[Massive intestinal hemorrhage as presentation of Behcet's disease].
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Biomedical subjects
Publications and source records attributed to R Solans.
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The case is reported of a patient who developed a vertebral osteomyelitis caused by Enterobacter cloacae. The organism was isolated in cultures of blood and vertebral puncture biopsy samples. The patient was satisfactorily treated with trimethroprim and sulphamethoxazole. Enterobacter cloacae, a Gram negative organism, has been confirmed as the cause of bacteremia in patients with burns, urinary infections, in adults with pneumonia, and in children with joint infections. Spondylodiscitis caused by Enterobacter cloacae has not previously been described.
BACKGROUND: The changes of nailfold capillaries detected by capillary microscopy is a characteristic frequently observed in systemic sclerosis. The relationship between the different capillary microscopic changes and clinical manifestation, organic disease and disease progression were studied. METHODS: Sixty-three patients were studied in whom capillary microscopy was performed and organic disease was determined by analytical and morphological examination. The presence of association between the capillary microscopic signs and clinical manifestation and disease progression were investigated by the chi-square and Fisher tests. RESULTS: Capillary microscopic alterations were found in 95% of the patients. The extense capillary loss was associated as statistically significant to the diffuse form of scleroderma. Statistically significant associations were not found between the different capillary microscopic signs and disease progression and organic disease (global and individual per each organ). CONCLUSIONS: Although capillary microscopic changes are present in most scleroderma patients they are not useful in the evaluation of organ involvement of the disease. The presence of extense capillary loss is linked to worse prognosis in its association to the diffuse form of scleroderma.
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Forty-eight patients fulfilling the criteria for carcinoma of unknown origin (CUO) between April 1983 and December 1987 were retrospectively analyzed. Mean age was 62 (33-83). Twenty-seven were males (56%) and 21 females (44%). The most common site of metastasis was the bone (35%), followed by the liver (19%) and lymph nodes (19%). 58% of cases were adenocarcinomas. Overall 274 studies for the detection of the primary tumor were carried out, the diagnosis being achieved in 10 cases (3.65%) which corresponded to lung neoplasms (5 cases), prostatic adenocarcinoma with negative markers (2 cases), bile duct neoplasms (2 cases) and pancreatic carcinoma (1 case). In our series, the most useful studies were computed tomography (CT) and fibrobronchoscopy. The necropsy, carried out in 11 patients, yielded 8 additional diagnoses: pulmonary neoplasm (one case), gastric adenocarcinoma (2 cases), malignant melanoma (2 cases), small intestine neoplasm (one case), parotid cancer (one case) and hepatocarcinoma (one case). Thirty-five patients were treated with chemotherapy and/or radiation; 12 objective responses (3 complete and 9 partial) were achieved, with a median duration of the response of 10 months (range 0.2-78 +). In view of the low diagnostic yield of the studies in patients with CUO we feel that the diagnostic study may be limited to CT scan with evaluation of the possible usefulness of bronchoscopy in individual patients. Regarding therapy, it is to be noted that there was a tendency for a longer survival in patients who responded.
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In 1992 interferon alpha (IFNalpha) was approved by the FDA for the treatment of chronic viral hepatitis B and C. Since then IFNalpha has been implicated in the development of several autoantibodies as well as in the development or exacerbation of various autoimmune disorders. Herein, we describe a 47-year-old female who developed a limited form of systemic sclerosis (SSc) with lung involvement 6 months after the institution of IFNalpha therapy for chronic active hepatitis C. There was no family or personal history of autoimmune diseases. We speculate that the immunomodulatory effects of IFNalpha triggered the clinical manifestations of SSc in this patient. To our knowledge, this is the second case of SSc developing after therapy with IFNalpha and the first in a patient treated for chronic viral hepatitis C.
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