ECZEMA/DERMATITIS
The word "ECZEMA" has a Greek origin. EC means "out" and Zeo means "boil" so Eczema means to boil out.

The development of eczema is a pruritic papulovesicular process. First there is superficial inflammation of the epidermis (outermost layer of the skin), then there is vesication which causes mild to severe itching. The disease progresses from erythema (redness of skin) to papules (small raised areas) with edema followed by vesicle (blisters) formation. It then goes through the stages of formation of watery discharge, crusting and finally scaling. Ultimately it heals without any scars. But if the eczema becomes chronic t here is lichenfication of the skin i.e. the skin becomes hardened and leathery.

There are two basic factors that work synergistically to cause dermatitis and eczema. The first of these two factors is ENDOGENIC (internal) which predisposes the skin to allergy thereby making it vulnerable. The second factor is EXOGENIC (external) and is made up of the various allergens that attack the body and invade it by contact with skin or by inhaling air and ingesting food and drink.

Once the skin has been irritated and sensitized, it becomes prone to further damage and insults. Scratching, chemical trauma, the weather and psychosomatic stresses keep the process going with the result that it becomes chronic. In such cases there is usually a FAMILY HISTORY of allergy e.g. urticaria, allergic rhinitis, asthma etc.

The main symptom of eczema is SEVERE ITCHING. There is a saying that in dermatitis, "It is an itch that rashes rather than a rash that itches". There are a multitude of allergens that cause eczema. These can be categorized as follows:

• Irritants: Physical; chemical or electromagnetic .
• Sensitizers: Plants; cosmetics; clothing; ointments, alkalis such as soaps and various occupational hazards.
• Climate: Temperature and Humidity.
• Drugs: Systemically administered drugs can produce a number of morphologically distinct cutaneous eruptions. Macular and maculopapular lesions & urticaria are the most undesirable side effects produced by drugs along with itching, fever, eosinophilia etc.
• Psychosomatic: Stress and strain caused by mental and emotional conflicts.
  
  

The development of urticaria occurs when the body releases histamines into the blood stream or tissues as an allergic response. This causes the capillaries to distend. The distention of the capillaries causes their walls to become thinner. This in turn allows the blood plasma to leak through the thinned capillary walls. The leaked plasma settles as swellings on the skin surface.

• Symptoms: Urticaria appear as red or white blotches on the skin accompanied by an itching, burning sensation. They may disappear as suddenly as they appear or they may last for several days. Usually: Severe itching proceeds the attack. Eruptions of various sizes usually appear. In a few minutes the eruptions may develop, spread and coalesce to form larger hives. Any part of the body may be affected.
• Complications: The most serious complication is the development of giant hives known as Angio-neurotic edema. This condition appears on the eyelids; lips or tongue accompanied by swelling. Then the swelling is internal especially in the air-passages, it can lead to obstruction in breathing.

ACNE
Acne is a disorder of the skin which usually occurs in adolescence especially in people with a strong family history of allergic disorders.

Acne which affects approximately 80% of all teenagers is closely associated with the onset of puberty. At puberty, the reproductive organs begin the process of maturing. As a result many glands get active and secrete many hormones within the body. This really causes the body to get excited. All this exciting activity frequently causes an imbalance which leads to an increased production of sebum from the sebaceous glands in the skin. In girls this may be more pronounced at the premenstrual stage. At this time the consumption of food to which the teenager is allergic can also increase the activity of the sebaceous glands. The most common foods that cause this are chocolates, nuts, cheese and fatty foods.

If a hair follicle opening on the surface of the skin is small or is clogged by dirt or heavy cosmetics, the fatty substances secreted by the sebaceous glands accumulate and a "LUMP" develops in the glands of the skin. This appears as a Comedo ("white head" or "black head") on the surface of the skin and is the primary lesion of acne. Some comedos my persist and remain unchanged but often an inflammatory reaction occurs. Pitted scarring is usually a common sequel of acne. The scarring is most pronounced when the lesions are nodular and suppurated (filled with pus).

PEMPHIGUS VULGARIS
It is characterized by the appearance of bullae (large blisters) in clusters, mild to severe constitutional symptoms and a bad prognosis.

Though the exact cause is unknown, there is some evidence suggesting a link with the Auto Immune system.

• Pathology: The bullae of Pemphigus Vulgaris are intra-epidermal and irregular in shape with acute lateral margins. They are formed by the separation of the acantholytic epidermal cells.
• Clinical Features: Bullae are most frequently seen in the mouth and on the face, scalp and trunk though they may occur anywhere on the body. The lesions may be, sparse, few or extensive and they usually appear in crops. Light pressure on the bulla will enlarge it and the integument will peel of easily with slight or firm sliding pressure. This is called Nikolsky's sign. It signifies splitting of skin due to acantholysis.

  The contents of the bullae are at first clear and serous but later may become hemorrhagic or sero-purulent. Usually the bullae rupture exposing extensive red and raw areas from which considerable loss of serum occurs. Some of them may be covered with crust. The disease leaves dark pigmented scars and stains on healing.

• Mucosal Lesions: The mouth is most often involved but denuded areas may be seen on conjunctiva, vagina and nose. Patients have painful raw areas with detachable shreds of epithelium in the mouth. These may extend to the pharynx and larynx resulting in dysphagia and hoarseness. Lips and gums may be swollen.
• Constitutional Symptoms: The constitutional symptoms are usually slight. The temperature rises when the bullae erupt. Hypoprotenemia, severe hypochromic anemia and salt depletion are common. There may be leucocytosis and raised ESR.
• Complications:
  • Secondary impetigo; ulceration and even gangrene.
  • Gastro-intestinal upset and debility.
  • Respiratory complications such as pneumonia.
• Prognosis: It is a chronic disease marked with remissions and recurrent attacks of increasing severity that sooner or later end in death.

HERPES
The term "HERPES" signifies a group of vesicles on an inflammatory base like a bunch of grapes. There are two main types of Herpes.

HERPES SIMPLEX: It is associated with stress. Psychosomatic stress, injury, fever particularly malaria, pneumonia, meningitis, general weakness all predispose the body to succumb to the Herpes virus. It is caused by the Herpes Simplex virus.

• Clinical Features: Herpes simplex starts with a sensation of burning or itching after there has been an exposure to cold, wind, sun etc. Erythematous macules appear on which clusters of pinhead sized superficial vesicles develop. They may rupture or become crusted or dry up and leave faint reddish stains. The course of herpes simplex is about 7 - 14 days.

HERPES ZOSTER: Also known as "Shingles" is caused by the Vericella-Zoster virus. The site of the infection is the posterior root ganglion. The skin is the secondary site of infection. The lowered resistance of the body and skin due to injury, illness, drugs, pyschosomatic stress etc. predispose the body to an attack by the Vericella-zoster virus.

• Clinical Features: An attack starts with neuralgic pain, local increased sensitivity of the skin (hyperaesthesia) and fever. Cutaneous lesions develop three days after the onset of the attack. The rash develops in the segmental distribution of the affected nerve root and consists of typical herpetic lesions. The lesion develops in several crops, each crop lasting a week or so. Ultimately the lesions rupture or dry up to form crusts which sloughs off leaving temporary pigmentation and faint scarring. The lymph glands near the affected area may be enlarged and painful. The attack lasts 2 to 3 weeks. The sites of predilection are the trunk (intercostal nerves), neck (cervical) and the face (trigeminal distribution). The sequela are post herpetic neuralgia and rarely muscular paralysis. Neuralgic pain lasts for months to years.

LEUCODERMA
It is an acquired idiopathic depigmentary condition. It is characterized by completely depigmented macules and patches of varying sizes and shapes. Besides loss of color, there is no structural change. Early lesions may be pale white and ill defined. Patches enlarge slowly and may affect the whole body. However that is rare. Any part of the body can be affected but the sites most predisposed to this condition are the face, dorsa of feet and hands, waist and the legs. The mucous membrane especially the lips are also frequently affected and can precede discoloration of the skin by several years. The onset is slow and the course insidious but enigmatic. It may continue to increase slowly or come to a halt and then increase again.

ETIOLOGY: Important known causative factors are:

• Nutritional - A diet deficient in copper, proteins and vitamins; gastrointestinal upsets brought on by amoebiasis, helminthes, chronic diarrhea, dysentery etc.
• Endocrines - Association with thyrotoxicosis and diabetes.
• Trophoneurosis and autonomic imbalance - emotional stress and strain..
• Drugs & Chemicals - like quinones, guanofuracin, amylphenol, chlorthiazide, broad spectrum antibiotics and chloroquin.