Hirsutism is the growth of terminal (thick) hair in male pattern in females. It is often, but not always, a manifestation of hyperandrogenism.

Basics: Androgens have a profound effect on many components of the skin like the hair, sebaceous glands (oil glands), apocrine glands (responsible for normal body odour), dermal collagen and subcutaneous fat. Androgens are normally secreted at puberty and are responsible for certain characteristics seen at puberty (growth of axillary and pubic hair, secretion of sebum, change in the voice etc.)

According to the sensitivity to androgens, body hair can be divided into:

  • Independent of androgen influence – Eyebrows, eye lashes, lanugo hair (fine body hair)
  • Sensitive to small amounts of androgens produced by adrenals – axillary and pubic hair
  • Sensitive to high levels of androgens as seen in males and some females – hair on the face, chest, upper pubic triangle, ears

Hirsutism results from both increased production of and increased sensitivity of the hair follicles to androgens. Increased androgens could be of ovarian or adrenal origin.

The causes of hirsutism are:

Mild hirsutism without other signs of hyperandrogenism:

  • Stress
  • Pregnancy
  • Menopause
  • Puberty

Hirsutism with other signs of hyperandrogenism:

  • Ovarian causes – PCOD (common), tumors
  • Adrenal causes – congenital adrenal hyperplasia, tumors
  • Cushing’s syndrome – pituitary origin, adrenal tumors, ectopic ACTH
  • Prolactinoma
  • Gonadal dysgenesis
  • Drugs – anabolic steroids, oral contraceptives with androgenic progesterones
  • Obesity

Most common cause of hirsutism is polycystic ovarian syndrome (PCOD). A small proportion of patients with hirsutism may not have hormonal abnormalities (idiopathic, racial, familial).

Signs and symptoms of hyperandrogenism which may or may not be associated with hirsutism are:

  • Cutaneous virilism – Acne (severe), seborrhoea, androgenic alopecia (loss of hair in male pattern)
  • Systemic virulism – amenorrhoea, oligomenorrhoea, cliteromegaly, loss of female body contour, coarsening of the skin
  • Other signs – obesity, striae, acanthosis nigricans (thick, dark skin over the neck and other body folds)

The accompanying symptoms and signs are of vital importance in investigating the cause of hirsutism.

Diagnostic Approach:

History should be elicited regarding:

  • Duration of hirsutism
  • Onset – sudden/gradual
  • Family history of similar complaints
  • Menstrual cycles
  • Associated signs and symptoms (baldness of the scalp, acne, striae etc.)
  • History of drug intake (oral contraceptives with androgenic progesterone, anabolic steroids, corticosteroids)

Look for the following on clinical examination:

  • Body contour
  • Fat distribution (trunkal obesity, buffalo hump, moon face)
  • Hair over the scalp (baldness)
  • Hair over body areas
  • Acne (particularly severe acne)
  • Seborrhoea (oily complexion)
  • Thickened skin over the neck (acanthosis nigricans)
  • Striae
  • Genital examination

The following investigations should be done based on the clinical details; no investigations are required in cases of long standing mild hirsutism with regular menstrual cycles and no other associated features of hyperandrogenism.

  • Serum testosterone (Total and free)
  • Serum FSH, LH, Prolactin
  • Dehydroepiandrosterone sulfate (DHEAS) – for adrenal causes
  • ACTH and Cortisol (Cushing’s syndrome)
  • Urinary 17 keto steroids
  • Ultra sound examination of the abdomen
  • Special tests like dexamethasone suppression test, ACTH stimulation test etc. may be needed in some cases


Physical modalities

  • Temporary: Shaving, waxing, hydrogen peroxide bleaching, depilation with chemicals
  • Permanent: Electrolysis, laser epilation (permanent hair reduction)

Medical treatment:

  • Ovarian suppression – oral contraceptives, cyproterone acetate, Gonadotrophin releasing hormone agonists
  • Androgen suppression – glucocorticoids
  • Androgen receptor blockers – spironolactone, flutamide, cyproterone acetate
  • 5α reductase inhibitors – Finasteride

Any underlying cause (tumors) should be treated accordingly.

hirs1 hirs2
Hirsutism Hirsutism – After Laser
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Hirsutism Hirsutism – After three electrolysis



Alopecia areata is a condition presenting with symptomless, well circumscribed, smooth, bald patches. It is often noticed by chance by a parent, spouse, hair dresser or a friend. It usually starts on the scalp and may involve beard region or some times the whole body. Progression of the disease is varied. In a few cases, the initial patch of hair loss may re-grow spontaneously within a few months while in others, new areas of hair loss may develop sometimes resulting in total hair loss.

Causes: The exact cause is uncertain, many factors may play a role.

  1. Genetic constitution
  2. Autoimmune origin (organ specific auto immune disease)
  3. Non-specific immune reaction
  4. Atopic state (Those with personal/family history of bronchial asthma, allergic rhinitis)
  5. Emotional stress

Alopecia areata has to be differentiated from other causes of bald patches like trichotillomania (habitual plucking of the hair), following inflammatory type of tinea capitis (fungal infection of scalp) etc. In doubtful cases, biopsy of the patch is indicated.


  1. Glucocorticoids (Topical, intra lesional, oral): In case of a few localised, stable patches, intra-lesional (injection to the site) steroids show beneficial effects. Oral steroids are indicated in the presence of rapidly progressing disease and many patches. Although steroids prevent the progression of the disease, a relapse cannot be prevented. Oral steroids are associated with adverse effects that can be minimised with proper dosing, timing and regular follow-up.
  2. Sensitizers: This type of treatment involves use of chemicals that cause dermatitis at the site of hair loss. The chemicals used include
    1. Dinitrochlorobenzene (DNCB) 2%: Success rate ranges from 10-78%
    2. Squaric acid dibutyl ester (SADBE)
    3. Diphencyprone
    4. Primula obconica

    Dermatitis and the other adverse effects caused by these agents have lead many dermatologists to abandon this treatment

  3. Psoralen and Ultra Violet light A (PUVA): It is beneficial in up to 60% of cases and patients with alopecia totalis and history of atopy respond poorly.
  4. Topical minoxidil: Though it is tried by some, the results are less encouraging.
  5. Cyclosporine (oral), tacrolimus (topical)

The prognosis of this condition depends upon the age of onset (earlier the onset, poorer the prognosis), co-existent history of atopy (atopics more likely to go in for alopecia totalis) and genetic predisposition.

alopeciaareata1a alopeciaareata1b
Alopecia Areata Before Treatment Alopecia Areata After OMP
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Alopecia Areata Before Treatment Alopecia Areata After OMP



Vitiligo is an acquired skin disorder caused by the disappearance of pigment cells from the epidermis, and results in well defined white patches that are often symmetrically distributed. It is a cosmetically disfiguring and stigmatizing condition that may lead to psychological problems in daily life.

It occurs worldwide in about 1% of the population and in more than 50% of patients, it occurs between the ages of 10-30 years. It affects both sexes equally, though women more often seek remedy.

Pigment loss in vitiligo, secondary to melanocyte loss, results from a complex interplay of genetic, immunological, environmental and biochemical events in a permissible genetic milieu. Various recent studies have shown that oxidative stress is largely responsible for biochemical and immunological loss of melanocytes. These result from defects in the handling of reactive oxygen species (ROS), particularly H2O produced in the melanocytes and the neighbouring keratinocytes. ROS and T-cells act in concert to destroy or incapacitate melanocytes in a vicious cycle of cellular fatigue, cytokine imbalance, immune attack and apoptosis. The synthesis of melanin by melanocytes also predisposes to ROS generation, and melanocytes, therefore, operate in a potentially hostile environment. Melanocytes seem to be uniquely fragile in people with a tendency to vitiligo.


Numerous endogenous and exogenous sources of H2O2 and other ROS have been described in vitiligo, which are deleterious to a variety of melanocytic cellular processes, particularly in the context of impaired cellular antioxidant defense.

This immune response principally involves cytotoxic T-cells. Failure of regulatory T-cell mechanisms allows the process to continue indefinitely, in keeping with the chronic, relentless course of generalized vitiligo.

Insight into these pathogenetic mechanisms of this common and distressing disorder will offer the potential for better therapies and might even facilitate effective strategies for primary prevention in genetically susceptible individuals.

Between 30-40% of patients with vitiligo have a positive family history suggesting genetic causation. The exact mode of inheritance is not known it is characterized by multiple susceptibility loci, incomplete penetrance and genetic heterogeneity and may involve genes asso- ciated with the biosynthesis of melanin, antioxidant system and regulation of autoimmunity.The risk of vitiligo for children of affected individuals is unknown, but may be less than 10%. Individuals from families with increased prevalence of thyroid disease, diabetes mellitus and vitiligo appear to be at increased risk.

Vitiligo is often associated with other diseases with autoimmune mechanism like thyroid disease, diabetes mellitus, Addison’s disease, pernicious anemia, hypoparathyroidism, alopecia areata, systemic lupus etc.

Precipitating causes for vitiligo in a patient with susceptibility include physical trauma or illness, emotional stress and sunburn.

Clinical Features: Clinically, patients present with white patches that could be focal, segmental, generalised (wherein the lesions are symmetrically distributed), lip and tip or acrofacial pattern (where the lesions are seen around the mouth, fingers, toes and lips, nipples and genitalia). Areas subjected to repeated friction and trauma are also likely to be affected. In long standing cases, the hairs within the patches also appear white.

Differential Diagnosis: Vitiligo should be differentiated from many conditions that present with pigment dilution like pityriasis alba (dry, scaly patches commonly seen on the face), post-inflammatory hypopigmentation, leprosy, lupus erythematosus, chemical leukoderma and certain nevi (present since birth and non-progressive). Confirmation is by histopathological examination of skin biopsy that shows absence of melanocytes with mild lymphocytic infiltrates.

Associated Disorders: Vitiligo can be associated with certain cutaneous diseases like alopecia areata (presenting with smooth, bald patches) and premature greying of the hair. Less than 10% of patients may have uveitis in the eye. Vitiligo can also be associated with systemic diseases like thyroid diseases (40% of cases), pernicious anemia (<5%), diabetes mellitus (1-7%, particularly late onset vitiligo) and can be a part of multiple endocrinopathy syndrome.

Course and Prognosis: Spontaneous repigmentation is noted in 10-20% of patients, most frequently in sun-exposed areas in younger patients. This pigmentation is trivial and mainly starts around the hairs. Course is unpredictable; sudden onset followed by a period of stability or slow progression is characteristic.

Management: Certain investigations need to be done based on the complete medical examination to rule out/confirm associated disorders. These include thyroid profile, fasting blood glucose, blood profile for pernicious anemia, early morning cortisol estimation, anti nuclear antibody etc.

vitiligoVitiligo: Before and With Treatment


General measures: Reassurance forms the mainstay of the treatment. Vitiligo is usually mistaken for leprosy and the patients fear of deformities resulting form leprosy. Vitiligo is not contagious. Emotional upsets can worsen the disease. Sunscreens should be used to avoid sunburns of the depigmented patches and also to avoid new lesions when the disease is active. Camouflage using coloured cosmetics is an immediate remedy that the patient can try.

Specific treatment should be done in consultation with a dermatologist. This includes

  • Topical glucocorticoids (when the lesions are few)
  • Systemic glucocorticoids (in the form of minipulse; when the disease is extensive and progressing)
  • Photochemotherapy (use of psoralens and exposure to ultraviolet light A – See PUVA)
    • Topical photochemotherapy – application of psoralens to the skin and then exposure to UV-A light; for children under the age of 12 years and adults with localised patches
    • Systemic photochemotherapy – ingestion of psoralens and exposure to UV light
  • Phototherapy using narrow band UVB – treatment with ultraviolet light B without the use of psoralens; preferable in children
  • Other immunomodulating drugs – levamisole, topical tacrolimus
  • Surgical – mini punch grafting, split thickness grafting, blister roof grafting. These procedures are done for the patches that are resistant to photochemotherapy and for those patches without black hair.

Vitiligo is a treatable disease with any of these methods, provided the right method is started at the right time and continued till the cosmetic improvement is acceptable.

Patches that have totally repigmented usually remain so in the absence of injury or sunburn in 85% cases up to 10 years. Those partially repigmented will reverse back when the treatment is discontinued.

Skin Infections

Common skin infections could be of viral, fungal and bacterial origin. All these conditions are curable, provided they are diagnosed rightly at the right time and treated.

Viral | Bacterial | Fungal

Viral Infections:

  • Molluscum contagiosum
  • Viral warts
  • Herpes infections
  • Viral exanthems
Bacterial Infections:

  • Impetigo
  • Folliculitis
  • Furuncle (Boil)
  • Erysepelas
  • Cellulitis
  • Abscess
Fungal Infections:

  • Pityriasis versicolor
  • Tinea
  • Candidiasis
  • Seborrhoic dermatitis

molscontagMolluscum Contagiosum:

It is a viral infection caused by Molluscum contagiosum Virus belonging to pox virus family. The disease follows contact with the infected persons or contaminated objects. It is commonly seen in children. It is commonly seen in the head and neck region as pearly white, hemispherical lesions with central depression. It easily spreads from one area to the other.

Treatment is extraction or curettage; cryotherapy can be tried.

Viral Warts: These are benign tumors of the skin caused by Human Papilloma Virus (HPV). They can occur at any age but are unusual in infancy. It is spread by direct or indirect contact. Impairment of the epithelial barrier by trauma, xerosis (dry, cracked skin) or maceration (excessive moisture) are pre-requisites for the infection. Warts are commonly seen around the nails, hands, face, feet and genital area. They can spread to other parts of the body through scratching and trauma. Clinically they are seen as asymptomatic, raised, round lesions with rough or velvety surface. On the face, they are seen as fleshy, finger like projections. Patients with defective immunity and those belonging to families with atopy usually develop large number of warts, sometimes resistant to treatment.
Treatment includes

  • Chemical cautery – by using chemicals such a salicylic acid and lactic acid, gluteraldehyde, trichloroacetic acid etc.
  • Electrosurgery
  • Cryotherapy using liquid nitrogen
  • Immunomodulators like podophylline, alpha interferon, 5 fluorouracil, imiquimod
  • CO2 laser

Herpes Infections: These are one of the commonest viral infections of the mucocutaneous surfaces caused by Herpes Simplex Virus (HSV) Type 1 and HSV Type 2. Herpes viruses cause primary mucocutaneous infection on contact with mucosal surfaces or abraded skin following which they replicate and enter the cutaneous neurones. Here they remain dormant and cause recurrent disease whenever the viral reactivation occurs.

herlabHSV Type 1 usually affects the oral cavity and occasionally the eyes. It presents as primary infection or recurrent infection.

Pic: Recurrent herpes labialis

Primary infection usually occurs at younger age and most of the time, goes unnoticed. It is characterised by fever and grouped, fluid filled lesions inside the mouth, leading to multiple, tiny ulcers.

Recurrent herpes labialis is the commonest presentation. It is characterised by a few grouped fluid filled lesions in and around the mouth. It can occur in any individual who had a primary infection (clinical or subclinical) in the past and may be precipitated by fever, stress, UV radiation, dental treatment, surgeries on the face including chemical peeling

Herpes Simplex Type 2 infection occurs over the genitals and is usually sexually transmitted. It also presents as primary and recurrent infection. Primary infection is seen 5-12 days after sexual contact and is clinically characterised by multiple, tiny, grouped, fluid filled lesions which rupture, leaving behind multiple, tiny ulcers over the genitals and is associated with fever and lymph node enlargement. The person with a primary infection will be shedding the virus for about 11-14 days and should avoid sexual contact during this period. Healing occurs in 18-21 days.

Recurrence with HSV 2 infection is more common than HSV 1 infection. However the recurrent attacks are less severe than the primary infection. Recurrence is precipitated by stress, trauma and immunocompromised state. In a recurrence, the viral shedding lasts for 3-4 days and healing occurs in 9-10 days.

Primary genital infection during the third trimester of pregnancy will lead to herpes infection in the neonates which can be severe. With recurrent genital infection, the risk of transmission to the newborn is lower.

Treatment: It should be started early for better results. In addition to the local measures to prevent the infection, acyclovir should be given in appropriate dose for appropriate duration.

Chicken Pox (Varicella): It is an acute infectious disease caused by the Varicella zoster virus. It spreads by inhalations of the viral particles. The duration between the infection and onset of eruption is usually 14-21 days. Most commonly it occurs during childhood when it is less severe and sometimes subclinical. Those who did not have the infection during childhood may develop it later, which might be severe.

Clinically it is characterised by fever, body ache and rash, consisting typically of clear, fluid filled (dew-drop) lesions starting on the trunk and extending on to the face. The lesions crust in 2-4 days and new lesions appear in crops over a period of one week. Patients with varicella are infectious to others when they are having these clear, fluid filled lesions. The lesions of chicken pox usually get secondarily infected resulting in scarring.

Treatment includes rest, use of drying preparations (calamine) in the presence of fluid filled lesions, antibacterial creams for ruptured lesions and antipyretics. Acyclovir is the drug of choice and should be given as early as possible (within 48 hours).

herpeszosterHerpes Zoster: It is a manifestation of reactivation of the Varicella zoster virus that usually remains dormant in a sensory ganglion following chicken pox. It occurs commonly in the elderly, diabetics, immunocompromised and following stress and trauma.

It presents clinically as severe pain along the affected nerve, followed by rash consisting of grouped, fluid filled lesions along the affected nerves. A person with herpes zoster can cause the spread of chicken pox in the family members who did not suffer from it earlier.

Treatment is the same as for chicken pox.

Prevention of varicella is very important in neonates and immunocompromised individuals. Passive immunization is by administering varicella zoster immunoglobulin (VZIg) to abort or modify the clinical infection and should be administered within 4 days of exposure to the infected case. Active immunization with a live attenuated VZ virus reduces the risk of acquiring infection; however it should be given within 48 hours to high risk individuals.

Bacterial Infections

Bacterial infections of the skin are commonly referred to as pyoderma, which literally means pus in the skin. Pathogenic bacteria most commonly causing infections of the skin are coagulase positive Staphylococcus aureus and Streptococcus pyogenes. Conditions predisposing for bacterial infections are moisture, damage to the skin, pre-existing skin disease etc.

While damage to the skin is a pre-requisite for Streptococcal infections, Staphylococcal infections can occur even on intact skin.

Disinfection of the skin using antiseptics can remove the resident flora (non-disease causing bacteria normally present on the skin) that provide defense against infection and hence can predispose to more frequent infections by Staphylococcus aureus. On the other hand, as resident flora do not hinder the growth of Streptococcus pyogenes, disinfecting the skin does not offer protection against this organism either.

bulimpetImpetigo: It is a common, contagious, superficial infection of the skin caused by either Streptococcus pyogenes or Staphylococcus aureus or both. It is commonly seen in children and young adults. It is common in lower socio-economic groups due to poor hygiene, poor nutrition and over-crowding. The peak incidence is seen in late summer. Precipitating factors include breach in the skin due to trauma, insect bite or any other skin diseases like eczema, infestations (Scabies)

Pic: Bullous Impetigo

Common sites include face, especially around the nose and mouth, scalp and legs.

Treatment: Compresses to remove the crusts followed by application of antibacterial creams.

For mild and localised infections, topical antibiotics like mupirocin, fucidic acid, neomycin and bacitracin combination may suffice.

impetigoIn the presence of wide spread and severe infections or with associated lymphadenopathy, oral antibiotics are indicated.

Pic: Non-Bullous Impetigo

Once the infection is controlled, the underlying skin disease should be identified and treated.

Info on Bacteria here: www.typesofbacteria.co.uk/home.htm


carbuncleCarbuncle is a deep seated infection of the skin, produced by the infection of neighbouring hair follicles, caused by Staphylococcus aureus. It is predominantly seen in middle aged and elderly men with predisposing causes like diabetes, malnutrition, immunocompromised state (diseases and drugs) and debility. Clinically it presents as painful, hard, red lump with multiple openings discharging pus. Common sites include back of the neck, shoulders, hips and thighs. It is usually associated with fever and generalised weakness. In elderly and debilitated individuals, if not treated in time, it can lead to toxemia and could even be fatal.

Treatment: Pus should be drained. Antibiotics against Staphylococcus aureus should be started as early as possible, drug of choice being cloxacillin or penicillinase resistant antibiotics. Underlying cause should be sought and treated.

Erysepelas: It is the infection of the dermis and the subcutaneous tissue including lymphatics, caused by Streptococcus pyogenes. Clinically it is seen as sharply demarcated, painful, raised, red lesions with orange peel (peau-de-orange) appearance. It is usually associated with fever and lymphadenopathy. The common sites are face and legs. In the presence of lymphatic obstruction secondary to surgery and radiation, it can occur on the upper limbs also. Most important predisposing cause is lymphatic obstruction (filarial lymphedema, varicose veins with chronic edema of limb). It can also occur following injuries, insect bites etc., that act as portal of entry toStreptococcus pyogenes.
Without effective treatment, complications like subcutaneous abscess, cellulitis and septicemia can occur. Sometimes, systemic reactions like nephritis and scarlet fever can follow.

erysepTreatment: Penicillin is the drug of choice. In the presence of severe infection with systemic reaction, injectable penicillin or first generation cephalosporins are indicated. In very early infections and in patients allergic to penicillin, erythromycin is the alternative. Vancomycin can also be used for penicillin sensitive patients with severe infection. Foot end elevation may help in patients with lymphedema. Recurrent erysepelas can occur in patients with chronic lymphedema. In recurrent cases, long term penicillin (Penicillin LA 12L Units once in 3 weeks) can be given. Supportive stockings may also help.

Fungal Infections

Superficial fungal infections of the skin are the most commonly encountered, curable skin diseases. They are caused by fungi belonging to three groups: dermatophytes, Candidaspecies and Malassezia furfur. The fungi affect the skin, hair and nails.

Dermatophytes cause the skin disease known as Tinea (Ring Worm). Dermatophytes infecting the skin could be anthropophilic (human to human), zoophilic (animal to human) or geophilic (soil to human). Most commonly encountered infections are caused by the anthropophilic species. Predisposing factors for dermatophytoses include excessive sweating, occlusive dressing, topical and systemic steroids, underlying skin diseases like ichthyosis and atopic dermatitis, immunocompromised state and environmental factors like high humidity.

The clinical presentation depends upon factors like site of infection, immunological response of the host and species of the fungus (anthropophilic cause less severe and zoophilic cause more severe inflammatory response). Commonly it is seen as ring like lesions with peripheral activity and central clearance. Common sites are the scalp in case of children (Tinea capitis) and body folds (intertriginous) in adults. Itching is a characteristic feature of tinea.

The diagnosis of tinea is to a large extent based on the clinical features. Difficulty arises when the patient presents with tinea incognito (hidden tinea) which results from misdiagnosis and mistreatment with topical steroids, over-the-counter products and home remedies. Tinea is one skin disease that, when diagnosed right and treated right (proper antifungals for proper duration), is curable. Treatment with topical steroids leads to chronic disease.

Differential Diagnosis: Clinically tinea has to be differentiated from common skin diseases like subacute and chronic eczema, psoriasis etc. The points that favour tinea are:

  • Intense itching
  • Sharply demarcated lesions
  • Peripheral activity and central clearance (absent when treated with topical steroids)
  • Asymmetric presentation

In case of doubt, scrapping for fungal elements should be done (if scales are present). If the patient has already used topical steroids, they should be stopped and lesions should be observed or plain antifungals could be advised.



Tinea Capitis resulting in alopecia Tinea Capitis resulting in alopecia
kerion tconcentricum
Kerion Tinea Concentricum

Treatment of Tinea: Treatment of tinea includes local application of medicines and oral medications. When the disease is of short duration and localised, local application of medicines is usually sufficient. Long term disease, extensive disease and recurrent infection should be treated with oral medications.

The antifungals used in the treatment of tinea are of two types:

  • Fungistatic agents (inhibit the multiplication of the fungus): Azoles like clotrimazole, miconazole, ketoconazole, oxyconazole etc.
  • Fungicidal agents (kill the fungus): Allylamines like terbinafine, butenafine, naftifine, griseofulvin.

Drugs of choice for dermatophytes are allylamines and griseofulvin.

Duration of treatment depends upon the site of infection. Skin infection usually requires treatment for 4-6 weeks, hair infection for 6-8 weeks and nail infection for months (3-4 months for finger nails, 6-12 months for toe nails).

Treatment should not be discontinued once the itching subsides; it should be continued for the recommended duration to ensure fungal clearance and prevention of immediate relapse. Preventive measures like keeping the area dry, avoiding wet clothes and avoiding friction should be practiced.

Candidiasis: It is the infection of the skin and mucous membranes by yeast like fungus Candida albicans and other species. Cutaneous candidiasis usually affects the web spaces of the fingers and toes, around the nails, body folds and angles of the mouth and genitals.
Cutaneous candidiasis: The factors that favour cutaneous candidiasis are

  • High moisture levels (sweat and prolonged immersion in water)
  • Mechanical trauma (maceration)
  • Obesity
  • Diabetes
  • Immunocompromised states (HIV/AIDS, other causes)
  • Nutritional deficiencies (vitamin, iron deficiency)
  • Cushing’s syndrome (drug induced or neoplastic)
  • Pregnancy
  • Extremes of age

Cutaneous Candidiasis

cutcandClinically, cutaneous candidiasis is characterised by erythema (redness) and maceration with sodden white scales at the periphery of the erythema. In severe cases, there may be tiny, pus filled lesions in the surrounding skin (satellite lesions). There may be associated symptoms of itching and burning.

It has to be differentiated from other types of fungal infections of the folds like tinea and seborroeic dermatitis, Pseudomonas infections of the web spaces, bacterial intertrigo and psoriasis (flexural). Diagnosis can be confirmed by KOH mount.

Treatment: The precipitating factors should be corrected. Topical and systemic antifungals can be used; the drugs of choice would be antifungals belonging to azoles like clotrimazole, miconazole, oxyconazole topically or fluconazole orallly.

Mucosal Candidiasis: It is the Candidal infection of oro-pharyngeal and genital mucosa. It is commonly seen in neonates, elderly, diabetics, immunocompromised (HIV/AIDS), following intake of steroids or of broad spectrum antibiotics, in those wearing dentures, nutritional deficiency etc.


Pics: Oral Candidiasis

Clinically it presents with curdy white patches on the background of erythema (redness) along with a burning sensation. It can affect any part of the oral mucosa or genital mucosa. The most common variety is called the thrush. Following intake of antibiotics, oral candidiasis presents as red mucous membranes with pain, without any white patches. Candidal infection at the angles of the mouth is seen in the elderly due to sagging of the angles and in denture wearers due to ill fitting dentures. It is characterised by erythema, maceration, fissuring and crust formation.

It should be differentiated from other causes of white patches such as leukoplakia, oral lichen planus, lupus eythematoses, frictional keratosis etc.

Treatment: The precipitating factors should be corrected. Topical and systemic antifungals can be used. Nystatin suspension, clotrimazole mouth paints/vaginal tablets topically or fluconazole and itraconazole orallly are used.

Tinea versicolor: It is a common, chronic, non-inflammatory, superficial infection caused by the fungus variably known as Pityrosporum orbiculare, Pityrosporum ovale or Melassezia furfur. It is very common in places with high humidity (tropical climate), affecting 40% of the population. The fungus causing this infection belongs to the normal flora of the skin and the manifestations of the disease occur when there is an increase in the number of the fungi and/or change in the form of the fungi under favourable conditions in the host. The precipitating factors include:

  1. Genetically determined susceptibility
  2. Increased humidity (excessive sweating)
  3. Increased sebum secretion (oily complexion)
  4. Chronic illness
  5. Immunocompromised state
  6. Cushing’s syndrome or prolonged use of glucocorticoids
  7. Excessive use of oils
  8. Pregnancy

Clinically it is characterised by asymptomatic, hypo and/or hyper pigmented tiny patches with fine scaling which becomes prominent on rubbing. The common sites affected are upper trunk, upper arms, neck, axillae (arm pits), face and thighs.

The diagnosis is made on the basis of the clinical presentation and the sites involved. Sometimes it may have to be differentiated from Pityriasis alba (dry, white patches), early vitiligo, indeterminate leprosy, post inflammatory hypopigmentation etc. In case of doubt KOH examination of the scales should be done.

Treatment: Common antifungal agents used are

  • Selenium sulfide 2.5%
  • Topical azoles like clotrimazole, ketoconazole
  • Oral medications like ketoconazole, itraconazole, fluconazole

Duration of treatment is 3 weeks. Repigmentation may take a few months. Relapses are very common and need re-treatment with same drugs.


Psoriasis is a chronic inflammatory disease of the skin characterised by a relapsing and remitting course. It manifests as pink, scaly, raised lesions on the elbows, knees, lower back and scalp along with certain nail changes like pitting, discolouration, subungual hyperkeratosis and onycholysis in about 25-50% of the cases. In 5-10% of patients, the disease can be associated with joint involvement.

It is multifactorial in aetiology, with genetic factors and environmental insults playing their role. A positive family history is present in about one third of the patients; when neither parents are affected the risk is about 7.5%, when one parent is affected it is about 15% and when both parents affected, it is 50%. Psoriasis is not contagious.

The following factors may exacerbate the disease:

  • Stress
  • Trauma
  • Infections (Streptococcal upper respiratory tract infections)
  • Medications (Lithium, Antimalarials, Propranolol and other beta blockers, NSAIDS, Terfenadine and steroid withdrawal)
  • Winter season

Age of onset is usually 16-22 years and 57-60 years. The lesions vary from a few to numerous and when numerous, tend to be symmetrically distributed.

At the microscopic level, the skin shows excessive cellular proliferation, poor differentiation and inflammation.

Co-Morbidities: Psoriatic patients have been identified as having higher frequencies of hyperlipidemia, coronoray artery disease and myocardial infarction, hypertension, insulin resistance, diabetes mellitus and homocysteinemia. A hospital based case control study has shown an increased prevalence of metabolic syndrome in psoriatic patients that is independent of psoriasis severity.[See Kimball AB below]. Results of a new study at Reykjavik’s Landspitali, the National University hospital of Iceland suggest that patients — especially women — with psoriasis may be at increased risk for metabolic syndrome. The study involving more than 6,500 people found the prevalence of metabolic syndrome to be higher among patients with psoriasis (40 percent) than among those without (23 percent)[See Love TJ et al below]

pso_guttate pso_guttate2
Guttate Psoriasis Guttate Psoriasis

Role of Diet: Diet has been suggested to play a role in the aetiology and pathogenesis of psoriasis. Diets with low carbohydrates and rich in vegetables and omega 3 polyunsaturated fatty acids (fish such as meckerel, salmons, sardines) improved psoriatic symptoms in some studies.

Animal studies indicate that fatty acids can modulate pro-inflammatory cytokine production and actions. Omega 6 polyunsaturated fatty acids such as arachidonic acid (from meat, refined vegetable oils) enhance interleukin 1 production and tissue responsiveness to cytokines whereas omega 3 polyunsaturated fatty acids such as eicosa pentanoic acid (EPA) and docosa hexanoic acid (DHA) (from fish such as meckerel, salmons, sardines) have the opposite effect. Arachidonic acid is converted to prostaglandin (PG) E2 and leukotreine (LT) B4 which are proinflammatory whereas EPA and DHA are converted into PGE3 and LT B5 which are anti inflammatory. Overproduction of arachidonic acid derived eicosanoids have been implicated in many inflammatory and autoimmune disorders including psoriasis. A diet rich in vegetables and fish is beneficial because it is associated with reduced arachidonic acid intake. Low calorie diet helps in reducing the oxidative stress and thereby improves psoriasis. Weight reduction in obese also helps in improvement of psoriasis.

Low glycemicfood improvespsoriasis
Diet, metabolic syndrome and psoriasis: Emerging evidence

  • Kimball AB et al. National Psoriasis Foundation clinical consensus on psoriasis comorbidities and recommendations for screening. J Am Acad Dermatol. 2008 Jun;58(6):1031-42. Epub 2008 Mar 4. Full Text
  • Love TJ et al. Prevalence of the Metabolic Syndrome in Psoriasis. Arch Dermatol. Published online December 20, 2010. doi:10.1001/archdermatol.2010.370. Abstract | Report
  • Cohen AD. Psoriasis and the Metabolic Syndrome. Acta Derm Venereol 2007;87:506–509. Full Text
  • Gottlieb AB et al. Psoriasis and the Metabolic Syndrome. Journal of Drugs in Dermatology. June, 2008. Full Text
  • Sommer DM et al. Increased prevalence of the metabolic syndrome in patients with moderate to severe psoriasis Arch Derm Res. 2006;298(7):321-328. Abstract
  • Gisondi P et al. Prevalence of metabolic syndrome in patients with psoriasis: a hospital-based case–control study
    British Journal of Dermatology. July 2007;157(1):68–73. Full text
  • Wolters M. Diet and psoriasis: experimental data and clinical evidence. Br J Dermatol. 2005 Oct;153(4):706-14. Full Text
  • More Evidence of Psoriasis Link to Metabolic Diseases Report 

Treatment: Treatment of psoriasis is aimed at reducing cellular proliferation (anti-tumor agents) and inflammation (anti-inflammatory agents) in addition to taking care of the precipitating factors. Treatment is long term with regular follow-up.


  • Emollients – liquid paraffin
  • Keratolytic agents – salicylic acid
  • Coal tar
  • Anthralin
  • Topical corticosteroids
  • Calcipotriene
  • Topical retinoids – Tazorotene


  • UVB
  • Narrow band UVB


  • PUVA


  • Methotrexate
  • Hydroxyurea
  • Azathioprine
  • Retinoids – Etritinate
  • Cyclosporine
  • Sulfasalazine (for arthritis)
  • Biological response modifiers


Eczema is the most common skin condition seen in day-to-day practice. It is a pattern of inflammatory response (dermatitis) of the skin characterised by itching, redness, flaking of the skin and raised, fluid filled lesions (papules and vesicles). The condition may be induced by a wide variety of external and internal factors acting alone or in combination.

Based on the causes, eczema can be classified as exogenous eczema or endogenous eczema. A detailed history of a patient with eczema is very important to identify the underlying cause/s, as long term remissions can be achieved only by eliminating the underlying cause/s. Sometimes, the tendency for eczema runs in the family and therefore occurrence of eczema in family members does not imply that it is contagious.

Exogenous causes:

  • Irritant dermatitis (detergents, soaps, chemicals)
  • Allergic dermatitis (rubber, cement, dyes, plants)
  • Photo-sensitive dermatitis (dermatitis caused or precipitated by sunlight and photosensitive agents)
  • Polymorphic light eruption (caused only by UV radiation present in the sunlight)
  • Infective dermatitis (dermatitis occurring in and around the infected wound)

Endogenous causes:

  • Atopic (dermatitis occurring in a person with personal or family history of asthma, allergic rhinitis)
  • Seborrhoeic dermatitis (dermatitis seen in areas rich in sebaceous glands; usually after puberty)
  • Asteatotic eczema (eczema associated with decrease in skin surface oils; common in the elderly)
  • Gravitational eczema (eczema associated with varicose veins; seen around the ankles)
  • Hand eczema (most common eczema; causes can be many)
  • Forefoot eczema (common eczema seen in childhood, involving predominantly the forefoot)
  • Pityriasis alba (dry, white patches seen on the face and sometimes elsewhere; occurs during childhood)
  • Metabolic eczema (eczema due to nutritional deficiencies of EFA, zinc, niacin, proteins)
  • Drug eruptions (exfoliative dermatitis)

Two or more types of eczema may be present in the same patient simultaneously or consecutively. Certain eczema are common in particular age groups:

  • Infants – atopic
  • Childhood – atopic, forefoot eczema, pityriasis alba
  • Adolescence – seborrhoic dermatitis, allergic and irritant dermatitis to cosmetics
  • Middle age – Stasis eczema, irritant and allergic dermatitis (occupational)
  • Elderly – asteatotic eczema

Based on the clinical presentation, eczemas are termed as-

  • Acute (when there is oozing, with tiny fluid filled lesions and swelling)
  • Subacute (scaly and red)
  • Chronic (thick and hyperpigmented skin)
eczema2 eczema1
Asteatotic eczema Asteatotic eczema


A detailed history is important to determine the cause (exogenous/ endogenous) and precipitating factors. Eczemas have to be differentiated from other common skin diseases like

  • Tinea (fungal infection/’ring worm’)
  • Psoriasis
  • Lichen planus etc.

Differentiation from Tinea is very important as the treatment is entirely different.

  • Eczemas are usually not sharply demarcated
  • Eczemas do not show clearance in the centre (unless partially treated)
  • Eczemas are usually bilateral and if unilateral, correspond to the site of contact with exogenous agent (contact dermatitis)
  • In acute stage, eczema is characterised by oozing.

In case of doubts, scraping should be taken from the scales to demonstrate the fungal elements.

Patch testing is required if clinical presentation (history and site of involvement) is suggestive of an exogenous cause. It is also indicated if eczema of endogenous origin does not respond to treatment or is persistent in spite of treatment.

Biopsy is required in unusual cases and unusual presentations.


Treatment should aim at removing or reversing the cause. Treatment should be such that the patient should have a long term remission with minimum or no side effects to the medications.

In the presence of acute exacerbation, compresses (potassium permanganate) should be given to reduce the oozing and oedema, following which bland preparations should be applied. Topical steroids can be used for quicker resolution. In the presence of infection (yellow crusting) topical steroids with antibiotics (other than gentamicin and neomycin) can be used. Oral antibiotics (targeting Streptococci and Staphylococci) and antihistamines (to reduce itching) may be required.

Subacute eczema: Sometimes eczemas can present in this stage or acute eczema after partial treatment may manifest in this form. Treatment includes avoidance of rubbing, use of emolients/moisturizers regularly during the day and topical steroids with or without moisturizers in the evenings.

Chronic eczema: Long term rubbing and scratching of eczematous or normal skin leads to chronic eczema. Treatment obviously includes avoidance of rubbing or scratching, emolients/moisturizers to protect and soothe the damaged skin during the day and topical steroids with salicylic acid, urea, lactic acid in the night. In addition, the area should be made inaccessible for scratching by occlusion of the area with clothing.

Maintenance therapy includes regular use of moisturizers, best suited for the type and site of the skin.

Points to remember regarding eczema:

  1. Do not try self-medication or home remedies
  2. Do not use potent topical steroids for long without doctor’s advice (not more than 2 weeks)
  3. Avoid the likely cause/precipitating factors
  4. Use the treatment for the specified duration continuously without interruption. Do not stop the treatment after the itching disappears; continue treatment until the skin comes back to its normal texture.
  5. Topical steroid is not the only form of treatment. It has to be continued or replaced with emolients/moisturizers simultaneously or later
  6. Stress can aggravate eczema