Omar Lupi da Rosa Santos

The Olmsted syndrome

A 35‐year‐old man had a hyperkeratotic disorder of the palmoplantar skin since the age of 6 months. The palmoplantar keratoderma progressed to thick and warty hyperkeratotic plaques, which enlarged and formed verrucous lesions and deep fissures. The acral keratoderma gradually involved the dorsal surface of the hands and feet with flexion contractures of the fingers and toes (Fig. 1). Since the age of 2 years, the patient also showed universal alopecia and small sharply marginated hyperkeratotic plaques around the nose and mouth, in the groin, and in the intergluteal area (Fig. 2). All of these keratotic lesions were strikingly symmetric.

Artrite psoriásica: entidade clínica distinta da psoríase?

Psoriasis and psoriatic arthritis are complex and heterogeneous clinical entities, whose presentations comprise multiple combinations of subtypes. There are doubts even if they are distinct entities or merely variants of the same disease. Epidemiologically, psoriasis can be considered a common disease because it affects about 2% of the world population. Regarding psoriatic arthritis, there is no consensus in the literature about its true incidence and prevalence in the general population. Genetic, immune, and environmental factors interact culminating in skin and joint manifestations of psoriatic disease. The central role of activated T lymphocytes in the pathogenesis of both psoriasis and psoriatic joints is now recognized. Furthermore, proinflammatory cytokines can be found in increased concentrations in both skin and synovium of patients with psoriatic arthritis. Since 1964, when the relationship between psoriasis and psoriatic arthritis was recognized, many studies have been conducted to better understand the common mechanism of both diseases. The HLA has already been considered the center of the psoriatic arthritis immunopathogenesis; today, TNF-α plays such a role. This paper is a review of various factors associating psoriasis and psoriatic arthritis leading to the hypothesis of a single disease with multiple presentations.

Obstructive Renal Failure due to Therapy with Sulfadiazine in an AIDS Patient

Luiz Paulo J. Marques, MD, University of Rio de Janeiro, Rua Major Avila 455/312, 20511 Rio, de Janeiro (Brasil) Dear Sir, Toxoplasmosis in one of the most common opportunistic infections in AIDS patients, and the treatment of choice is the synergistic combination of sulfadiazine and pyrimethamine for a prolonged period. Cry-stalluria and acute renal failure due to sulfadiazine have been described by several authors [1,2]. We report a case of obstructive renal failure due to the administration of sulfadiazine that resolved with rapid infusion of intravenous sodium bicarbonate and fluids without discontinuation of sulfadiazine therapy. A 35-year-old female AIDS patient was referred for evaluation of generalized seizure and weakness of the right arm that presented 3 days before admission. When she was admitted, her serum creatinine level was 0.6 mg%; total serum protein; 7.3 g%; albumin: 4.2%; globulin: 3.1 g%; hemoglobin level: 13.6 g/dl; hematocrit: 41%; normal urinalysis. Serology for toxoplasmosis was: IgG 1/2,048 and negative IgM. Cerebrospinal fluid examination showed only anti-HIV I (Elisa) posi-tivity and IgG 11.6%. Computed tomography scan revealed contrast enhancing left cerebral lesion. On day 3 hospitalization, she presented an other episode of generalized seizure and developed right hemiplegia. Oral sulfadiazine (1.0 g every 6 h), oral pyrimethamine (25 mg daily) and folinic acid were begun for suspected toxoplasmosis. On day 7 of therapy, she presented abdominal pain, dysuria and oliguria (36-hour urine output: 300 ml). Serum creatinine was 3.9 mg%; urinalysis revealed sulfa crystals and numerous red blood cells per high-power field, and renal ultrasound detected bilateral lithiasis with moderate hydronephrosis. Administration of intravenous sodium bicarbonate, 3 liters of fluids and furosemide (20 mg every 6 h were begun, without discontinuation of sulfadiazine. After few days of therapy, renal function returned of a normal level and she was discharged on day 19 of therapy with partial remission of neurologic signs; serum creatinine was 0.6 mg%, and she had normal urinalysis without the presence of sulfa crystals. Obstructive acute renal failure associated with sulfadiazine has been previously described due to the low solubility of the sulfo-namides as well as under appropriated conditions, such as dehydration and hypoalbu-minemia [3]. However, with adequate hydra-tion and alcalinization of urine, renal failure may be resolved without discontinuation of sulfadiazine. Physicians using sulfadiazine for the treatment of toxoplasmosis should be aware of the risk for crystalluria and renal failure, especially during