Common malignant cutaneous conditions among albinos in Kenya.

Background: Albinos in Africa are at constant risk of developing skin cancer due to the damage caused by ultra-violet exposure. This study identifies the common skin conditions among albinos in Kenya as a country located along the equator. Methods: In this descriptive study on albino patients who were admitted to Mbagathi District Hospital in Nairobi, Kenya the census method was used for sampling and a total of 151 albinos were registered. All necessary data including age, gender, type, site and the number of skin lesions were recorded. Suspected patients with malignant and premalignant lesions were studied individually through skin biopsy and histopathological investigation. Finally, the collected data were analyzed using SPSS software. Results: Albinos with serious skin lesions were 121(80%) patients. Females were 64 (52.9%). The frequency of the following premalignant and malignant skin lesions including actinic-cheilitis, solar elastosis, actinic keratosis (AK), basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) were 17.88%, 11.92%, 37.08%, 7.94% and 5.29%, respectively. Hands (20.52%), face (19.20%), head (18.18%), shoulder (14.56%) and neck (7.94%) were the most affected areas by malignant and premalignant lesions. Conclusions: BCC was the most common type of cutaneous malignancy on the face and shoulders while AK was the most common cutaneous pre-malignancy on the hands and face in albinos in Kenya. Therefore, appropriate physical protection, avoiding any trauma when carrying sharp, heavy or rough instruments by the shoulder and hands, and finally urgent and quality treatment for any lesion even a small erosion and ulcer, especially on exposed areas in albinos, are recommended.

Sézary syndrome, Kaposi sarcoma and generalized dermatophytosis 15 years after sulfur mustard gas exposure.

BACKGROUND: The relationship between compromised immune system and the development of malignancy, generalized dermatitis, and infection after sulfur mustard gas exposure has been established. MAIN OBSERVATION: We introduce a 58-year-old man with an abrupt, de novo and erythrodermic eruption in 2002 that was previously exposed to sulfur mustard during the Iran - Iraq war in 1987. Six weeks after the onset of diffuse eruption, he developed papules on the glans penis and generalized dermatophytosis. A biopsy of his eruption was consistent with cutaneous T-cell lymphoma/Sézary syndrome. A complete blood count demonstrated leukocytosis, eosinophilia and atypical lymphocytosis. Subsequently, Sézary syndrome was confirmed and T-cell count with increased CD4/CD8 in flow cytometry. The biopsy of his penile papules was consistent with Kaposi's sarcoma. CONCLUSION: These findings suggest a causative relationship between sulfur mustard gas exposure, cutaneous T cell lymphoma and immune compromised state with opportunistic infections.

Pathogenesis and treatment of skin lesions caused by sulfur mustard.

OBJECTIVE: Sulfur mustard (SM) exposure intensely causes lesions that range in severity from mild erythema to blister formation and necrosis. This review will discuss acute and long-term skin consequences due to exposure to SM and different kinds of medical prophylaxis and therapeutics against SM-induced skin lesions. METHODS: Literature survey of medical case reports, clinical studies, and original articles was performed using PubMed, Medline, and the Cochrane Database (1917-2011 March). Key words included sulfur mustard, skin, toxicity, pathogenesis, cancer, treatment. RESULTS: SM-induced damage to the skin is characterized by edema, inflammation, and cell death mainly of the basal keratinocyte layer, with varying immunological and pathological changes in the acute phase. Also, xerosis, hypo or hyper pigmentation, scars, and rarely, skin cancers are long-term cutaneous effects. So far,the combination therapy of topical drugs and oral antihistamines, also iodine and antitumor necrosis factor alpha antibodies, are effective remedies in the treatment of skin lesions. CONCLUSION: The requirement for preparedness in the dermatological community concerning SM exposure is underlined. Novel treatments for prevention and therapeutics against SM toxicity and carcinogenicity are reviewed.

Comparison late cutaneous complications between exposure to sulfur mustard and nerve agents.

BACKGROUND: Iraq used chemical weapons against thousands of Iranian militaries and civilians. This study aimed to compare the chronic cutaneous side effects of exposure to sulfur mustard (SM) with nerve agents (NA). METHODS: The study enrolled 154 SM exposed cases and 175 (NA) exposed cases. Presence of any late cutaneous manifestations was evaluated by a dermatologist via prior history of acute cutaneous complications extracted from medical achieves. RESULTS: only 18.1% mustard exposed group was asymptomatic compared to 62.4% nerve agent exposures. Mustard and non-mustard scars, intertrigo, xerosis, cherry angioma, hyper pigmentation, pilar keratosis, poikiloderma, and malignant tumors were significantly more frequent in mustard exposed patients (p < 0.05). Nerve agent exposed patients experienced significantly more frequent occurrence of acne a seborrheic dermatitis and tinea versicolor. CONCLUSIONS: Mustard induced dermaltologic lesions were more common and specific than (NA) skin injuries. (NA) cause few psychocutaneous disorders like acne and seborrheic dermatitis in addition to psychological stress disorders.

Darier disease associated with HIV infection: a case report.

AIDS is characterized with immune dysregulation and depletion of CD4+ T cells and increased vulnerability to different pathological conditions, including many dermatoses. The present report describes features of Darier disease (DD) in an HIV-positive patient. The subject of this report was a 45-year old Ghanaian man referred to the dermatology unit of the Iranian Red Crescent Society in Accra, Ghana. He presented with numerous follicular keratotic red-brown papules on the scalp, face, retroauricular regions, ears, sternum, upper trunk, hands, axilla, and inguinal regions. The lesions first appeared on the dorsal surface of the hands and face and subsequently appeared on the other parts of the body including the outline of the scalp. This is the first report of DD in the setting of HIV infection. Significant features of this case associated with HIV in comparison with non-HIV cases are negative family history of DD, late onset, and wide distribution of the disease without abnormality on the nails and mucous membranes beginning a few years after involvement with HIV virus.

Sulfur mustard-induced poikiloderma: a case report.

Sulfur mustard (SM) is a potent chemical warfare agent that was widely used during the First World War and the Iran-Iraq conflict. This vesicant agent causes several acute and chronic effects on the skin, eye, and respiratory system. We report the case of a 41-year-old man who was injured with SM in Iraq chemical attack in 1988. After exposure, he developed severe skin blisters on his upper trunk, dorsum of hands, and genitalia. Based on several clinical observations, such as atrophy, pigmentation, and vascular changes on genitalia with relevant findings in histopathological studies, persistent pigmentation, and damaged skin appendix in hand lesions, a diagnosis of "SM-induced poikiloderma" was postulated. The absence of any complication on the palmar aspect of hands is another remarkable finding in presented case, which suggests a plausible role of the palms as a vector for transporting SM to other sites of the skin.

Acute and chronic effects of sulfur mustard on the skin: a comprehensive review.

Sulfur mustard (2,2-dichlorodiethyl sulfide, SM) is one of the vesicant classes of chemical warfare agents that causes blistering in the skin and mucous membranes, where it can have lingering long-term effects for up to ten years (1). SM was employed extensively by the Iraqi army against not only Iranian soldiers but also civilians between 1983 and 1988, resulting in over 100,000 chemical casualties. Approximately 45,000 victims are still suffering from long-term effects of exposure (2,3). More than 90% of the patients exposed to SM exhibit various cutaneous lesions in the affected area. The human skin can absorb approximately 20% of the SM through exposure. Up to 70% of the chemical is concentrated in the epidermis and the remainder in the basement membrane and in the dermis (4).Sulfur mustard exists in different physical states. The liquid form of SM evaporates slowly in cold weather and can penetrate through the clothing, thereby increasing exposure. However, the gas form readily diffuses in the air and it can be inhaled, leading to systemic absorption. In addition, warm temperatures are ideal conditions that liquid SM present in the clothing of the exposed individual could be converted to gas form. SM-induced clinical cutaneous symptoms include itching and burning. Other clinical findings include erythema or painless sunburn, bulla, hypo- and hyper pigmentation in both exposed and unexposed areas (5,6) The mechanism and biochemical cascade of SM-induced cutaneous manifestations are not completely understood but several published pathways support many of the know facts. Our current understanding fails to explain the time interval between the acute chemical exposure and the late-onset and delayed tissue damage (7,8). The aim of this article is to review the acute and long-term cutaneous findings resulting from SM exposure. Also, cellular and molecular mechanism involved in SM-induced skin pathology have been discussed.

Extensive hypertrophic lichen planus in an HIV positive patient.

Individuals who are infected with Human Immunodeficiency Virus (HIV) suffer from numerous dermatoses. These disorders are often more severe than those observed in non HIV-infected persons afflicted with the same diseases. Lichen planus (LP) is a chronic inflammatory papulosquamous skin disorder. Herein, the diagnosis and treatment of a 40-year-old HIV+ Kenyan man afflicted with hypertrophic lichen planus (HLP) is described. In this case, lesions of HLP were widely distributed across the trunk and extremities, having become of such thickness on the dorsal surfaces of the hands and fingers as to make normal use of hands impossible. A significant distinguishing feature of this patient is prior history of tuberculosis, which is a known trigger for lichenoid skin lesions.