[On the clinical differential diagnosis of mesenteric lymphadenitis (Masshoff)].
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Biomedical subjects
Publications and source records attributed to L Bianchi.
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PURPOSE: The purpose of this study was to determine whether kidney size in patients who have autosomal dominant polycystic kidney disease (ADPKD) is related to renal function, hypertension, or extrarenal manifestations of the disease and to sonographically evaluate the abdominal manifestations of ADPKD. METHODS: Between 1994 and 1998, 400 individuals from 85 families with a history of ADPKD were examined. There were 213 persons with ADPKD and 187 unaffected family members; there were 182 males and 218 females, 1-82 years old (mean, 39.3 years). We obtained a complete medical history, performed a physical examination, measured the arterial blood pressure and serum creatinine levels, and performed abdominal sonography on each subject. The sonographic features that were studied were renal length and the presence and number of cysts on the kidneys, liver, and pancreas. RESULTS: There was a relationship between kidney size and age (p < 0.05), kidney size and renal function (p < 0.001), and kidney size and hypertension (p < 0.001). The overall prevalence of hepatic cysts in patients with ADPKD was 67%, and the prevalence increased with age. The presence of hepatic cysts was related to the severity of renal disease. Females had more severe polycystic liver disease, and massive polycystic liver disease (ie, hepatomegaly with innumerable cysts) was seen only in females. The prevalence of pancreatic cysts in the 187 persons in whom the pancreas was well evaluated sonographically was 5%. CONCLUSIONS: Kidney size in patients with ADPKD is related to renal function, hypertension, and extrarenal involvement and can be used to predict the outcome of the disease. Hepatic cysts are very common in patients with ADPKD and are related to age and renal function; pancreatic cysts are infrequent in these patients.
The finding that the recently described hepatitis B (HB)-associated delta antigen (delta Ag) is preserved in pronase-treated, formalin-fixed paraffin sections allowed a combined prospective and retrospective immunohistological study of its occurrence in 571 liver biopsies. Among 116 frozen biopsies (69 HBAg seropositive, 47 HBAg seronegative) and 455 paraffin-embedded biopsies (296 HBAg seropositive, 159 HBAg-negative), delta Ag was found in 10 HBAg seropositive patients. With the exception of 1 patient with chronic persistent HB, all had chronic-active HB and none had acute HB; 5 patients were i.v. drug abusers. In follow-up biopsies, the delta Ag persisted with HBsAg for as long as 6 years. The expression of delta Ag showed similarities to the HBcAg system including nuclear localization, mixed nuclear cytoplasmic expression, and coexistence with anti-delta in blood. The findings are compatible with the hypothesis that delta Ag represents a transmissible, defective viral agent which requires HBV as a helper and may modulate, but not terminate, ongoing HBV infection.
The presence of albumin receptors on the plasma membrane of isolated human hepatocytes was investigated employing albumin-coupled latex minibeads. Hepatocyte-latex reaction was visualized by phase contrast and scanning electron microscopy. The experiments demonstrate that hepatocytes exhibit binding activity for polymeric and monomeric forms of glutaraldehyde-treated albumin. Additionally, the reaction was shown to be species-nonspecific. These findings support the hypothesis that polymerized albumin may act as a bridge between receptors on hepatitis B virus and human hepatocytes.
Anti-HBc IgM was determined by a modified radioimmunoassay (RIA) in 35 patients with acute hepatitis B, 35 patients with chronic hepatitis B (7 with chronic persistent, and 28 with chronic active hepatitis), 157 HBsAg positive blood donors, and in 143 HBsAg negative but anti-HBc positive donors. The results of the RIA test were compared with those obtained by an ELISA technique. In chronic hepatitis, anti-HBc IgM was correlated with the occurrence of HBeAg, anti-HBe, Dane particles in the serum, HBsAg, and HBcAg in liver tissue and with biochemical and histological degrees of hepatic inflammatory activity. In acute self-limited hepatitis B, anti-HBc IgM (RIA and ELISA) was initially positive in all 35 patients. Twelve months after the acute illness, 94% of the patients were negative for anti-HBc IgM in the RIA test with only one patient showing a persistence of up to 18 months, whereas in the ELISA test anti-HBc IgM persisted in 17% of the patients over 2 years. In chronic hepatitis, the occurrence of anti-HBc IgM (RIA) showed a strong relation with the inflammatory activity, the anti-HBc IgM positive patients revealing a significantly more severe liver disease than did anti-HBc IgM negative patients. Anti-HBc IgM (RIA), however, did not correlate with the occurrence of HBeAg and Dane particles in the serum and HBcAg in liver tissue of patients with chronic hepatitis. Of the 157 HBsAg positive blood donors, anti-HBc IgM (RIA) could be demonstrated in 10 (6%), but in none of the 143 HBsAg negative, but anti-HBc positive donors, as compared to 43 (27%) and 9 (6%), respectively, in the ELISA test. Comparing the two test methods, the RIA exhibits higher specificity than did the ELISA due to a better blocking of nonspecific reactions, but possibly somewhat lower sensitivity. In this form, however, the RIA test is a more useful tool in the diagnosis of the different forms of hepatitis B virus infection and in determining the severity of chronic hepatitis B.
In an electron microscopic study, nuclear aggregates of virus-like spherical and tubular particles measuring 20 to 29 nm in diameter were found in 5 of 7 clinically healthy volunteers with normal liver histology, 6 of 10 patients with hepatitis B and 17 of 18 patients with hepatitis non-A, non-B. The incidence of hepatocytes containing nuclear particles was approximately 0.5 to 2% in all three groups. We conclude that these nuclear particles are not specific ultrastructural markers of hepatitis non-A, non-B in man as originally claimed for experimental hepatitis non-A, non-B in chimpanzees.
We have investigated, by scanning and transmission electron microscopy (SEM and TEM), the cell surface morphology of isolated human hepatocytes. For this purpose, liver cells were mechanically isolated from surgical or needle liver biopsies, fixed in 3% glutaraldehyde and post-fixed in 2% osmium tetroxide. In order to handle a low number of cells, a particular procedure for harvesting hepatocytes on coverslips has been developed for SEM and an in situ embedding procedure in polyethylene-embedding capsules was applied for TEM. A rough membrane exhibiting short, uniform microvilli and pores of 0.1 mu in diameter was the main feature of isolated liver cells. Furthermore, single hepatocytes showed no polarity and junctional or bile canaliculus remnants were rarely observed. However, differences in surface configuration were noted in relation to culture conditions, such as oxygen and temperature during isolation procedures. SEM, when controlled by TEM for intracellular preservation, is proposed as a reliable method for screening small quantities of hepatocyte suspensions, for intact cells and for the study of surface configuration under experimental conditions.
In a prospective study, 102 hospital patients with liver disease were evaluated in West Cameroon, Africa. Blood donors, pregnant women and patients without liver disease served as controls. A total of 757 individuals were tested for markers of hepatitis A, B, C and D and for immunological markers (autoantibodies, procollagen III, alpha-foetoprotein, CA50 antigen, alpha-1-antitrypsin and antibodies to human immunodeficiency virus types 1 and 2). One-third of the liver disease patients had focal lesions on ultrasound examination. Histologically, 20 cases of cirrhosis, 14 cases of chronic hepatitis, 15 hepatocellular carcinomas and 17 cases of acute hepatitis were detected. All hepatic patients and virtually all controls had had a previous hepatitis A virus infection. Over 85% of adult patients and controls had at least one marker of hepatitis B virus infection. Over 30% of patients with liver disease had markers of possible hepatitis B virus replication. Antihepatitis C virus antibody was present in 18% of hepatic patients and in 6% of controls. Hepatitis C virus infection seems to play an important role in the development of chronic liver pathology; 40% of cirrhotic patients had a combined hepatitis B and C virus infection. Serum autoantibodies were frequently found and were not correlated with the presence of autoimmune liver disease.
Metastasis to the gallbladder is rare. Malignant melanoma is the tumor that most often metastasizes to this site. For this reason, the finding of solid lesions in the gallbladder wall in patients with advanced stage melanoma should lead to the suspicion of metastatic disease. The aim of this report is to describe and illustrate a case of surgically confirmed malignant melanoma metastasis to the gallbladder and to review the most significant ultrasound findings described in the literature for gallbladder lesions caused by melanoma.
The release of glutamate, aspartate, GABA, and taurine from the striatum of young (3 months), mature (12 months), and old (22 months), freely moving male rats was investigated by using a microdialysis fiber inserted transversally in the striatum. In old rats basal extracellular glutamate and aspartate levels were decreased vs. young rats (-38 and -49%, respectively). GABA and taurine levels were unmodified by age. In the presence of the adenosine receptor antagonist 8-phenyltheophilline (8-pT) at the concentration of 50 microM, both K(+)-evoked releases of glutamate and aspartate were more than doubled in young, but not in mature and old rats. 8-pT at the concentration of 500 microM significantly decreased glutamate basal levels and K(+)-evoked aspartate release in old rats only. GABA and taurine releases were not affected by 8-pT at either dose. Our findings indicate a modified adenosine modulation on glutamate and aspartate release in aged rats, that could result from a change in the balance between A1 and A2a adenosine receptor density or an alteration of A1 and A2a receptor-effector coupling.