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Biomedical subjects

G Gaber

Publications and source records attributed to G Gaber.

4 recordsLinked to original sources

[American cutaneous leishmaniasis: special features in diagnosis and therapy].

HISTORY AND CLINICAL FINDINGS: Three weeks after returning from a trip to Guatemala, a 33-year-old man developed two ulcers with indurated edges on his right leg and painful lymph nodes in the right groin. His general condition was not impaired. EXAMINATIONS: Histological examination revealed cellular infiltrates of the corium by lymphocytes and plasma cells, always accompanied by epithelial cells and multinuclear giant cells. Special stainings were unable to detect pathogens but Leishmania brasiliensis was identified using PCR. The Leishmania culture remained negative. THERAPY AND COURSE: After 7-day intravenous therapy with 20 mg/kg/d pentostam (pentavalent antimonial compound), the patient developed gastrointestinal complaints, coupled with a marked elevation of transaminases. Therapy was discontinued until the transaminase values normalized, then continued in reduced dosage (12 mg/kg body weight) for 23 days. The ulcers and lymphadenitis healed under this therapy. CONCLUSION: The diagnosis of American cutaneous Leishmaniasis may be complicated by the relative lack of pathogens in the lesions. PCR diagnosis are very helpful here. The therapy must be systemic owing to the danger of progression to mucocutaneous Leishmaniasis. The standard therapeutic pentostam has, however, a high rate of side effects and administration is exclusively intravenous.

Adult↗

Dapsone in rosacea fulminans.

Rosacea fulminans is a rare disease with female predominance characterized by abrupt onset of pustules, papules, and confluent nodules on the face. The conventional treatment consists of systemic glucocorticoids and isotretinoin. We present the case of a 56-year-old woman with a marked facial papulopustular eruption that had followed an initial period of severe seborrhoea. Conventional treatment produced no clear improvement. Dapsone treatment achieved complete healing in 5 weeks.

Administration, Oral↗

Panniculitis, pancreatitis and very severe aplastic anemia in childhood: a challenge to treat.

In childhood, aplastic anemia is a rare disease of unknown etiology. Besides toxic effects, also an infectious or an autoimmune origin are discussed. We report on an 8-year-old boy with very severe aplastic anemia (VSAA) who developed pancreatitis together with panniculitis. Initially, active cytomegalovirus (CMV) infection was thought to be possibly contributive. Ganciclovir was tried resulting in clearance of CMV, but VSAA persisted. Two months after the onset of VSAA, oligosymptomatic pancreatitis was observed together with the onset of severe febrile panniculitis, occurring with multiple painful enlarged subcutaneous infiltrates of up to 7 cm in diameter. Treatment according to the Severe Aplastic Anemia-94 (SAA-94) protocol consisting of glucocorticoids, cyclosporin A (CsA), anti-thymocyte globulin and granulocyte colony-stimulating factor was instituted. Since this treatment did not lead to remission after day 110, escalation of the CsA dose up to 8 mg/kg body weight was tried. This regimen resulted in complete recovery of panniculitis and symptoms of pancreatitis. Incomplete hematological remission was reached and, to date, the patient has not required transfusions for 6 months. Because this boy suffered simultaneously from three rare disorders, which all responded to intense immunosuppression, this observation may underline common autoimmune mechanisms of these distinct diseases.

Anemia, Aplastic↗

Metastasising malignant lymphoma mimicking necrotising and hyperplastic gingivostomatitis.

This paper presents the case of a 65 year-old woman suffering from recurrent oral aphthoid ulcers which rapidly evolved towards hyperplastic and ulcerated lesions over the entire floor of the mouth. The initial lesions were interpreted as non-specific aphthoid ulcers. Later, a tentative diagnosis of necrotising stomatitis with secondary reactive proliferating epithelial hyperplasia was made. The clinical symptoms and the immuno-phenotyping of lymphocytes circulating in the peripheral blood suggested the diagnosis of CD30-positive large cell anaplastic lymphoma. The biopsy showed only a pseudoepitheliomatous hyperplasia, reactive infiltrates and no lymphoma cells. The disease ran a fulminant course leading to death within 4 weeks due to acute gastro-intestinal bleeding. Autopsy revealed infiltrates of CD30+ large cell anaplastic lymphoma in a submandibular lymph node, in a thrombus stenosing the right subclavian vein, in the spleen, the anterior and posterior gastric wall as well as in the depth of the tumour on the floor of the mouth. The clinical and histopathological spectrum of CD30+ large cell anaplastic lymphoma is considerably variable. The particular feature of pseudoepitheliomatous hyperplasia has been reported especially in CD30+ anaplastic large cell lymphomas. An early correct diagnosis is rendered difficult in insufficient biopsy size, becauses this type of lymphoma often simulates other inflammatory or neoplastic skin diseases. Thus, with a necrotising and hyperplastic gingivostomatitis, the diagnosis of a CD30+ anaplastic large cell lymphoma should be considered.

Aged↗