Biomedical subjects
Publications and source records attributed to E A Pariente.
A patient with long-standing Waldenström's disease and cryoglobulinemia, treated with chlorambucil, developed hepatocellular carcinoma. Although HBs antigen, anti-HBs, and anti-HBc antibodies were not detected in his serum by conventional polyclonal radioimmunoassays, immunofluorescence techniques showed HBs antigen to be present in hepatocytes.
We assessed the prevalence of overt and latent primary myeloproliferative disorders in hepatic vein thrombosis. Cultures of bone marrow or peripheral blood mononuclear cells were done in 20 patients with Budd-Chiari syndrome. Erythroid colony formation in the absence of erythropoietin, which is a reliable indicator for a primary myeloproliferative disorder, was seen in 16 patients in whom Budd-Chiari syndrome was due to hepatic vein thrombosis, including 13 women aged 18 to 45 years. Among these 16 patients, the conventional criteria for the diagnosis of a primary myeloproliferative disorder were met in only 2. Primary myeloproliferative disorder, often without peripheral blood changes, is a major cause of hepatic vein thrombosis in young women.
In a 37-year-old woman with chronic watery diarrhea of three years duration, the diagnostic of collagenous colitis was established by optical and ultrastructural examination of rectal and colonic biopsies. No other cause of diarrhea could be found. Moreover, this patient had also selective IgA deficiency, Grave's disease and chronic atrophic gastritis of auto-immune type. Sequential treatments with loperamide, cholestyramine and antibiotics did not modified diarrhea which improved with salazosulfapyridine and betamethasone enemas. These observations suggest that collagenous colitis might be a part of the spectrum of enteropathies associated with immunoglobulin deficiencies.
Glomerular metastases are rarely observed. Two cases of such metastases are reported. In one patient, proteinuria was detected and the diagnosis was made by kidney needle biopsy; light microscopy, immunofluorescence, and electron microscopy studies were performed. The second case was an autopsy finding. The histologic patterns were, respectively, an intracapillary metastasis and associated intra- and extracapillary metastases. These findings raise a number of questions concerning the early detection of such neoplastic diseases, the nature of primary tumors, and the mechanisms of malignant dissemination and glomerular localization.
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Systemic and splanchnic hemodynamics, renal blood flow, and renal function were studied in 13 patients with cirrhosis both before and 1 h after oral administration of 40 mg of propranolol (acute administration) and 1 mo after continuous administration of this substance at doses reducing the heart rate by 25% (chronic administration). Cardiac output and the gradient between wedged and free hepatic venous pressures significantly decreased after acute and chronic administration of propranolol; mean arterial pressure did not change significantly and systemic vascular resistance significantly increased. Renal blood flow and renal vascular resistance did not change significantly after acute administration of propranolol and renal function did not change significantly after acute or chronic administration of propranolol. We conclude that propranolol does not alter renal function in patients with cirrhosis who are in good physical condition.
Sixty-one patients with symptomatic endoscopically confirmed duodenal ulcer, 5 mm or more in diameter, were treated with omeprazole 30 mg once daily in the morning for 4 weeks. Complete ulcer healing was assessed by endoscopy performed after 15 and, if necessary, 29 days of treatment. The healing rate as 83 p. 100 (49/59 patients) after 2 weeks, and 98 p. 100 (58/59 patients) after 4 weeks. Only 5 patients remained symptomatic on day 15. Fifty-six patients did not take any antacid during the course of treatment. There were few adverse effects. No clinically significant changes in laboratory parameters were observed. These results confirm: the remarkable efficiency of omeprazole in short-term treatment of duodenal ulcer, the good tolerance to this drug, at least in short duration treatment.
Six episodes of acute rhabdomyolysis were observed within a two-year period in 5 male adult alcoholic patients hospitalised in a hepatology intensive care unit. Painful muscle swelling was discrete of absent in 4 of the 5 patients. Acute rhabdomyolysis was preceded by grand mal seizures in 4 patients, delirium tremens in 1 and high fever with shivers in 3. All cases were rapidly diagnosed on the finding of very high serum creatinine phosphokinase levels. One patient developed acute respiratory failure and recovered after prolonged mechanical ventilation. Three patients had acute renal failure with severe hyperkalemia in one but none required dialysis. Three patients died within 2 to 6 days of the diagnosis, but the deaths were not directly related to rhabdomyolysis. It would appear that in alcoholic patients: the prevalence of rhabdomyolysis is probably underestimated; any muscular hyperactivity as seen in seizures, delirium tremens and prolonged shivers may be a precipitating factor; the condition is easily diagnosed by measuring serum creatinine kinase activity; some cases of acute renal failure in patients with alcoholic cirrhosis might be explained by acute rhabdomyolysis with minimal symptoms.
The authors report the case of a patient with hepatitis after the administration of dihydralazine, an analogue of hydralazine which is widely used in Europe. Hepatitis occurred during the administration of dihydralazine, quickly improved when the administration of dihydralazine was interrupted, and worsened again when it was resumed. Hepatitis was severe with hepatic encephalopathy and prolonged prothrombin time. There was centrizonal and bridging necrosis. After interruption of the drug administration, the outcome was favorable, but fibrotic sequelae were observed on a follow-up histologic examination.
We report the cases of four adult patients suffering from acute hepatitis due to isaxonine phosphate (Nerfactor), a drug recently proposed for the treatment of the lesions of peripheral nerves. Hepatitis developed 14 to 166 days after the beginning of the administration of the drug. In all the patients, predominantly centrilobular hepatocytic necrosis was present. In two of our patients, the course of hepatitis was fatal. Hepatitis induced by isaxonine phosphate is likely to be due to an immuno-allergic mechanism.
We describe two patients with alcoholic cirrhosis in whom staphylococcal right-sided endocarditis developed after insertion of a peritoneovenous shunt (PVS). Massive pulmonary embolism caused early death in one patient. In the other patient, staphylococcal septicemia was cured after shunt removal and antibiotic treatment; recurrent endocarditis due to Corynebacterium xerosis ultimately caused the patient's death. No clinical manifestation of tricuspid valve dysfunction was noted in either patient, and right-sided endocarditis was recognized only at autopsy. The protracted contact of the tip of the venous line of PVS with the atrial wall is likely to be a major factor in the development of right-sided endocarditis in these patients.
A 39-year-old moderately obese and alcoholic man complained of abdominal pain and nausea. An ultrasound examination of the liver showed large hyperechoic areas surrounding a limited pseudotumorous zone of relatively decreased echogenicity. CT scan showed a decreased density (35 UH) in the hyperechoic areas, suggesting fatty liver which was confirmed histologically; conversely, the hypoechoic area appeared normal on CT scan. Six months later, after reduction of caloric intake and cessation of alcohol ingestion, ultrasound examination and CT scan of the liver were normal.
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The influence of the initial upper GI tract exploration upon the accuracy and cost of diagnosis was evaluated in 103 in- and out-patients of a hepato-gastroenterology unit. The patients were divided at random into two groups of comparable number, age, sex and clinical findings. One group was first examined by fiberoptic gastroscopy and the other by barium meal. In patients whose first examination was by endoscopy a second examination was less frequently needed (3/53 versus 14/50; p less than 0.01), significant lesions (e.g. oesophagitis, oesophageal varices, gastroduodenal losses of substance or tumours) were more often diagnosed (22/53 versus 11/50; p less than 0.05) and the time required for a diagnosis to be made was shorter (mean 7 +/- 6 days versus 14 +/- 16 days; p less than 0.01), even when only one examination was performed (7 +/- 6 days versus 12 +/- 15 days; p less than 0.05), than in patients first examined by barium meal. It is concluded that fiberoptic gastroscopy should be the initial method of exploration of the upper GI tract.
The presence of PAS-positive, diastase-resistant inclusions in the cytoplasm of the hepatocytes is characteristic of alpha-1-antitrypsin deficiency. The purpose of this investigation was to determine whether the presence of these inclusions is a specific feature, permitting the recognition of alpha-1-antitrypsin deficiency in patients with liver disease. We examined the liver specimens from 20 patients suffering from alcoholic cirrhosis with the Pi M phenotype, i.e., in whom alpha-1-antitrypsin deficiency was excluded. In seven of these patients, PAS-positive, diastase-resistant inclusions were seen in the hepatocytes; in two patients, these inclusions contained a material antigenically similar to alpha-1-antitrypsin. These inclusions might represent deposits of glycoproteins poorly excreted by the diseased hepatocytes. It is concluded that, in patients with liver disease, the presence of PAS-positive, diastase-resistant inclusions--even containing alpha-1-antitrypsin--in the cytoplasm of the hepatocytes does not permit the hepatic lesions to be ascribed to alpha-1-antitrypsin deficiency.