Jaskin

Keratosis Pilaris (aka “chicken skin”) is a condition in which the skin takes on a sandpaper like appearance with small, acne-like bumps and rough patches appearing most commonly on the back, upper arms, buttocks, and thighs. While less common, bumps may also appear on the face causing the disease to be confused with acne. Keratosis Pilaris is a common condition and estimates indicate that as many as 40-50% of adults and 50-80% of adolescents worldwide are impacted by this disorder with varying severity. While anyone can get this disease, it appears to be more common in children and adolescents. Fortunately, KP is not a serious condition and is not contagious. Nevertheless, the skin is unpleasant to look at and the condition is difficult to treat.

KP tends to be worse during the winter and periods of low humidity when the skin dries out. The condition may appear or worsen during pregnancy or after child birth. Medications and self care measures can, however, improve the appearance of the skin. Additionally, studies have shown that KP usually improves with age.

The exact causes of KP are unknown but is believed to be related to the overproduction of keratin (a hard protein in skin, nails, and hair). The bumps on the skin are the result of excess accumulation of keratin at the opening of hair follicles. This condition is believed to have a partial genetic basis as well. It is related to other conditions like ichtyosis vulgaris, dry skin, xerosis, eczema, asthma, allergies, and atopic dermatitis.

Treatment

There is no cure for Keratosis Pilaris but various treatment options exist. While results may be discouraging at first, persistence is the key to seeing improvement. The most effective form of treatment is intense moisturizing and lubrication of the skin. Application of creams such as Acid mantle, Vaseline, or Complex 15 following baths followed by re-applying them several times a day has been proven to be effective. If symptoms persist, medicated creams containing urea (e.g Carmol, Vanomide, and U-Kera) can be applied twice a day. In more serious cases where the pimples are very red, prescription medications including antibiotics (e.g. Erythromycin, Bactrim) and Tazorac cream can also be used.

Stevens-Johnson syndrome (aka Erythema multiforme major) is a rare and potentially life threatening inflammatory disease in which the skin and mucous membranes react severely to a particular type of medication or infection. Stevens-Johnson syndrome starts with flu-like symptoms and is followed by painful red or purple colored rashes that spread and form blisters across the skin, eventually causing the top layer to shed and die.

Causes

Stevens-Johnson Syndrome has most often been caused by drugs, especially sulfas, non-steroidal anti-inflammatory drugs (NSAIDs), and anticonvulsants such as phenytoin. Any drug, however, is a potential cause.

Coxsackievirus, echovirus, and most commonly, herpes simplex viruses as well as mycoplasma have been known to trigger the syndrome. Vaccines, such as those used to treat tuberculosis and polio, have also been linked to the disease. In about 50 percent of cases, no causes was identified.

Victims of Stevens-Johnson generally tend to be between the second and fourth decades of their lives. However, the disease has affect children as young as three months and any age group is susceptible.

Symptoms

Stevens-Johnson syndrome typically affects the mucous membranes of the oral cavity, nostril, eyes, and both the anal and genital regions. It may or may not be associated with skin lesions elsewhere on the body. Oropharyngeal (mouth) lesions can be especially intolerable and can hinder eating. There may also be recurring oral ulcers. Often, the skin lesions may look like a target-lesion (3 concentric zones of color change) or as bullae (bubble-like).

A painful conjunctivitis may occur in the eye, frequently with a pus discharge, and can lead to corneal scarring and loss of vision. In addition to the mucous membrane lesions, fever and exhaustion are usual.

Approximately one-third of patients have pulmonary involvement with cough and patchy infiltrates (material that has permeated into the tissues) on chest x-ray. In fatal cases, renal failure and pneumonia may occur.

Diagnosis

Diagnosis of Stevens-Johnson Syndrome is based on the clinical appearance and distribution of the skin and mucosal lesions. Skin biopsies are often performed to detect Stevens-Johnson syndrome.

Treatment

Every attempt should be made to identify a precipitating agent, and to remove it if possible. Antibiotics are appropriate if superinfection (a fresh infection added to one of the same nature already present) is suspected, or if bacterial disease, such as mycoplasma, is suspected to be the cause. Intensive supportive care is important in severe cases, including specialized care in a burn unit.

Fluid replacement is often required, and meticulous oral hygiene is necessary to prevent superinfection. Examination by an ophthalmologist is recommended for patients with eye lesions so that precautions can be taken to avoid permanent eye damage. Oral and topical corticosteroids are often used.

Sources:

HealthScout.com

Aplasia cutis congenita is a skin disorder in which an infant is born with a patch of skin missing, usually on the scalp. This may occur by itself or be associated with other physical syndromes or disorders. Many forms of aplasia cutis congenita are inherited. The disorder affects both males and females of all ethnic backgrounds and is rare, but exactly how often it occurs is unknown.
A classification system exists for aplasia cutis congenita consisting of 9 groups based on the number and location of the skin defects and the presence or absence of other malformations.

Symptoms

The infant born with aplasia cutis congenita has a patch of skin missing, usually on the scalp (70% of individuals), but it may also occur on the trunk, arms, or legs. There may also be more than one missing patch. The affected area is usually covered with a thin transparent membrane, is well-defined, and is not inflamed.

If aplasia cutis congenita occurs on the scalp, there may be a defect of the skull underneath the missing patch. In this case, there is often distorted hair growth around the patch, known as the hair collar sign.

Diagnosis

Diagnosis of aplasia cutis congenita is made based on the physical appearance of the infant’s skin. No specific laboratory test is needed. Very large scalp defects, especially those with the hair collar sign, should be investigated for possible underlying bone or soft tissue defects.

Treatment

Usually the only treatment required for aplasia cutis congenital is gentle cleansing of the affected area and the application of a silver sulfadiazine or other ointment to prevent the patch from drying out. Most affected areas will heal on their own over several weeks, resulting in the development of a hairless scar. Small bone defects also usually close on their own within the first year of life. Surgical repair is not usually needed unless the missing area of skin is large, or there are several areas on the scalp affected.

Sources:

About.com

Crowe, M. (2005). Aplasia cutis congenita. eMedicine, accessed at http://www.emedicine.com/derm/topic32.htm
National Organization for Rare Disorders. Aplasia Cutis Congenita