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Biomedical subjects

R Behrens

Publications and source records attributed to R Behrens.

At least 37 records · Page 2Linked to original sources
PubMed1997

Congenital microvillous atrophy: report of two cases.

2 infants with chronic severe diarrhoea from birth and with lethal outcome have been studied. Small intestinal biopsies were examined by light and electron microscopy. Severe villous atrophy, complete loss of microvilli or rudimentary forms, intracytoplasmic vesicles, and microvillous inclusions are the characteristic features of the disease. The etiology is unknown. A disturbance in the transport of brush-border proteins to the cell surface is assumed to be the reason for congenital microvillous atrophy.

Atrophy↗
PubMed1996

Different expression of Helicobacter pylori gastritis in children: evidence for a specific pediatric disease?

BACKGROUND: Infection with Helicobacter pylori causes active chronic gastritis. Once the infection is acquired, gastritis will persist for almost the rest of one's life. To date, very few data are available on H. pylori gastritis in relation to age. Therefore, we attempted to investigate whether H. pylori gastritis in children exhibits features different from H. pylori gastritis in adults of two different age groups. MATERIALS AND METHODS: Fifty consecutive children with a median age of 11 years (range, 3-18 years) were compared with two groups of 50 adult patients, one group with a median age of 43 (range, 19-56 years) and another group with a median age of 70 years (range, 59-86 years). All patients had H. pylori gastritis unrelated to active peptic ulcer disease. Two biopsy specimens were taken from the antrum and two from the corpus, and the following gastritis parameters were evaluated: degree and activity of gastritis, H, pylori colonization, replacement of foveolar epithelium by regenerative epithelium, mucous depletion, presence of atrophic gastritis with intestinal metaplasia, and presence of lymphoid follicles. RESULTS: Degree and activity of gastritis, extent of H. pylori colonization, degree of replacement by regenerative epithelium, extent of mucous depletion, degree of atrophic gastritis with intestinal metaplasia, and the presence of lymphoid follicles in the antrum, as well as the presence of lymphoid follicles in the corpus differed significantly (chi-square test: p < .05). All these differences--except the once frequent occurrence of atrophic gastritis with intestinal metaplasia in adults--were attributable to a higher expression of these gastritis parameters in children. CONCLUSIONS: We conclude that H. pylori gastritis, particularly in the antrum, is more severely expressed in childhood. One reason for this might be a child-specific immune response to an infection with H. pylori. Alternatively, infection may represent a pediatric disease characterized by a nonatrophic, highly expressed form of gastritis, which changes its appearance once the host becomes adapted over time.

Adolescent↗
PubMed1995

Effect of growth hormone on IGF-I levels in a patient with growth hormone deficiency and Wilson disease.

This is a case report of a boy with a combination of two rare disorders:growth hormone deficiency (GHD) and Wilson disease. To our knowledge, no comparable case has yet been published in the literature. GHD was diagnosed at the age of 4.5 years (height standard deviation score (SDS) -4.85). However, because of a difficult family background, growth hormone (GH) therapy could not be started. The boy was not seen again until the age of 7.7 years (height SDS -4.77), when GHD was reconfirmed and GH therapy could be initiated (dose 0.6 IU/kg/week). At that time, elevated liver enzymes (GPT 128 U/l, GOT 67 U/l, gamma-GT 28 U/l) confused diagnostic procedures. On GH, growth velocity SDS increased from -1.86 to +4.50 in the first year and +3.87 in the second year, and height SDS increased to -4.26 and -3.59. However, serum IGF-I levels did not normalize (max. 67 ng/ml), and liver enzymes were still elevated. At the age of 10 years, Wilson disease was diagnosed in view of low concentration of serum ceruloplasmin, elevated urinary copper excretion and high copper content in a liver biopsy sample. Under a combined therapy with D-penicillamine and GH, serum liver enzymes decreased, and IGF-I levels increased to normal. Height SDS for chronological age has improved constantly.

Ceruloplasmin↗
PubMed1994

Frequency of stress lesions of the upper gastrointestinal tract in paediatric patients after cardiac surgery: effects of prophylaxis.

BACKGROUND: Stress lesions of the upper gastrointestinal tract are well recognised in adult patients in intensive care. There are no controlled studies of the incidence of these lesions and the effects or side effects of prophylactic treatment in high risk paediatric patients. METHODS: 79 paediatric patients in intensive care were studied prospectively after operation for congenital heart disease. All patients had at least one endoscopic examination. The first 36 patients were not given prophylactic medication: later 43 children were treated randomly either with pirenzepine (n = 21) or with famotidine (n = 22). Gastric and tracheal secretions were taken daily for culture in those patients given prophylactic medication. RESULTS: Severe inflammation or ulceration of the upper gastrointestinal tract was less common in those patients who were given prophylactic medication (18% v 44%). Prophylactic treatment did not, however, reduce the total incidence of postoperative stress lesions: it shifted the severity of these changes towards mild lesions and reduced the incidence of ulcerations from 25% to 2%. None of the patients developed a pneumonia caused by an organism previously isolated from the stomach. CONCLUSIONS: The incidence of stress lesions in children after cardiac surgery resembles that in high risk adult patients. Children in intensive care after cardiac surgery should be treated prophylactically with famotidine or pirenzepine until they can be fed by mouth.

Adolescent↗
PubMed1993

[Endogenous digitalis-like factor in liver cirrhosis and cholestasis].

Endogenous digitalis-like factor (EDLF), an inhibitor of membrane Na+/K(+)-ATPase, is discussed to be involved in the pathogenesis of cirrhogenic portal hypertension, ascites formation and development of functional hepatorenal failure. Therefore, we investigated the serum content of this mediator in patients with liver cirrhosis Child-Pugh stage A, B, and C (n = 27) by means of enzyme immunoassay with a specific digoxin antibody. Furthermore, a correlation analysis was performed in order to find out correlations between signs of cell injury, cholestasis, synthetic cell function, ascites formation, and hepatorenal failure. Our results demonstrate that EDLF is significantly elevated in Child C cirrhosis (0.61 +/- 0.15 ng/ml) in comparison to Child A cirrhosis (0.013 +/- 0.2 ng/ml) and is also higher than in Child B cirrhosis (0.23 +/- 0.25 ng/ml). In patients without ascites EDLF (0.056 +/- 0.19 ng/ml) differs significantly from that of patients with non-complicated ascites (0.156 +/- 0.176 ng/ml) and from that of patients with therapy refractory ascites (0.66 +/- 0.17 ng/ml) or hepatorenal failure (1.56 ng/ml). There are no correlations between EDLF and renal function. Significant correlations were demonstrated for cholestasis (serum bilirubin), synthesis function (serum protein, Quick's value, cholinesterase, fibrinogen, albumin), and the degree of portasystemic encephalopathy (number connection test). We conclude that EDLF may act as a mediator in the process of progressive portal hypertension and its complications due to cirrhosis. This process of progression is caused by the inhibition of Na+/K(+)-ATPase, vasoconstriction, and endothelin secretion.

Adult↗
PubMed1993

[Congenital cystic bile duct dilatation. Presentation of clinical symptoms, diagnostic possibilities and therapy based on 6 cases].

BACKGROUND AND METHODS: Congenital cystic dilatation of the bile ducts represents an uncommon anomaly of the biliary system. We report on 6 patients suffering from cystic biliary duct dilatations which were treated in our hospital between 1980 and 1992. Clinical signs included upper abdominal pain, white or clay-colored stool, icterus and/or palpable tumor. According to the classification of Todani, 4 children had type Ia cysts, 1 child a type Va cyst and 1 child a type Ia cyst with extrahepatic biliary atresia. RESULTS: Among the diagnostic methods sonography is preeminent and permitted demonstration of intra- and extrahepatic biliary duct dilatations in all of our patients. In 2 patients small cystic dilatations could be distinguished from hepatic vessels by colour-coded Doppler sonography. CONCLUSION: The treatment of choice is the resection of the dilated extrahepatic biliary ducts followed by hepaticojejunostomy using the Roux-en-Y-technique.

Abnormalities, Multiple↗
PubMed1993

[Caustic burns of the upper gastrointestinal tract. Diagnosis and therapy].

Out of 81 patients with suspected caustic injury 27% showed esophageal lesions. In 5% the lesions were severe and strictures developed and dilatations were necessary. The diagnosis has to be made by endoscopy in each suspected injury to rule it out or to control its steroid therapy. Even without oropharyngeal lesions caustic injury of the esophagus is possible. Endoscopy and dilatation were made under sedation and did not hurt the patients. No complications occurred. Steroids seem to be useful only in severe caustic ingestions.

Adolescent↗