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Biomedical subjects

B Högemann

Publications and source records attributed to B Högemann.

12 recordsLinked to original sources
PubMed1992

[What is reliable in therapy of liver fibrosis?].

Therapy of chronic active liver diseases associated with fibrotic transformation is usually restricted to unspecific antiinflammatory and immunosuppressive agents. However, recent advances in the biochemistry of collagen have allowed to define specific levels of collagen metabolism at which pharmacologic intervention can lead to reduced collagen deposition. The mode of action of some substances which interfere with collagen biosynthesis and degradation is described. However, the efficacy of these agents was tested in vitro exclusively or in animal experiments. Only few agents like colchicine were also studied in clinical trials. Reliable, safe, and specific antifibrotic agents for the clinical management of liver fibrosis do not exist up to now. Advances can be expected, however, from the development of novel inhibitors of prolyl-4-hydroxylase.

Collagen↗
PubMed1990

[Ultrasonic findings in aggressive abdominal fibromatosis].

A case of aggressive abdominal fibromatosis is reported. Ultrasonography revealed multiple inhomogenous, hypoechoic tumours within the mesenterium and the anterior abdominal wall. Some of these lesions had a hyperechogenic margin.

Abdominal Muscles↗
PubMed1989

Significance of a sonographic secretin test in the diagnosis of pancreatic disease. Results of a prospective study.

In a prospective study the pancreatic duct diameter was measured sonographically before and after secretin stimulation in 20 healthy controls and 59 patients with upper abdominal pain, weight loss, and/or diarrhea. Whereas healthy controls and patients without pancreatic disease after secretin stimulation showed a distinct pancreatic duct dilatation of more than 90% of basal duct diameter, no distinct secretin-induced duct enlargement was observed in most patients with chronic pancreatitis. Patients with circumscript pancreatic duct stenosis even had a marked and longer-lasting duct dilatation after stimulation. In patients with anomalies of the pancreatic duct system, no uniform response was found after secretin injection. In this study the sonographic secretin test showed a sensitivity of 92% and a specificity of 95% for diagnosis of chronic pancreatitis. The results confirm that this diagnostic method can be recommended as a reliable screening test for pancreatic disease.

Adult↗
PubMed1989

Evaluation of serum laminin P1, procollagen-III peptides, and N-acetyl-beta-glucosaminidase for monitoring the activity of liver fibrosis.

Chronic liver diseases are characterized by an increase in connective tissue components in liver tissue. The determination of Col 1-3 peptide of type III procollagen (P-III-P) in serum of patients seems to be a useful parameter of hepatic fibroplasia. Specific radioimmunoassays are available for Col 1-3 (P-III-P) and the Col 1 and Col 1-3 (P-III-P-Fab) peptides of type III procollagen and for laminin P1 fragment. These proteins and the activity of N-acetyl-beta-glucosaminidase (beta-NAG) were measured in 94 patients with chronic liver diseases, and in 74 healthy controls. In addition, direct immunofluorescence studies were done for laminin P1 in normal and fibrotic liver tissues. In normal human liver, laminin was found in the basement membrane of bile ducts and in blood vessel walls. In fibrotic liver tissue, laminin additionally occurred in periportal areas and in sinusoids co-distributed with other connective tissue components. In serum concentrations of P-III-P, P-III-P-Fab and laminin were higher in patients than in healthy subjects. Laminin concentration was increased in early stages of chronic liver disease, possibly as a marker of regeneration; the highest concentrations were in active cirrhosis and chronic active hepatitis. The determination of P-III-P and P-III-P-Fab provided information on synthesis and degradation of type III collagen: In inactive cirrhosis, Col 1 peptide was increased in relation to Col 1-3 peptide.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗
PubMed1987

Sonographic imaging of the pancreatic duct. New diagnostic possibilities using secretin stimulation.

The pancreatic duct or at least parts of this structure can be demonstrated today by sonography in 75-85% of all persons examined. In 84 persons we have now measured the caliber of the sonographically visualized pancreatic duct in the region of the proximal body of the pancreas with special attention to dependence on age. The diameter of Wirsung's duct ranged from 1 to 3 mm (mean 1.9 mm) and increased significantly from the fifth decade of life onwards. After intravenous injection of the hormone secretin, healthy persons usually show a distinct duct enlargement, which also depends on age. Nine persons aged 19 through 35 (median 28) years showed a dilatation of the main pancreatic duct by about 110% following secretion injection. Nine further probands, 50-74 (median 58) years old, had a dilatation of about 70%. Eighteen patients with confirmed chronic pancreatitis and a pancreatic duct diameter not exceeding 4 mm generally showed no duct enlargement after secretin stimulation. We believe that periductal fibrosis, which is common in chronic pancreatitis, is the most important reason for these results. The use of the sonographic secretin test in the diagnosis of chronic pancreatitis should be considered.

Adult↗
PubMed1987

[Primary sonographic diagnosis of pancreatic duct calculi: the non-uniform aspect].

Four cases of sonographically visualised intraductal pancreatic calculi are reported. In three of these cases the calculi had been caused by chronic pancreatitis, and in one case by carcinoma of the head of the pancreas. The calculi did not present a uniform sonographic pattern, especially as regards echogenicity. A dorsal echo extinction was observed in three cases only. The non-uniform sonographic aspect of intraductal pancreatic calculi can probably be ascribed to differences in the lime content.

Adult↗
PubMed1986

Concentrations of 7S collagen and laminin P1 in sera of patients with diabetes mellitus.

Specific radioimmunoassays were used to quantify two basement membrane components, 7S collagen and laminin P1, in sera of 70 patients suffering from diabetes mellitus types I and II with and without clinical signs of chronic diabetic complications. Serum levels of both antigens were increased in diabetics compared to controls (p less than 0.001). Concentrations of 7S collagen were significantly different in diabetics with signs of microvascular damage compared to those without small vessel disease (p less than 0.05). The difference between laminin P1 concentrations in the two groups of diabetics was not significant (p less than 0.2). The augmented levels of circulating 7S collagen and laminin P1 may reflect alterations of basement membrane metabolism. Thus, the measurement of concentrations of these basement membrane components in serum may be a useful tool for monitoring the development of chronic diabetic complications.

Adolescent↗
PubMed1986

Basement membrane components (7S collagen, laminin P1) are increased in sera of diabetics and activate platelets in vitro.

Serum concentrations of two basement membrane components (7S collagen and laminin P1) were detected by specific radioimmunoassays in 70 patients suffering from diabetes mellitus type I and II with and without clinical signs of microangiopathy. Serum levels of both antigens were increased compared to controls. 7S collagen concentrations were significantly different between the diabetics with signs of microvascular damage and those without small-vessel disease (p less than 0.05). Laminin P1 concentrations were also elevated, but the difference between the two groups of diabetics was not significant (p less than 0.2). Raised levels of circulating basement membrane proteins may indicate connective tissue activity and development of diabetic microangiopathy. In vitro 7S collagen is a moderate platelet activator inducing platelet spreading, aggregation, and malondialdehyde production. Laminin activates platelet spreading. As a part of the altered hemostatic system the activation of basement membrane components may contribute to the development of microvascular damage.

Adult↗