[Diagnostic value of laparoscopy in liver metastasis].
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Biomedical subjects
Publications and source records attributed to D Boixeda.
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We have prospectively studied the evolution of 13 patients with liver hydatid cysts treated with mebendazole. Two patients also had peritoneal hydatid disease in addition to liver cysts. One of the two also had a retrovesical cyst. Liver cysts disappeared in three patients. In one, the liver cyst reappeared and in another a new cyst was observed after treatment was stopped. Therapy was most effective in young patients, in small cysts, in one case of peritoneal hydatid disease and in one case of a retrovesical cyst. Side effects warranted interruption of therapy in three cases, although we cannot be sure that they were due to mebendazole treatment. We recommend long-term patient follow-up once the cyst can no longer be identified by ultrasound.
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Human Yersinia enterocolitica septicemia is an uncommon condition. Four new cases are reported here and a review is made of 51 others taken from medical literature. Septicemia caused by this microorganism occurs more frequently in the young and in the elderly, and usually involves patients havig previous liver or blood disorders, diabetes mellitus, and other debilitating diseases. Clinically it is indistinguishable from sepsis caused by other organisms of Enterobacteriaceae, but it is important that the clinician bear its existence in mind, since Yersinia enterocolitica strains are usually resistant to beta-lactam antibiotics, whereas they are susceptible to the aminoglycosides and co-trimoxazole, among others. Susceptibilities in the blood isolates from our patients, and in another ten fecal isolates from eight other patients showed the previously described pattern. Our isolates, however, were all susceptible to the new cephalosporins, cefamandole and cefoxitin, and to the experimental ones, HR-756, T-1551, and Ly-127.935.
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The correction of hepatopulmonary syndrome (HPS) after liver transplantation (LT) remains controversial. The aims of our study were to: 1) analyze whether LT reverses HPS; 2) note any relationship between HPS and the systemic hemodynamic disturbance; and 3) note changes in circulating sex hormones and the possible association with pulmonary and systemic hemodynamic changes. Systemic hemodynamic parameters, cardiac output and systemic vascular resistance (SVR), sex hormones, and intrapulmonary vasodilatation assessed by contrast transesophageal echocardiography, and gas exchange abnormalities were investigated in 19 patients with advanced cirrhosis prior to and 6 months (176.8+/-30 days) after LT. LT was followed by a marked reduction in cardiac output (6.6+/-1.7 vs 3.5+/-0.5 l/min; p<0.001) and SVR (1039+/-460 vs 1978+/-294 dyn x sec x cm(-5); p<0.005). Before LT, circulating estradiol and progesterone levels were invariably elevated (66+/-22 pg/ml and 1.8+/-1.1 ng/ml, respectively, normal values <31 pg/ml and 0.35 ng/ml, respectively), and dropped after LT (28+/-12 pg/ml p<0.001 and 0.38+/-0.2 ng/ml; p<0.001, respectively). Seventeen of 19 patients had intrapulmonary vasodilatation and increased alveolar-arterial oxygen difference, thereby fulfilling diagnostic criteria for HPS. Patients with HPS presented higher cardiac output (p<0.05), lower SVR (p<0.01), and higher progesterone and estradiol levels than patients without HPS (p<0.05). LT produced normalization of intrapulmonary vasodilatation in all patients. LT normalized hyperdynamic circulation and is a useful therapeutic option in patients with HPS. Normalization of sex hormone levels after LT suggests that they could play a pathogenic role in the development of HPS.
OBJECTIVE: To study histologic gastric mucosa lesions in patients with gastric ulcer disease and to assess their evolution in the year after Helicobacter pylori eradication. METHODS: Seventy-three patients with gastric ulcer were prospectively studied. On endoscopy, biopsy specimens were taken from the antrum and gastric body for hematoxylin and eosin staining and urease testing. Serology and 13C-urea breath test were carried out. Fifty-six patients treated for H. pylori infection were monitored with histologic study at months 1, 6 and 12 after therapy to eradicate H. pylori infection. RESULTS: In patients with gastric ulcer, the prevalence of H. pylori was 86.3% (95% CI: 76-92%). Similar percentages in patients with chronic gastritis (CG) and in those with active chronic gastritis (ACG) were noted in the antrum and gastric body. However, severe active chronic gastritis was more prevalent in the antrum (p < 0.01). In patients with H. pylori infection who were not treated with non-steroidal anti-inflammatory drugs (NSAIDs), the percentages of both CG and ACG were higher than those observed in patients with both risk factors (p < 0.01) and in those treated with NSAIDs and with no infection (p < 0.0001). The prevalence of glandular atrophy (17.8%; 11-28%) and of intestinal metaplasia (68.5%; 57-78%) was higher in the antrum than in the gastric body (4.1%; 1-11% and 16.4%; 10-26%, respectively) (p < 0.01). In the antrum of patients with successful treatment, the percentages of CG:ACG before treatment and 1, 6, and 12 months after treatment completion were: 100%:97%, 74%:14%, 44%:11% and 11%:2%, respectively. In the gastric body these rates were: 88%:86%, 51%:14%, 23%:4% and 4%:0%. Improvement of CG was observed at month 1 after treatment completion, which was then confirmed at months 6 and 12 (p < 0.01) whereas improvement of ACG was most often achieved at month 1 after treatment completion (p > 0.001). No changes in atrophy and intestinal metaplasia were observed after H. pylori eradication. CONCLUSIONS: Histologic gastritis associated with gastric ulcer disease involves both the antrum and gastric body, although prevalence of severe ACG, atrophy and intestinal metaplasia were higher in the antrum. Histologic gastritis were closely related to H. pylori infection but is unrelated to NSAIDs. H. pylori eradication results in progressive CG improvement over the first year, as well as in early ACG improvement (as soon as 1 month after treatment completion); however, atrophy and intestinal metaplasia remain unchanged.
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