produce a mild, chronic inflammation. Zoophilic organisms are found primarily in animals and cause marked inflammatory reactions in humans who have contact with infected cats, dogs, cattle, horses, birds, or other animals. Geophilic species are usually recovered from the soil but occasionally infect humans and animals. They cause a marked inflammatory reaction, which limits the spread of the infection and may lead to a spontaneous cure but may also leave scars. Infections or infestations occur when dermatophytes grow and multiply in the skin.
Growth of the athlete’s foot fungus is promoted by a dark, warm, moist environment such as that found inside shoes. The fungi persist for a long time in the environment, facilitating transmission of the disease in communal areas such as locker rooms and showers.
Athlete’s foot causes scaling, flaking and itching of the affected skin. Blisters and cracked skin may also occur, leading to exposed raw tissue, pain, swelling, and inflammation. The infection can be spread to other areas of the body, such as the armpits, knees, elbows, and the groin, and usually is called by a different name once it spreads (such as jock itch or tinea cruris for an infection of the skin and groin respectively).
Since the fungus thrives in a moist warm environment keeping the feet dry and cool can cure the infection. It’s is recommended to wear open sandals, or even better, go barefoot as much as possible. However, avoid walking barefoot in warm moist environments since you may infect other people, and allowing your feet to stay wet can help the fungus grow.
Keep the feet clean – but make sure they are fully dry after washing them. This may require showering in the evening instead of the morning, and staying barefoot afterwards.
Change socks daily, and try to alternate shoes on different days, to allow the shoes to fully dry out.
Placebo controlled studies report that good foot hygiene alone can cure athlete’s foot even without medication in 30-40% of the cases.
The infection is often treated with topical antifungal agents such as miconazole, itraconazole, terbinafine and a keratolytic such as salicylic acid. Topical agents only clear the infection about 30% of the time and provide mycologic cures (absence of organisms) less than 15% of the time. The time line for cure may be long, often 45 days or longer. However, because the itching associated with the infection subsides quickly, patients may not complete the courses of therapy prescribed. Washing socks, underwear and bed clothes at 60C or 140F will also help prevent any reinfection.
Some topical applications such as Castellani’s Paint, often used for intertrigo, work well but in small selected areas. Carbol Fuscin Red dye used in this treatment like many other vital stains is both fungicidal and bacteriocidal; however, because of the staining are cosmetically undesirable. For many years gentian violet was also used for interdigital and other bacterial and fungal infections.
Oral treatment with griseofulvin was begun early in the 1950s. Because of the tendency to cause liver problems and to provoke aplastic anemia the drugs were used cautiously and sparingly. Over time it was found that those problems were due to the size of the crystal in the manufacturing process and microsize and now ultramicrosize crystals are available with few of the original side effects. Oral treatment provides long lasting mycologic cure.
If the fungal invader is not a dermatophyte but a yeast, other medications such as fluconazole may be used. Typically diflucan is used for candidal vaginal infections moniliasis but has been shown to be of benefit for those with cutaneous yeast infections as well. The most common of these infections occur in the web spaces (intertriginous) and at the base of the fingernail or toenail. The hall mark of these infections is a cherry red color surrounding the lesion and a yellow thick pus. Undecylenic acid (Castor oil derivative) is an effective fungicide for fungal skin infections such as athlete’s foot.
Users report instant relief from itching after topical application of Tea Tree Oil (Melaleuca Oil) or crocodile oil, allowing lesions to heal due to the cessation of scratching the itch.
Proponents of urine therapy claim that urine is very effective at killing athlete’s foot. Urea, the “active ingredient” in urine, is already used in many drugs and treatments made by pharmaceutical companies to treat athlete’s foot. This controversial treatment method recommends urinating on the infected area once a day in the shower. According to supporters, urine therapy not only kills existing fungi, it prevents new fungi from growing in the infected area.
One biochemist states that urea is only used to soften the outer layers of skin so that antifungal drugs can reach fungi below the surface, and that the urea must be concentrated and applied for a long period of time in order to be effective. According to another article about high-concentration urea cream, the compound is used to “dissolve proteins and as a denaturant. The ability of urea to macerate [tissue] has been attributed to a ‘proteolytic effect’, but others attribute the maceration to the hydrating properties of urea.”This use requires a high concentration of urea, up to 40%, and extended exposure. Urea itself without the presence of an additional antifungal drug is not referred to in scholarly literature as having antifungal properties. Thus, it is unlikely that urinating on one’s feet in the shower will significantly improve a case of athlete’s foot.
Acne (Acne Vulgaris)
Acne vulgaris is an inflammatory disease of the skin, caused by changes in the pilosebaceous units (skin structures consisting of a hair follicle and its associated sebaceous gland). Acne lesions are commonly referred to as pimples, spots or “zits”.
The condition is most common in puberty, especially among Western societies most likely due to a higher genetic predisposition. It is considered an abnormal response to normal levels of the male hormone testosterone. The response for most people diminishes over time and acne thus tends to disappear, or at least decrease, after one reaches their early twenties. There is, however, no way to predict how long it will take for it to disappear entirely, and some individuals will continue to suffer from acne decades later, into their thirties and forties and even beyond. Acne affects a large percentage of humans at some stage in life.
The term acne comes from a corruption of the Greek (acme in the sense of a skin eruption) in the writings of Aëtius Amidenus. The vernacular term bacne or backne is often used to indicate acne found specifically on one’s back.
The most common form of acne is known as “acne vulgaris”, meaning “common acne.” Excessive secretion of oils from the sebaceous glands accompanies the plugging of the pores with naturally occurring dead skin cells (corneocytes) blocking hair follicles. The accumulation of these corneocytes in the duct appears to be due to a failure of the normal keratinization process in the skin which usually leads to shedding of skin cells lining the pores. Oil secretions are said to build up beneath the blocked pore, providing a perfect environment for the skin bacteria Propionibacterium acnes and the lipophilic (oil/lipid-loving) yeast Malassezia to multiply uncontrollably. Under the microscope, however, there is no evidence of pooled trapped sebum. Indeed the oil percolates through the plugged duct onto the surface. In response to the bacterial and yeast populations, the skin inflames, producing the visible lesion. The face, chest, back, shoulders and upper arms are especially affected.
The typical acne lesions are: comedones, papules, pustules, nodules and inflammatory cysts. These are the more inflamed form of pus-filled or reddish bumps, even boil-like tender swellings. Non-inflamed ‘sebaceous cysts’, more properly called epidermoid cysts, occur either in association with acne or alone but are not a constant feature. After resolution of acne lesions, prominent unsightly scars may remain.
Aside from scarring, its main effects are psychological, such as reduced self-esteem and depression or suicide. Acne usually appears during adolescence, when people already tend to be most socially insecure. Early and aggressive treatment is therefore advocated to lessen the overall impact to individuals.
Causes of acne
Exactly why some people get acne and some do not is not fully known. It is known to be partly hereditary. Several factors are known to be linked to acne:
|Hormonal activity, such as menstrual cycles and puberty.|
|Stress, through increased output of hormones from the adrenal (stress) glands.|
|Hyperactive sebaceous glands, secondary to the three hormone sources above.|
|Accumulation of dead skin cells.|
|Bacteria in the pores, to which the body becomes ‘allergic’.|
|Skin irritation or scratching of any sort will activate inflammation.|
|Use of anabolic steroids.|
|Any medication containing halogens (iodides, chlorides, bromides), lithium, barbiturates, or androgens.|
|Exposure to high levels of chlorine compounds, particularly chlorinated dioxins, can cause severe, long-lasting acne, known as Chloracne.|
Traditionally, attention has focused mostly on hormone-driven over-production of sebum as the main contributing factor of acne. More recently, more attention has been given to narrowing of the follicle channel as a second main contributing factor. Abnormal shedding of the cells lining the follicle, abnormal cell binding (“hyperkeratinization”) within the follicle, and water retention in the skin (swelling the skin and so pressing the follicles shut) have all been put forward as important mechanisms. Several hormones have been linked to acne: the male hormones testosterone, dihydrotestosterone (DHT) and dehydroepiandrosterone sulfate (DHEAS), as well as insulin-like growth factor 1 (IGF-I). In addition, acne-prone skin has been shown to be insulin resistant.
Development of acne vulgaris in later years is uncommon, although this is the age group for Rosacea which may have similar appearances. True acne vulgaris in adults may be a feature of an underlying condition such as pregnancy and disorders such as polycystic ovary syndrome or the rare Cushing’s syndrome. Dermatologists are seeing more cases of menopause-associated acne as fewer women replace the natural anti-acne ovarian hormone estradiol whose production fails as women arrive at menopause. The lack of estradiol also causes thinning hair, hot flashes, thin skin, wrinkles, vaginal dryness, and predisposes to osteopenia and osteoporosis as well as triggering acne (known as acne climacterica in this situation).
Misconceptions about causes
There are many misconceptions and rumors about what does and does not cause the condition:
|Diet. One study suggested that chocolate, french fries, potato chips and sugar, among others, affect acne. A high GI (glycemic index) diet that causes sharp rises in blood sugar worsens acne. If this study’s conclusions are verified then a low GI diet may help acne, but a recent review of somewhat dated scientific literature cannot affirm either way. A recent study, based on a survey of 47,335 women, did find a positive epidemiological association between acne and consumption of partially skimmed milk, instant breakfast drink, sherbet, cottage cheese and cream cheese. The researchers hypothesize that the association may be caused by hormones (such as several sex hormones and bovine IGF-I) present in cow milk. Although the association between milk and acne has been definitively shown, the ingredient in the milk responsible for the acne is still unclear.Most dermatologists are awaiting confirmatory research linking diet and acne but some support the idea that acne sufferers should experiment with their diets, and refrain from consuming such fare if they find such food affects the severity of their acne. Seafood, on the other hand, may contain relatively high levels of iodine. Iodine is known to make existing acne worse but there is probably not enough to cause an acne outbreak. Still, people who are prone to acne may want to avoid excessive consumption of foods high in iodine.It has also been suggested that there is a link between a diet high in refined sugars and other processed foods and acne. According to this hypothesis, the startling absence of acne in non-westernized societies could be explained by the low glycemic index of these cultures’ diets. Others have cited possible genetic reasons for there being no acne in these populations, but similar populations shifting to Western diets do develop acne. Note also that the populations studied consumed no milk or other dairy products. Further research is necessary to establish whether a reduced consumption of high-glycemic foods (such as soft drinks, sweets, white bread) can significantly alleviate acne, though consumption of high-glycemic foods should in any case be kept to a minimum, for general health reasons. Avoidance of ‘junk food’ with its high fat and sugar content is also recommended . On the other hand there is no evidence that fat alone makes skin oilier or acne worse.|
|Deficient personal hygiene. Acne is not caused by dirt. This misconception probably comes from the fact that comedones look like dirt stuck in the openings of pores. The black color is simply not dirt but compact keratin. In fact, the blockages of keratin that cause acne occur deep within the narrow follicle channel, where it is impossible to wash them away. These plugs are formed by the failure of the cells lining the duct to separate and flow to the surface in the sebum created there by the body. The bacteria involved are normally present on the skin but they multiply preferentially in the very low oxygen environment of these plugged pores. Very little variation among individuals with acne is due to hygiene. Anything beyond very gentle cleansing can actually worsen existing lesions and even encourage new ones by damaging or overdrying skin. On the other hand some commercial cleansers have been shown to help empty plugged pores.|
|Sex. Common myths state that masturbation causes acne and, conversely, that celibacy or sexual intercourse can cure it. Though it has been widely accepted that these are not true due to lack of scientific study on the subject, it is also important to note sexual activity has been observed to result in hormonal spikes, which has been linked to acne.|
Timeline of acne treatment
The history of acne reaches back to the dawn of recorded history. In Ancient Egypt, it is recorded that several pharaohs were acne sufferers. From Ancient Greece comes the English word ‘acne’ (meaning ‘point’ or ‘peak’). Acne treatments are also of considerable antiquity:
|Ancient Rome: bathing in hot, and often sulfurous, mineral water was one of the few available acne treatments. One of the earliest texts to mention skin problems is De Medicina by the Roman writer Celsus.|
|1800s: Nineteenth century dermatologists used sulphur in the treatment of acne. It was believed to dry the skin.|
|1920s: Benzoyl Peroxide is used.|
|1930s: Laxatives were used as a cure for what were known as ‘chastity pimples’.|
|1950s: When antibiotics became available, it was discovered that they had beneficial effects on acne. They were taken orally to begin with. Much of the benefit was not from killing bacteria but from the anti-inflammatory effects of tetracycline and its relatives. Topical antibiotics became available later.|
|1960s: Tretinoin (original Trade Name Retin A) was found effective for acne. This preceeded the development of oral isotretinoin (sold as Accutane and Roaccutane) since the early 1980s.|
|1990s: Laser treatment introduced.|
|2000s: Blue/red light therapy.|
Some old treatments, like laxatives, have fallen into disuse but others, like spas, are recovering their popularity.
There are many products sold for the treatment of acne, many of them without any scientifically-proven effects. Generally speaking successful treatments give little improvement within the first week or two; and then the acne decreases over approximately 3 months, after which the improvement starts to flatten out. Treatments that promise improvements within 2 weeks are likely to be largely disappointing. Short bursts of cortisone, quick bursts of antibiotics and many of the laser therapies offer a quick reduction in the redness, swelling and inflammation when used correctly, but none of these empty the pore of all the materials that trigger the inflammation. Emptying the pores takes months.
Modes of improvement are not necessarily fully understood but in general treatments are believed to work in at least 4 different ways (with many of the best treatments providing multiple simultaneous effects):
|normalizing shedding into the pore to prevent blockage|
|killing P. acnes|
A combination of treatments can greatly reduce the amount and severity of acne in many cases. Those treatments that are most effective tend to have greater potential for side effects and need a greater degree of monitoring, so a step-wise approach is often taken. Many people consult with doctors when deciding which treatments to use, especially when considering using any treatments in combination. There are a number of treatments that have been proven effective:
Exfoliating the skin
This can be done either mechanically, using an abrasive cloth or a liquid scrub, or chemically. Common chemical exfoliating agents include salicylic acid and glycolic acid, which encourage the peeling of the top layer of skin to prevent a build-up of dead skin cells which combine with skin oil to block pores. It also helps to unblock already clogged pores. Note that the word “peeling” is not meant in the visible sense of shedding, but rather as the destruction of the top layer of skin cells at the microscopic level. Depending on the type of exfoliation used, some visible flaking is possible. Moisturizers and anti-acne topicals containing chemical exfoliating agents are commonly available over-the-counter. Mechanical exfoliation is less commonly used as many benefits derived from the exfoliation are negated by the act of mechanically rubbing and irritating the skin.
Widely available OTC bactericidal products containing benzoyl peroxide may be used in mild to moderate acne. The gel or cream containing benzoyl peroxide is rubbed, twice daily, into the pores over the affected region. Bar soaps or washes may also be used and vary from 2 to 10% in strength. In addition to its therapeutic effect as a keratolytic (a chemical that dissolves the keratin plugging the pores) benzoyl peroxide also prevents new lesions by killing P.acnes. Unlike antibiotics, benzoyl peroxide has the advantage of being a strong oxidizer (essentially a mild bleach) and thus does not appear to generate bacterial resistance. However, it routinely causes dryness, local irritation and redness. A sensible regimen may include the daily use of low-concentration (2.5%) benzoyl peroxide preparations, combined with suitable non-comedogenic moisturizers to help avoid overdrying the skin.
Care must be taken when using benzoyl peroxide, as it can very easily bleach any fabric or hair it comes in contact with.
Externally applied antibiotics such as erythromycin, clindamycin, Stiemycin or tetracycline aim to kill the bacteria that are harbored in the blocked follicles. Whilst topical use of antibiotics is equally as effective as oral, this method avoids possible side effects of stomach upset or drug interactions (e.g. it will not affect the oral contraceptive pill), but may prove awkward to apply over larger areas than just the face alone.
Oral antibiotics used to treat acne include erythromycin or one of the tetracycline antibiotics (tetracycline, the better absorbed oxytetracycline, or one of the once daily doxycycline, minocycline or lymecycline). Trimethoprim is also sometimes used (off-label use in UK). However, reducing the P. acnes bacteria will not, in itself, do anything to reduce the oil secretion and abnormal cell behaviour that is the initial cause of the blocked follicles. Additionally the antibiotics are becoming less and less useful as resistant P. acnes are becoming more common. Acne will generally reappear quite soon after the end of treatment—days later in the case of topical applications, and weeks later in the case of oral antibiotics.
In females, acne can be improved with hormonal treatments. The common combined oestrogen/progestogen methods of hormonal contraception have some effect, but the anti-testosterone, Cyproterone, in combination with an oestrogen (Diane 35) is particularly effective at reducing androgenic hormone levels. Diane-35 is not available in the USA, but a newer oral contraceptive containing the progestin drospirenone is now available with fewer side effects than Diane 35 / Dianette. Both can be used where blood tests show abnormally high levels of androgens, but are effective even when this is not the case. Along with this, treatment with low dose spironolactone can have anti-androgenetic properties, especially in patients with polycystic ovarian syndrome.
If a pimple is large and/or does not seem to be affected by other treatments, a dermatologist may administer an injection of cortisone directly into it, which will usually reduce redness and inflammation almost immediately. This has the effect of flattening the pimple, thereby making it easier to cover up with makeup, and can also aid in the healing process. Side effects are minimal, but may include a temporary whitening of the skin around the injection point. This method also carries a much smaller risk of scarring than surgical removal.
Normalizing the follicle cell lifecycle. A group of medications for this are topical retinoids such as tretinoin (brand name Retin-A), adapalene (brand name Differin) and tazarotene (brand name Tazorac). Like isotretinoin, they are related to vitamin A, but they are administered as topicals and generally have much milder side effects. They can, however, cause significant irritation of the skin. The retinoids appear to influence the cell creation and death lifecycle of cells in the follicle lining. This helps prevent the hyperkeratinization of these cells that can create a blockage. Retinol, a form of vitamin A, has similar but milder effects and is used in many over-the-counter moisturizers and other topical products. Effective topical retinoids have been in use over 30 years but are available only on prescription so are not as widely used as the other topical treatments. Topical retinoids often cause an initial flare up of acne within a month or so, which can be severe.
Reducing the secretion of oils from the glands. This is done by a daily oral intake of vitamin A derivatives like isotretinoin (marketed as Accutane, Sotret, Claravis) over a period of 4-6 months. It is believed that isotretinoin works primarily by reducing the secretion of oils from the glands, however some studies suggest that it affects other acne-related factors as well. Isotretinoin has been shown to be very effective in treating severe acne and can either improve or clear well over 80% of patients. The drug has a much longer effect than anti-bacterial treatments and will often cure acne for good. The treatment requires close medical supervision by a dermatologist because the drug has many known side effects (many of which can be severe). About 25% of patients may relapse after one treatment. In those cases, a second treatment for another 4-6 months may be indicated to obtain desired results. It is often recommended that one lets a few months pass between the two treatments, because the condition can actually improve somewhat in the time after stopping the treatment and waiting a few months also gives the body a chance to recover. Occasionally a third or even a fourth course is used, but the benefits are often less substantial. The most common side effects are dry skin and occasional nosebleeds (secondary to dry nasal mucosa). Oral retinoids also often cause an initial flare up of acne within a month or so, which can be severe. There are reports that the drug has damaged the liver of patients. For this reason, it is recommended that patients have blood samples taken and examined before and during treatment. In some cases, treatment is terminated due to elevated liver enzymes in the blood, which might be related to liver damage. Others claim that the reports of permanent damage to the liver are unsubstantiated, and routine testing is considered unnecessary by some dermatologists. Blood triglycerides also need to be monitored. However, routine testing are part of the official guidelines for the use of the drug in many countries. Some press reports suggest that isotretinoin may cause depression but as of September 2005 there is no agreement in the medical literature as to the risk. The drug also causes birth defects if women become pregnant while taking it or take it while pregnant. For this reason, female patients are required to use two separate forms of birth control or vow abstinence while on the drug. Because of this, the drug is supposed to be given as a last resort after milder treatments have proven insufficient. Restrictive rules (see iPledge Program) for use were put into force in the USA beginning in March 2006 to prevent misuse. This has occasioned widespread editorial comment.
Blue and red light
It has long been known that short term improvement can be achieved with sunlight. However, studies have shown that sunlight worsens acne long-term, presumably due to UV damage. More recently, visible light has been successfully employed to treat acne (Phototherapy) – in particular intense blue light generated by purpose-built fluorescent lighting, dichroic bulbs, LEDs or lasers. Used twice weekly, this has been shown to reduce the number of acne lesions by about 64%; and is even more effective when applied daily. The mechanism appears to be that a porphyrin (Coproporphyrin III) produced within P. acnes generates free radicals when irradiated by blue light. Particularly when applied over several days, these free radicals ultimately kill the bacteria.Since porphyrins are not otherwise present in skin, and no UV light is employed, it appears to be safe, and has been licensed by the U.S. FDA. The treatment apparently works even better if used with red visible light (660 nanometer) resulting in a 76% reduction of lesions after 3 months of daily treatment for 80% of the patients; and overall clearance was similar or better than benzoyl peroxide. Unlike most of the other treatments few if any negative side effects are typically experienced, and the development of bacterial resistance to the treatment seems very unlikely. After treatment, clearance can be longer lived than is typical with topical or oral antibiotic treatments; several months is not uncommon. The equipment or treatment, however, is relatively new and reasonably expensive.
In addition, basic science and clinical work by dermatologists Yoram Harth and Alan Shalita and others has produced evidence that intense blue/violet light (405-425 nanometer) can decrease the number of inflammatory acne lesion by 60-70% in 4 weeks of therapy, particularly when the P.acnes is pretreated with delta-aminolevulinic acid (ALA), which increases the production of porphyrins. However this photodynamic therapy is controversial and apparently not published in a peer reviewed
Less widely used treatments:
|Azelaic acid – (brand names Azelex, Finevin, Skinoren) is suitable for mild, comedonal acne.|
|Zinc – Orally administered zinc gluconate has been shown to be effective in the treatment of inflammatory acne, although less so than tetracyclines.|
|Tea Tree Oil – (Melaleuca Oil) has been used with some success, and has been shown to be an effective anti-inflammatory in skin infections.|
|Heat therapy – Zeno product uses heat at a specific temperature to kill bacteria and to treat mild to moderate acne.|
|Niacinamide – (Vitamin B3) used topically in the form of a gel, has been shown in a 1995 study to be more effective than a topical antibiotic used for comparison, as well as having less side effects. Topical niacinamide is available both on prescription and over-the-counter. Some users choose to make their own at home, mixing together crushed niacinamide pills with aloe vera gel. The property of topical niacinamide’s benefit in treating acne seems to be it’s anti-inflammatory nature. It is also purported to result in increased synthesis of collagen, keratin, involucrin and flaggrin.|
|In some cases, people bathing in salt water (pure from the ocean) noticed lessened redness and decreased size in their acne.|
Laser surgery has been in use for some time to reduce the scars left behind by acne, but research is now being done on lasers for prevention of acne formation itself. The laser is used to produce one of the following effects:
|to burn away the follicle sac from which the hair grows|
|to burn away the sebaceous gland which produces the oil|
|to induce formation of oxygen in the bacteria, killing them|
Since lasers and intense pulsed light sources cause thermal damage to the skin there are concerns that laser or intense pulsed light treatments for acne will induce hyperpigmented macules (spots) or cause long term dryness of the skin. As of 2005, this is still mostly at the stage of medical research rather than established treatment.
Because acne appears to have a significant hereditary link, there is some expectation that cheap whole-genome DNA sequencing may help isolate the body mechanisms involved in acne more precisely, possibly leading to a more satisfactory treatment. (Crudely put, take the DNA of large samples of people with significant acne and of people without, and let a computer search for statistically strong differences in genes between the two groups). However, as of 2005 DNA sequencing is not yet cheap and all this may still be decades off. It is also possible that gene therapy could be used to alter the skin’s DNA. Phage therapy has been proposed to kill P. acnes, and has seen some use, particularly in Georgia.
Preferred treatments by types of acne vulgaris
|Comedonal (non-inflammatory) acne: local treatment with azelaic acid, salicylic acid, topical retinoids, benzoyl peroxide.|
|Mild papulo-pustular (inflammatory) acne: benzoyl peroxide or topical retinoids, topical antibiotics (such as erythromycin).|
|Moderate inflammatory acne: benzoyl peroxide or topical retinoids combined with oral antibiotics (tetracyclines). Isotretinoin is an option.|
|Severe inflammatory acne, nodular acne, acne resistant to the above treatments: isotretinoin, or contraceptive pills with cyproterone for females with virilization or drospirenone.|
Most physicians state that topical retinoids are the preferred treatment for all forms of acne vulgaris.
Severe acne often leaves small scars where the skin gets a “volcanic” shape. Acne scars are difficult and expensive to treat, and it is unusual for the scars to be successfully removed completely. In those cases, acne scar treatment may be appropriate.
The psychological and emotional effects caused by acne scars can be as devastating to one’s confidence as the acne itself.
Acne scars generally fall into two categories: physical scars and pigmented scars. Physical acne scars are often referred to as “Icepick” scars. This is because the scars tend to cause an indentation in the skins surface. Pigmented scars is a slightly misleading term, suggesting a change in the skin’s pigmentation. This is not true. Pigmented scars are usually the result of nodular or cystic acne (the painful ‘bumps’ lying under the skin). They often leave behind an inflamed red mark. Often, the pigmentation scars can be avoided simply by avoiding aggravation of the nodule or cyst. When sufferers try to ‘pop’ cysts or nodules, pigmentation scarring becomes significantly worse, and may even bruise the affected area. Pigmentation scars often fade with time, and those who suffered from acne before, and have developed scars are generally relieved that the acne has gone, and emotional effects of acne scars tend to be less distressing.
Acne scars are unsightly, and it is for this reason they can be psychologically and emotionally distressing. However, there are a range of treatments available. If acne scars are causing severe psychological distress, social withdrawal and/or emotional ill-health, a physician should be contacted.
Blackheads and Pimples
A blackhead (technically known as an open comedo) is a yellowish or blackish bump or plug on the skin. An open comedo or blackhead is a type of acne vulgaris. It is caused by excess oils that have accumulated in the sebaceous gland’s duct. Blackheads are typically caused by excessive oil and makeup. While the contents inside may look dark, it is not dirt; the substance found in these bumps mostly consists of keratin and modified sebum (an oily secretion of the sebaceous gland).
Possible factors that cause blackheads include:
|Excess dead cells blocking the opening to the pore|
|Excess production of facial oil|
|Improper cleansing routine, facial oil not being removed|
|Excess scrubbing of the skin (Scrubs)|
|Use of products/makeup (foundations, sunscreens, and moisturizers) that may contain too much oil|
|Use of low quality facial cleansing products|
|Removal of the skin bumps or plugs by your dermatologist or certified beautician or by oneself (if possessing the skills to do so).|
|Use of exfoliants such as Beta Hydroxy Acid (salicylic acid).|
|Application of benzoyl peroxide.|
|Phototherapy with blue/red light.|
|Frequent, thorough cleansing of the skin.|
|Using a steel blackhead remover tool called a comedo extractor.|
|The strategic application of pressure around the affected area. Most commonly exerted by the index fingers of both hands.|
|In cases of severe recalcitrant nodular acne, by the use of the drug Accutane (isotretinoin).|
|Using one Q-tip in each hand to push out black/whiteheads – this way you do not touch and spread the bacteria and you do not scratch your face using your bare fingers.|
From the greek “pimplhsi”: fills or infects
A pimple is a type of skin lesion that is caused by inflamed and/or obstructed pores. The most common cause of pimples is acne.
A pimple is a result of a blockage of the skin’s pore.
Inside the pore are sebaceous glands which produce sticky sebum. When the outer layers of skin shed (as it does continuously), the dead skin cells left behind may become ‘glued’ together by the sticky sebum. This causes a blockage in the pore. The sebaceous glands produce more sebum which builds up behind the blockage, and this sebum harbors bacteria (P.Acnes bacteria). Since the body’s natural defense against bacteria is primarily phagocytes (white blood cells), these rush to the site behind the blockage (where the bacteria are). This is what gives some pimples the ‘whiteheads’ (unless the Phagocytes are deeper in the skin, which means you can’t see the ‘white’ caused by them). The white blood cells then destroy (by phagocytosis) the bacteria to prevent infection.
Common over-the-counter medications for pimples are Benzoyl peroxide and/or salicylic acid. Both medications can be found in many creams and gels used to treat acne through topical application. Both medications help skin slough off easier, which helps to remove bacteria faster. A regimen of keeping the affected skin area clean plus the regular application of these topical medications is usually enough to keep acne under control, if not at bay altogether. 1-2% of the population is allergic to Benzoyl peroxide treatments.
Severe acne usually indicates the necessity of prescription medication to treat pimples. Prescription medications used to treat acne include isotretinoin or Accutane, which is a retinoid. Historically, prescription antibiotics such as tetracyclines and erythromycin were used to treat acne. While they were more effective than topical applications of benzoyl peroxide, the bacteria eventually grew resistant to the antibiotics and the treatments became less and less effective. Also, antibiotics had more side effects than topical applications (erythromycin can cause stomach cramps).
Commercial products include Murad Acne Complex® and Proactiv Solution®. Both of these products are subscription-based services where you sign up with the company and receive their products (usually on a monthly basis) at various prices.
See the treatment of Acne Vulgaris for more information on treating pimples.
Keratosis Pilaris (KP) is a very common genetic follicular condition that is manifested by the appearance of rough bumps on the skin and hence colloquially referred to as “chicken skin”. It most often appears on the back and outer sides of the upper arms (though the lower arms can also be affected), and can also occur on the thighs and tops of legs, flanks, buttocks or any body part except glabrous skin (like the palms or soles of feet). Less commonly, lesions appear on the face and may be mistaken for acne.
Worldwide, KP affects an estimated 40 to 50% of the adult population and approximately 50 to 80% of all adolescents. It is more common in women than in men. Varying in degree, cases of KP can range from minimal to severe.
There are several different types of Keratosis Pilaris, including Keratosis Pilaris Rubra (red, inflamed bumps), Alba (rough, bumpy skin with no irritation), Rubra Faceii (reddish rash on the cheeks) and related disorders.
Many people with Keratosis Pilaris do not know they have it (if the condition is mild). While KP resembles goose bumps, it is characterized by the appearance of small rough bumps on the skin. As a result, it is often confused with acne.
Keratosis Pilaris occurs as excess keratin, a natural protein in the skin, accumulates within the hair follicles forming hard plugs (process known as hyperkeratinization). Bearing only cosmetic consequence, the condition most often appears as a proliferation of tiny hard bumps that are seldom sore or itchy. Though people with Keratosis Pilaris experience this condition year round, it’s during the colder months when moisture levels in the air are lower that the problem can become exacerbated and the “goose bumps” are apt to look and feel more pronounced in color and texture.
There is no known cure for Keratosis Pilaris, though it may improve with age and even disappear completely in adulthood; however, some will show signs of Keratosis Pilaris for life.
Treatments are largely symptomatic and must be repeated. Regardless, exfoliation, intensive moisturizing cremes, lac-hydrin, and medicated lotions containing alpha hydroxy acids or urea may be used to temporarily improve the appearance and texture of affected skin.
Scratching and picking at KP bumps causes them to redden (if they do not already appear red), and in many cases will cause bleeding. Excessive picking can lead to scarring.
Wearing clothing that is looser around the affected areas can also help reduce the marks, as constant chafing from clothing (such as tight fitting jeans) is similar to repeatedly scratching the bumps.
Many KP bumps contain an ingrown hair that has coiled. This is a result of the keratinized skin “capping off” the hair follicle, preventing the hair from exiting. Instead, the hair grows inside the follicle, often encapsulated, and can be removed if the bump is picked or squeezed (which can lead to scarring.)
Rosacea is a common but often misunderstood condition that is estimated to affect over 45 million people worldwide. It affects fair-skinned people of mostly north-western European descent, and has been nicknamed the ‘curse of the Celts’ by some in Ireland. It begins as erythema (flushing and redness) on the central face and across the cheeks, nose, or forehead but can also less commonly affect the neck and chest. As rosacea progresses, other symptoms can develop such as semi-permanent erythema, telangiectasia (dilation of superficial blood vessels on the face), red domed papules (small bumps) and pustules, red gritty eyes, burning and stinging sensations, and in some advanced cases, a red lobulated nose (rhinophyma). The disorder can be confused and co-exist with acne vulgaris and/or seborrheic dermatitis. Rosacea affects both sexes, but is almost three times more common in women, and has a peak age of onset between 30 and 60. The presence of rash on the scalp or ears suggests a different or co-existing diagnosis, as rosacea is primarily a facial diagnosis.
There are four identified rosacea subtypes and patients may have more than one subtype present.
|1.||Erythematotelangiectatic rosacea: Permanent redness (erythema) with a tendency to flush and blush easily. It is also common to have small blood vessels visible near the surface of the skin (telangiectasias) and possibly burning or itching sensations.|
|2.||Papulopustular rosacea: Some permanent redness with red bumps (papules) with some pus filled (pustules) (which typically last 1-4 days); this subtype can be easily confused with acne.|
|3.||Phymatous rosacea: This subtype is most commonly associated with rhinophyma, an enlargenent of the nose. Symptoms include thickening skin, irregular surface nodularities, and enlargement. Phymatous rosacea can appear on the nose, chin, forehead, cheeks, and ears. Small blood vessels visible near the surface of the skin (telangiectasias) may be present.|
|4.||Ocular rosacea: Red, dry and irritated eyes and eyelids. Some other symptoms include foreign body sensations, itching and burning.|
Rosacea sufferers often report periods of depression stemming from cosmetic disfigurement, painful burning sensations, and decreases in quality of life.
The precise pathogenesis of rosacea still remains unknown, but most experts believe that rosacea is a disorder where the blood vessels become damaged when repeatedly dilated by stimuli. The damage causes the vessels to dilate too easily and stay dilated for longer periods of time or remain permanently dilated, resulting in flushing and redness. Immune cells and inflammatory mediators can leak from the microvascular bed causing inflammatory pustules and papules, especially with those with papulopustular rosacea.
Rosacea has a hereditary component and those that are fair-skinned of European or Celtic ancestry have a higher genetic predisposition to developing it. Women are more commonly affected but when men develop rosacea it tends to be more severe. People of all ages can get rosacea but there is a higher instance in the 30-50 age group. The first signs of rosacea are said to be persisting redness due to exercise, changes in temperature, and cleansing.
Triggers that cause episodes of flushing and blushing play a part in the development of rosacea. Exposure to temperature extremes can cause the face to become flushed as well as strenuous exercise, heat from sunlight, severe sunburn, stress, cold wind, moving to a warm or hot environment from a cold one such as heated shops and offices during the winter. There are also some foods and drinks that can trigger flushing, these include alcohol, foods and beverages containing caffeine, foods high in histamine and spicy food.
Certain medications and topical irritants can quickly progress rosacea. If redness persists after using a treatment then it should be stopped immediately. Some acne and wrinkle treatments that have been reported to cause rosacea include microdermabrasion, chemical peels, high dosages of isotretinoin, benzoyl peroxide and tretinoin. Steroid induced rosacea is the term given to rosacea caused by the use of topical or nasal steroids. These steroids are often prescribed for seborrheic dermatitis. Dosage should be slowly decreased and not immediately stopped to avoid a flare up.
Studies of rosacea and demodex mites have revealed that some people with rosacea have increased numbers of the mite, especially those with steroid induced rosacea. When large numbers are present they may play a role along with other triggers.
It has also been suggested that rosacea might be a neurological disorder resulting from hypersensitization of sensory neurons following activation of the plasma kallikrein-kinin system by exposure to intestinal bacteria in the digestive tract.
Treating rosacea varies from patient to patient depending on severity and subtypes. Dermatologists are recommended to take a subtype-directed approach to treating rosacea patients.
Trigger avoidance can help reduce the onset of rosacea but alone will not normally cause remission for all but mild cases. The National Rosacea Society recommends that a diary be kept to help identify and reduce triggers.
It is important to have a gentle skin cleansing regimen using non-irritating cleansers. Protection from the sun is important and daily use of a sunscreen of at least SPF 15 containing a physical blocker such as zinc oxide or titanium dioxide is advised.
Oral tetracycline antibiotics (tetracycline, doxycycline, minocycline) and topical antibiotics such as metronidazole are usually the first line of defense prescribed by doctors to relieve papules, pustules, inflammation and some redness. Oral antibiotics may also help to relieve symptoms of ocular rosacea. If papules and pustules persist, then sometimes isotretinoin can be prescribed. Isotretinoin has many side effects and is normally used to treat severe acne but in low dosages is proven to be effective against papulopustular and phymatous rosacea.
The treatment of flushing and blushing has been attempted by means of the centrally-acting agonist clonidine, but there is no evidence whatsoever that this is of any benefit. The same is true of the beta-blockers nadolol and propanolol. If flushing occurs with red wine consumption, then complete avoidance helps. There is no evidence at all that antihistamines are of any benefit in rosacea.
People who develop infections of the eyelids must practice frequent eyelid hygiene. Daily scrubbing the eyelids gently with diluted baby shampoo or an over-the-counter eyelid cleaner and applying warm (but not hot) compresses several times a day is recommended.
Dermatological vascular laser (single wavelength) or Intense Pulsed Light (broad spectrum) machines offer one of the best treatments for rosacea, in particular the erythema (redness) of the skin. They use light to penetrate the epidermis to target the capillaries in the dermis layer of the skin. The light is absorbed by oxy-hemoglobin which heat up causing the capillary walls to heat up to 70şC, damaging them, causing them to be absorbed by the body’s natural defense mechanism.
CO2 lasers can be used to remove excess tissue caused by phymatous rosacea. CO2 lasers emit a wavelength that is absorbed directly by the skin. The laser beam can be focused into a thin beam and used as a scalpel or defocused and used to vaporize tissue.
Famous people with Rosacea include:
|J. P. Morgan|
|Diana, Princess of Wales|
|W. C. Fields|
|Melanoma is a malignant tumor of melanocytes and, less frequently, of the eye. While it represents one of the rarer forms of skin cancer, melanoma underlies the majority of skin cancer-related deaths. Despite many years of intensive laboratory and clinical research, the sole effective cure is surgical resection of the primary tumor before it achieves a thickness of greater than 1 mm.Melanoma of the skin accounts for 160,000 new cases worldwide each year, and is more frequent in white men. It is particularly common in white populations living in sunny climates. According to the WHO Report about 48,000 deaths worldwide due to malignant melanoma are registered annually.
The diagnosis of melanoma requires experience, as early stages may look identical to harmless moles or not have any color at all. Moles that are irregular in color or shape are suspicious of a malignant melanoma or a premalignant lesion.
The treatment includes surgical removal of the tumor; adjuvant treatment; chemo- and immunotherapy, or radiation therapy.
Although melanoma is not a new disease, evidence for its occurrence in antiquity is rather scarce. However, one example lies in a 1960s examination of nine Peruvian Inca mummies, radiocarbon dated to be approximately 2400 years old, which showed apparent signs of melanoma: melanotic masses in the skin and diffuse metastases to the bones.
John Hunter is reported to be the first to operate on metastatic melanoma in 1787. Although not knowing precisely what it was, he described it as a “cancerous fungous excrescence”. The excised tumor was preserved in the Hunterian Museum of the Royal College of Surgeons of England. It was not until 1968 that microscopic examination of the specimen revealed it to be an example of metastatic melanoma.
The French physician René Laennec was the first to describe melanoma as a disease entity. His report was initially presented during a lecture for the Faculté de Médecine de Paris in 1804 and then published as a bulletin in 1806. The first English language report of melanoma was presented by an English general practitioner from Stourbridge, William Norris in 1820. In his later work in 1857 he remarked that there is a familial predisposition for development of melanoma (Eight Cases of Melanosis with Pathological and Therapeutical Remarks on That Disease). American physician, Dr. Roger Turkington, discovered the human melanoma gene.
The first formal acknowledgement that advanced melanoma as untreatable came from Samuel Cooper in 1840. He stated that the ‘… only chance for benefit depends upon the early removal of the disease … More than one and a half centuries later this situation remains largely unchanged.
Generally, an individual’s risk for developing melanoma depends on two groups of factors: intrinsic and environmental. “Intrinsic” factors are generally an individual’s family history and inherited genotype, while the most relevant environmental factor is sun exposure.
Epidemiologic studies suggest that exposure to ultraviolet radiation (UVA and UVB) is one of the major contributors to the development of melanoma. UV radiation causes damage to the DNA of cells, which when unrepaired can create mutations in the cell’s genes. When the cell divides, these mutations are propagated to new generations of cells. If the mutations occur in oncogenes or tumor suppressor genes, the rate of mitosis in the mutation-bearing cells can become uncontrolled, leading to the formation of a tumor. Occasional extreme sun exposure (resulting in “sunburn”) is causally related to melanoma. Those with more chronic long term exposure (outdoor workers) may develop protective mechanisms. Melanoma is most common on the back in men and on legs in women (areas of intermittent sun exposure) and is more common in indoor workers than outdoor workers (in a British study). Other factors are mutations in or total loss of tumor suppressor genes. Use of sunbeds (with deeply penetrating UVA rays) has been linked to the development of skin cancers, including melanoma.
Possible significant elements in determining risk include the intensity and duration of sun exposure, the age at which sun exposure occurs, and the degree of skin pigmentation. Exposure during childhood is a more important risk factor than exposure in adulthood. This is seen in migration studies in Australia where people tend to retain the risk profile of their country of birth if they migrate to Australia as an adult. Individuals with blistering or peeling sunburns (especially in the first twenty years of life) have a significantly greater risk for melanoma.
Fair and red-headed people, persons with multiple atypical nevi or dysplastic nevi and persons born with giant congenital nevi are at increased risk.
A family history of melanoma greatly increases a person’s risk because mutations in CDKN2A, CDK4 and several other genes have been found in melanoma-prone families. Patients with a history of one melanoma are at increased risk of developing a second primary tumor.
The incidence of melanoma has increased in the recent years, but it is not clear to what extent changes in behavior, in the environment, or in early detection are involved.
Familial melanoma is genetically heterogeneous, and loci for familial melanoma have been identified on the chromosome arms 1p, 9p and 12q. Multiple genetic events have been related to the pathogenesis of melanoma. The multiple tumor suppressor 1 (CDKN2A/MTS1) gene encodes p16INK4a – a low-molecular weight protein inhibitor of cyclin-dependent protein kinases (CDKs) – which has been localized to the p21 region of human chromosome 9.
Minimizing exposure to sources of ultraviolet radiation (the sun and sunbeds), following sun protection measures and wearing sun protective clothing (long-sleeved shirts, long trousers, and broad-brimmed hats.) can offer protection. Using a sunscreen with an SPF rating of 30 or better on exposed areas has preventive effect.
To prevent or detect melanomas (and increase survival rates), it is recommended to learn what they look like (see “ABCDE” mnemonic below), to be aware of moles and check for changes (shape, size, color, itching or bleeding) and to show any suspicious moles to a doctor with an interest and skills in skin malignancy.
A popular method for remembering the signs and symptoms of melanoma is the mnemonic “ABCDE“:
People with a personal or family history of skin cancer or of dysplastic nevus syndrome (multiple atypical moles) should see a dermatologist at least once a year to be sure they are not developing melanoma.
Moles that are irregular in color or shape are suspicious of a malignant or a premalignant melanoma. Following a visual examination and a dermatoscopic exam (an instrument that illuminates a mole, revealing its underlying pigment and vascular network structure), the doctor may biopsy the suspicious mole. If it is malignant, the mole and an area around it needs excision. This may require a referral to a surgeon or dermatologist.
The diagnosis of melanoma requires experience, as early stages may look identical to harmless moles or not have any color at all. Where any doubt exists, the patient will be referred to a specialist dermatologist. Beyond this expert knowledge a biopsy performed under local anesthesia is often required to assist in making or confirming the diagnosis and in defining the severity of the melanoma.
Excisional biopsy is the management of choice; this is where the suspect lesion is totally removed with an adequate ellipse of surrounding skin and tissue. The biopsy will include the epidermal, dermal, and subcutaneous layers of the skin, enabling the histopathologist to determine the depth of penetration of the melanoma by microscopic examination. This is described by Clark’s level (involvement of skin structures) and Breslow’s depth (measured in millimeters).
If an excisional biopsy is not possible in certain larger pigmented lesions, a punch biopsy may by performed by a specialist hospital doctor, using a surgical punch (an instrument similar to a tiny cookie cutter with a handle, with an opening ranging in size from 1 to 6 mm). The punch is used to remove a plug of skin (down to the subcutaneous layer) from a portion of a large suspicious lesion, for histopathological examination.
Lactate dehydrogenase (LDH) tests are often used to screen for metastases, although many patients with metastases (even end-stage) have a normal LDH; extraordinarily high LDH often indicates metastatic spread of the disease to the liver. It is common for patients diagnosed with melanoma to have chest X-rays and an LDH test, and in some cases CT, MRI, PET and/or PET/CT scans. Although controversial, sentinel lymph node biopsies and examination of the lymph nodes are also performed in patients to assess spread to the lymph nodes.
Sometimes the skin lesion may bleed, itch, or ulcerate, although this is a very late sign. A slow-healing lesion should be watched closely, as that may be a sign of melanoma. Be aware also that in circumstances that are still poorly understood, melanomas may “regress” or spontaneously become smaller or invisible – however the malignancy is still present. Amelanotic (colorless or flesh-colored) melanomas do not have pigment and may not even be visible. Lentigo maligna, a superficial melanoma confined to the topmost layers of the skin (found primarily in older patients) is often described as a “stain” on the skin. Some patients with metastatic melanoma do not have an obvious detectable primary tumor.
Types of primary melanoma
Any of the above types may produce melanin (and be dark in color) or not (and be amelanotic – not dark). Similarly any subtype may show desmoplasia (dense fibrous reaction with neurotropism) which is a marker of aggressive behavior and a tendency to local recurrence.
When melanomas have spread to the lymph nodes, one of the most important factors is the number of nodes with malignancy. Extent of malignancy within a node is also important; micrometastases in which malignancy is only microscopic have a more favorable prognosis than macrometastases. In some cases micrometastases may only be detected by special staining, and if malignancy is only detectable by a rarely-employed test known as polymerase chain reaction (PCR), the prognosis is better. Macrometastases in which malignancy is clinically apparent (in some cases cancer completely replaces a node) have a far worse prognosis, and if nodes are matted or if there is extracapsular extension, the prognosis is still worse.
When there is distant metastasis, the cancer is generally considered incurable. The five year survival rate is less than 10%.The median survival is 6 to 12 months. Treatment is palliative, focusing on life-extension and quality of life. In some cases, patients may live many months or even years with metastatic melanoma (depending on the aggressiveness of the treatment). Metastases to skin and lungs have a better prognosis. Metastases to brain, bone and liver are associated with a worse prognosis.
There is not enough definitive evidence to adequately stage, and thus give a prognosis for ocular melanoma and melanoma of soft parts, or mucosal melanoma (e.g. rectal melanoma), although these tend to metastasize more easily. Even though regression may increase survival, when a melanoma has regressed, it is impossible to know its original size and thus the original tumor is often worse than a pathology report might indicate.
Stage 0: Melanoma in Situ (Clark Level I), 100% Survival
Stage I/II: Invasive Melanoma, 85-95% Survival
Stage II: High Risk Melanoma, 40-85% Survival
Stage III: Regional Metastasis, 25-60% Survival
Stage IV: Distant Metastasis, 9-15% Survival
Based Upon AJCC 5-Year Survival With Proper Treatment
Treatment of advanced malignant melanoma is performed from a multidisciplinary approach including dermatologists, medical oncologists, radiation oncologists, surgical oncologists, general surgeons, plastic surgeons, neurologists, neurosurgeons, otorynolaryngologists, radiologists, pathologists / dermatopathologists, research scientists, nurse practitioners and physician assistants, and palliative care experts. Nurse practitioners (NPs) and physician assistants (PAs) are qualified to evaluate and treat patients on behalf of their supervising physicians.
Diagnostic punch or excisional biopsies may appear to excise (and in some cases may indeed actually remove) the tumor, but further surgery is often necessary to reduce the risk of recurrence.
Complete surgical excision with adequate margins and assessment for the presence of detectable metastatic disease along with short and long term follow up is standard. Often this is done by a “wide local excision” (WLE) with 1 to 2 cm margins. The wide excision aims to reduce the rate of tumor recurrence at the site of the original lesion. This is a common pattern of treatment failure in melanoma. Considerable research has aimed to elucideate appropriate margins for excision with a general trend toward less aggressive treatment during the last decades. There seems to be no advantage to taking in excess of 2 cm margins for even the thickest tumors.
Mohs micrographic surgery is sometimes used in the treatment of melanoma. In this surgery, performed by specially-trained dermatologists, a small layer of tissue is excised and prepared as a frozen tissue section. This section can be prepared and examined by the dermatologist / dermatopathologist within one hour, and the patient will return for further stages of excision as needed, with each excised tissue layer being examined until clear margins are obtained. However, the usefulness of Moh’s surgery in melanoma is limited because of the difficulty of identifying melanocytic atypia on a frozen section, which may lead to incomplete resection of the melanoma.
Other issues to consider with Moh’s technique are risks of tumor implantation and possible false negative margins due to suboptimal melanocytic staining. Deviation from recommended 1-2 cm margins of excision should thus be approached carefully.
Melanomas which spread usually do so to the lymph nodes in the region of the tumor before spreading elsewhere. Attempts to improve survival by removing lymph nodes surgically (lymphadenectomy) were associated with many complications but unfortunately no overall survival benefit. Recently the technique of sentinel lymph node biopsy has been developed to reduce the complications of lymph node surgery while allowing assessment of the involvement of nodes with tumor.
Although controversial and without prolonging survival, “sentinel lymph node” biopsy is often performed, especially for T1b/T2+ tumors, mucosal tumors, ocular melanoma and tumors of the limbs. A process called lymphoscintigraphy is performed in which a radioactive tracer is injected at the tumor site in order to localize the “sentinel node(s)”. Further precision is provided using a blue tracer dye and surgery is performed to biopsy the node(s). Routine H&E staining, and immunoperoxidase staining will be adequate to rule out node involvement. PCR (Polymerase Chain Reaction) tests on nodes, usually performed to test for entry into clinical trials, now demonstrate that many patients with a negative SLN actually had a small number of positive cells in their nodes. Alternatively, a fine-needle aspiration may be performed, and is often used to test masses.
If a lymph node is positive, depending on the extent of lymph node spread, a radical lymph node dissection will often be performed. If the disease is completely resected the patient will be considered for adjuvant therapy.
High risk melanomas may require referral to a medical or surgical oncologist for adjuvant treatment. In the United States most patients in otherwise good health will begin up to a year of high-dose interferon treatment, which has severe side effects, but may improve the patients’ prognosis. This claim is not supported by all research at this time and in Europe interferon is usually not used outside the scope of clinical trials. Metastatic melanomas can be detected by X-rays, CT scans, MRIs, PET and PET/CTs, ultrasound, LDH testing and photoacoustic detection.
Chemotherapy and immunotherapy
Various chemotherapy agents are used, including dacarbazine (also termed DTIC), immunotherapy (with interleukin-2 (IL-2) or interferon (IFN)) as well as local perfusion are used by different centers. They can occasionally show dramatic success, but the overall success in metastatic melanoma is quite limited. IL-2 (Proleukin®)is the first new therapy approved for the treatment of metastatic melanoma in 20 years. Studies have demonstrated that IL-2 offers the possibility of a complete and long-lasting remission in this disease, although only in a small percentage of patients. A number of new agents and novel approaches are under evaluation and show promise.
Some superficial melanomas (lentigo maligna) have resolved with, an experimental treatment, imiquimod (Aldara®) topical cream, an immune enhancing agent. Application of this cream has been shown to decrease tumor size prior to surgery, reducing the invasiveness of the procedure. This treatment is used especially for smaller melanoma in situ lesions located in cosmetically sensitive regions. Several published studies demonstrate a 70% cure rate with this topical treatment. With lentigo maligna, surgical cure rates are no higher. Some dermasurgeons are combining the 2 methods: surgically excise the cancer, then treat the area with Aldara® cream post-operatively for 3 months.
Radiation and other therapies
Radiation therapy is often used after surgical resection for patients with locally or regionally advanced melanoma or for patients with unresectable distant metastases. It may reduce the rate of local recurrence but does not prolong survival.
In research setting other therapies, such as gene therapy, may be tested. Radioimmunotherapy of metastatic melanoma is currently under investigation.
Experimental treatment developed at the National Cancer Institute (NCI), part of the National Institutes of Health in the US was used in advanced (metastatic) melanoma with moderate success. The treatment, adoptive transfer of genetically altered autologous lymphocytes, depends on delivering genes that encode so called T cell receptors (TCRs), into patient’s lymphocytes. After that manipulation lymphocytes recognize and bind to certain molecules found on the surface of melanoma cells and kill them.