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Biomedical subjects

J Rahier

Publications and source records attributed to J Rahier.

At least 127 records · Page 7Linked to original sources
PubMed1987

Biosynthesis of gastrin. Localization of the precursor and peptide products using electron microscopic-immunogold methods.

Antibodies to different peptides produced from the gastrin precursor have been used in light microscopic- and electron microscopic-immunogold studies of gastrinoma tissue and normal antral mucosa. Antibodies to the C terminus of progastrin, which are known to react with the intact precursor, revealed immunoreactive material in the rough endoplasmic reticulum, Golgi region, and electron-dense granules in gastrinoma cells. In normal antrum these antibodies again revealed the Golgi region and a population of electron-dense granules. Other antibodies that react with the products of progastrin processing, but not the precursor, e.g., C-terminal and N-terminal gastrin 17 specific antibodies, revealed only granules. In addition to electron-dense granules already mentioned, the latter antibodies also revealed electron-lucent and intermediate granule populations, which in antrum were the major granule types. It is proposed that the intact precursor occurs in rough endoplasmic reticulum and Golgi; thereafter, in the immature electron-dense granules, and subsequently in electron-lucent granules, biosynthetic processing liberates gastrin 17 and gastrin 34, which are the major active products of gastrin gene expression.

Gastrins↗
PubMed1985

Epidermal changes in atopic dermatitis.

The epidermal changes occurring in various lesions of atopic dermatitis are reported. Quantitative evaluation or epidermal thickening suggests that both differentiated and undifferentiated compartments are increased in lichenified lesions. In dry skin (xerosis) of atopic dermatitis moderate but obvious inflammatory changes are observed. There is a mild increase of the epidermal volume without folding of the dermo-epidermal interface. The latter is most prominent in exudative and lichenified lesions where a fourfold overall increase of epidermal volume is observed.

Biopsy↗
PubMed1985

[Liver transplantation in children].

Liver transplantation has become a clinical therapeutic modality for end stage liver diseases. The results achieved in children are better than in adults: in T.E. Starzl unique experience in Pittsburgh, USA, the survival rate at one and four years are 75 and 70% respectively. Complete rehabilitation of these children can nowadays be expected. Between March 1984 and June 1985, 8 children received an orthotopic liver transplantation at the University of Louvain Medical School in Brussels, Belgium; one child received two transplantations after acute and irreversible rejection of a first ABO incompatible graft. The indications were biliary atresia in five (polysplenia in one), biliary hypoplasia in one, alpha-1-antitrypsine deficiency in one and Crigler-Najjar syndrome type I in one. The age of the patients at the time of liver replacement was 12 to 18 months in four, 8 to 13 years in four. Six patients are alive after 17, 14, 12, 10, 3 and 3 months; the two youngest children deceased during the first postoperative month. The Kaplan-Meyer one year survival rate is 75%; all surviving children are in excellent clinical condition with a normal liver function. The 9 transplanted livers were harvested from multiorgan cerebral death donors with the exception of one neonate whose liver alone was removed; 4 were retrieved locally, the five others were offered by foreign hospitals through the organ procurement agencies (Eurotransplant, France-Transplant, U.K. Transplant). Due to appropriate logistics with air flight transportation of the harvesting team when indicated, the total ischaemia time was kept below 6 hours in every case. Two small children underwent a left lobe orthotopic transplantation after ex vivo right trisegmentectomy of the liver retrieved from an older donor with one long term survival. The indications for liver transplantation in children are end-stage liver diseases consisting of a) cholestatic diseases among which the most frequent is biliary atresia after unsuccessful Kasai procedure followed by familial cholestasis (Byler syndrome) and the paucity of the intrahepatic bile ducts of the syndromatic (Alagille syndrome) or non syndromatic type. b) the metabolic diseases resulting either in cirrhosis with liver failure (alpha-1-antitrypsin deficiency, Wilson disease, glycogen storage disease type I and IV, protoporphyria) or in extrahepatic complications of enzymatic deficiency of an otherwise normally functioning liver (Crigler-Najjar syndrome type I, familial hypercholesterolemia and perhaps oxalosis). c) the hepatocellular diseases either chronic with cirrhosis of various origin or acute, eg. toxic hepatitis.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1985

A case of cholestatic hepatitis associated with D-penicillamine therapy for rheumatoid arthritis.

A male aged 72 years suffering from erosive seropositive rheumatoid arthritis developed jaundice after one month on D-penicillamine after a cumulative dose of 5.625 g. The biological abnormalities were characteristic of cholestasis. There were no gall-stones. The liver biopsy showed severe intrahepatocellular cholestasis with a slight degree of cellular cholangitis and with eosinophils in the portal tracts. There was no sign of cellular necrosis. After cessation of D-penicillamine, the jaundice cleared within three weeks and the enzymes were normalized within two months. The aetiology is discussed and the cases of the literature are reviewed. This case represents a further instance of D-penicillamine-induced cholestatic hepatitis.

Aged↗
PubMed1985

[Our experience in the study and treatment of medullary carcinomas of the thyroid. Apropos of 2 familial cases].

Between July 1976 and July 1984, 1106 cold thyroid nodules have been operated on UCL. Teaching Hospital; 128 were diagnosed as carcinoma (11,5%) and 15 were diagnosed as medullary carcinoma of the thyroid gland (1,3% of all the cold nodules and 12% of all carcinomas of the thyroid). This article presents the case of two families exhibiting a characteristic clinical history of Medullary Carcinoma of the thyroid or CMT. The authors describe briefly the clinical signs; they point out that it is absolutely necessary to ask for a blood calcitonine level control in case of cold thyroid nodule or cervical lymphadenopathie. Once the diagnosis of Medullary Carcinoma of the thyroid gland is reached, screening of the Family, at least the first degree relatives should be undertaken, in order to reveal subclinical cases, which could be detected by laboratory investigations at an early subclinical stage. The treatment of the CMT is always surgery; it consists of total thyroidectomy with a modified neck dissection or a radical neck dissection, if lymph nodes are more than 3 cm or are fixed. Any way the recurrent nerve nodes have to be looked for, and if positive a Mediastinal lymph node dissection should be carried out. A control of the calcitonine hormone blood level should be asked for twice a year to detect any metastases or recurrence.

Adult↗
PubMed1984

The basic structural lesion of persistent neonatal hypoglycaemia with hyperinsulinism: deficiency of pancreatic D cells or hyperactivity of B cells?

Pancreatic tissue obtained at subtotal pancreatectomy from 15 infants with persistent hypoglycaemia with hyperinsulinism, and autopsy specimens from 23 age-matched normoglycaemic controls, were studied with morphometric methods after immunocytochemical staining of the four main islet cell types (A, B, D and pancreatic polypeptide cells). In three cases, a focal lesion was detected by gross examination. Macroscopic or microscopic examination did not distinguish the 12 other cases from controls. As found previously, nesidioblastosis was not a specific feature of the pancreas in infantile hypoglycaemia, being observed in age-matched controls as well. In cases with hypoglycaemia the volume density of B cells was not significantly increased; that of the A cells was within normal range. The volume density of pancreatic polypeptide cells was markedly augmented and that of somatostatin cells was significantly decreased. The mean nuclear volume of the B cells was increased by 40% in cases with diffuse changes, but in cases with a focal lesion this increase was restricted to the abnormal area. This finding is of decisive importance for diagnosis and has therapeutic implications. The increase in B-cell nuclear size is thought to reflect an enhanced functional activity of these cells. On the other hand, the figures obtained for the volume density of B and D cells must be viewed with some reservation because degranulation may interfere with accurate detection of these cells.

Cell Count↗
PubMed1984

Immunohistochemical localization of secretory component in the liver of guinea pigs and dogs versus rats, rabbits, and mice.

Secretory component (SC) was localized in the liver of guinea pigs, dogs, rabbits, rats, and mice. In rabbits, rats, and mice SC localized predominantly in bile canaliculi and on hepatocyte sinusoidal membranes but was doubtful in cholangiocytes . In dogs and guinea pigs SC-staining was not detected in/on hepatocytes and canaliculi but was strong in/on cholangiocytes , as reported for humans. In guinea pigs IgA biliary output was small (0.23 mg/kg/day), as for dogs and humans, and below IgG output (1.4 mg), in contrast to rats, whose IgA biliary output (38 mg/kg/day) was much larger than IgG output (2mg). Biliary obstruction in guinea pigs induced only minor increases in serum IgA (+ 26% over 24 h), as reported for dogs and humans, in contrast to rats (+ 800% over 24h) and rabbits. Hepatocyte SC expression correlates with IgA hepatobiliary excretion, being low in guinea pigs, dogs, and humans but high in rats, rabbits, and mice.

Animals↗
PubMed1984

Localization and serum concentration of secretory component during massive necrosis of human liver.

The serum concentration of secretory component was monitored in 9 patients with massive liver necrosis. During acute cytolysis, no increase in serum secretory component levels was observed. Later on, patients with fulminant evolution displayed minor elevations. Values as high as those usually found in acute hepatitis were only observed in cases with delayed liver failure. In these patients, levels were elevated before failure, dropped as liver failure developed, and rose again during recovery. This evolution of serum secretory component level cannot be accounted for by a defective liver clearance of circulating secretory component. It rather suggests a release into the blood of secretory component produced in the liver by cells other than damaged hepatocytes, possibly during liver regeneration. In 3 cases, secretory component localization in the liver was demonstrated by immunocytochemistry and was compared with that in normal liver and in obstructive jaundice. In normal liver, it was restricted to portal bile duct cells and lumens. In obstructive jaundice, additional secretory component staining was found in bile canaliculi. After fatal liver necrosis, secretory component was localized to portal ducts and to a variable proportion of the cholangiocytelike cells belonging to the numerous extraportal proliferating ducts. In these structures, 0.1%, 21%, and 4% of the cells were stained 3, 8, and 30 days after maximal cytolysis, respectively. Remaining hepatocytes and bile canaliculi or bile plugs were unstained. Therefore, portal cholangiocytes and extraportal cholangiocytelike cells are probably essential sources of secretory component in human liver. We propose that proliferation of extraportal cholangiocytelike cells, expression of secretory component synthesis by these cells, and their inability to secrete secretory component in a disorganized biliary tree result in the elevated serum concentration of secretory component observed after acute liver necrosis.

Acute Disease↗
PubMed1984

Glucose homeostasis in rats acutely and chronically treated with chloroquine.

Glucose homeostasis of normal rats was studied after chronic or acute administration of chloroquine. Male rats received, in drinking water, a daily dose of 5-20 mg chloroquine/kg, for 20 weeks. The high dose caused a slight decrease in food intake and weight gain. In these animals, plasma glucose levels were somewhat lower than in controls after an overnight fast and after oral administration of glucose or intravenous administration of insulin, but not after intravenous administration of glucose. Their insulin response to oral or intravenous glucose was normal. The insulin content of their pancreas was decreased by about 15%. Electron microscopy revealed the presence of myeloid bodies and numerous lysosomes in B cells. Acute intraperitoneal administration of chloroquine was without effect on glucose tolerance and insulin release. This study shows that chloroquine, at plasma concentrations similar to those reached in treated patients, does not impair glucose homeostasis in normal rats.

Animals↗
PubMed1984

Acute Wilson's disease and thalassemia minor: a case report.

The case of a 17-year-old Italian girl with thalassemia minor and fatal acute Wilson's disease together with severe hemolysis is reported. The fortuitous(?) occurrence of both genetically determined conditions in the same patient was the source of delayed diagnosis of the metabolic disorder.

Acute Disease↗