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Biomedical subjects

A Quinton

Publications and source records attributed to A Quinton.

At least 37 records · Page 2Linked to original sources
PubMed1989

Treatment of benign gastric ulcer: a comparative clinical trial of rioprostil and ranitidine.

This study is a multicentre, double-blind, double-dummy, two-way, parallel group comparison of the efficacy and safety of rioprostil and ranitidine in the treatment of active gastric ulcer. Ninety-one patients with gastric ulcer are randomly allocated to treatment with either rioprostil 300 micrograms b.d., or ranitidine, 150 mg b.d. The duration of treatment is 4 weeks, or 8 weeks for the patients who are improved but not healed at 4 weeks. Clinical, endoscopic and laboratory assessments are made before treatment, and after each treatment period. Therapeutic success is defined as complete endoscopic healing of the ulcer. At the end of the treatment period, either 4 or 8 weeks, healing rates are 69% in the rioprostil group, and 66% in the ranitidine group; this difference is not significant (p = 0.86). After the first 4 weeks of treatment the healing rates are 44% and 55% in the rioprostil and ranitidine groups, respectively. The incidence of adverse effects is 22% in the rioprostil group, and 7% in the ranitidine group (p = 0.036). Diarrhoea is the most common side effect (12%), but is usually intermittent and mild. We conclude that rioprostil, 300 micrograms b.d., for up to 8 weeks is as effective as ranitidine, 150 mg b.d., in the treatment of benign gastric ulcer.

Adult↗
PubMed1988

Chance discovery of hepatic fibrosis in patient with asymptomatic hypervitaminosis A.

A liver biopsy specimen was obtained from a 50-year-old patient whose clinical and functional liver tests showed no abnormalities but who had for some time a high vitamin A intake (109 X 10(6) IU over four years). Liver architecture was normal. Sinusoids were slightly dilated in zone 2. Perisinusoidal cells were numerous and enlarged. On Sirius red staining, there was mild fibrosis of the central veins, portal tracts, and terminal portal venules and perisinusoidal fibrosis in zone 1 of the acinus. Liver vitamin A level was increased. By electron microscopy, perisinusoidal cells filled with numerous lipid droplets had slightly dilated rough endoplasmic reticulum, numerous minute filament condensations below the plasma membrane, and stellate-shaped processes giving them the appearance of fibroblast-myofibroblast-like cells. Numerous collagen bundles, fibrils, amorphous material, and fragments of basement membrane-like material were identified in Disse's space. Immunocytochemistry showed increased amounts of collagen types I, III, IV, laminin, and fibronectin. This observation suggests that vitamin A per se, and not the cellular damage often seen in hypervitaminosis A, is responsible for fibrosis.

Biopsy↗
PubMed1988

The increase in the number of liver sinusoidal pit cells in four patients with primary or metastatic cancer of the liver.

Four patients with liver carcinoma (case 1: hepatocellular carcinoma; cases 2 and 3: metastases; case 4: adenocarcinoma possibly of hepatic origin) underwent a wedge liver biopsy taken at some distance from the tumor. Liver histology was normal in cases 2 and 3. Sinusoids were dilated in case 4. Fibrosis formed bridges between portal tracts in case 1. In all 4 cases, sinusoids contained lymphocytic cells. By electron microscopy (perfusion-fixation with glutaraldehyde) numerous lymphocytes could be identified as pit cells with characteristic dense granules and occasional rod-cored vesicles. The majority of the pit cells were luminal cells in contact with endothelial or Kupffer cells; some were in the Disse space. It is now accepted that pit cells are resident large granular lymphocytes with natural killer activity. The increase in the number of pit cells in liver carcinoma compared to the number observed in the control group (uncomplicated gallbladder lithiasis) could be hypothetically interpreted as a defense mechanism against tumor extension.

Aged↗
PubMed1987

Removal of cellular debris formed in the Disse space in patients with cholestasis.

Using electron microscopy, we investigated how cellular debris, formed in the Disse space during cholestasis, was cleared. Ten patients with cholestasis of varied origin and severity were studied and compared with 10 controls without liver disease. In cholestatic patients, sinusoidal cells contained variable amounts of amylase PAS-positive material. In clean perfusion-fixed sinusoids the endothelial cells often appeared swollen and active, with few fenestrations. Hepatocyte blebs and cellular debris were sometimes seen in the Disse space. Two mechanisms were apparently involved in the clearing process: phagocytosis by macrophages either infiltrated into the Disse space, or forming the barrier; and the passage of debris from the Disse space into the sinusoidal lumen through the endothelial wall. Debris was either forced through enlarged pores or through the wall, with a progressive invagination followed by an outpouching in the lumen. The force, possibly provided by endothelial massage, may not be sufficient to push out cellular debris from the Disse space; morphological data seemed to indicate that endothelial damage may be a necessary factor. Debris present in the lumen was phagocytized by numerous active macrophages. Cellular debris was not observed in the Disse space of control patients.

Adult↗
PubMed1987

Agnogenic myeloid metaplasia, portal hypertension, and sinusoidal abnormalities.

A patient with agnogenic myeloid metaplasia suffered from gastrointestinal bleeding due to ruptured esophageal varices. The portal vein and its intrahepatic branches were patent. Except for the presence of myeloid cells, mainly megakaryocytes, in the sinusoids, liver histology was more or less normal. However, on Sirius red staining there was marked perisinusoidal fibrosis. In addition to numerous collagen bundles in the Disse space, electron microscopy also revealed the presence of hemopoietic cells, the transformation of perisinusoidal cells into fibroblasticlike or myofibroblasticlike cells, or both, and fragmentary deposits of basement membrane-like material. In the pathogenesis of sinusoidal hypertension as it occurs in agnogenic myeloid metaplasia, all the factors mentioned above should probably be taken into consideration.

Biopsy, Needle↗
PubMed1987

Liver sinusoids and sinusoidal cells in patients with agnogenic myeloid metaplasia.

The origin of sinusoidal portal hypertension often remains unknown in patients with agnogenic myeloid metaplasia. Four consecutive patients with agnogenic myeloid metaplasia had liver biopsies examined under light and electron microscopy. Two of the four had obvious clinical portal hypertension; of these two, only one had portal vein thrombosis. All four cases showed sinusoidal infiltration by myeloid cells (from very mild to obvious) and an increased perisinusoidal collagen network. Under electron microscopy we observed (a) the collagenization of the Disse space, (b) myeloid cells in the lumen and the Disse space, (c) the transformation of perisinusoidal cells into transitional cells, and (d) fragments of basement membrane-like material. It is possible that all these abnormalities, and not only sinusoidal infiltration, contribute to increase vascular resistance, even when there is no clinical evidence of portal hypertension unrelated to vascular thrombosis.

Aged↗
PubMed1987

Benign recurrent cholestasis: a light and electron microscopic study with emphasis on sinusoidal cells.

A liver biopsy was performed on a patient with benign recurrent cholestasis. Cholestasis was mainly centrolobular with infiltration by sinusoidal macrophages. There was no necrosis. All the classic and specific ultrastructural criteria of cholestasis were observed in hepatocytes under electron microscopy. Perfusion-fixation of the biopsy allowed in addition a good visualization of sinusoids and sinusoidal cells. Numerous macrophages (Kupffer cells) with intense phagocytic activity were present in the lumen; some formed the sinusoidal barrier or were infiltrated in the Disse space. Endothelial cells contained numerous dense bodies and had few fenestrae. Cellular debris of hepatocytic origin which were not phagocytized in the Disse space were extruded in the lumen either through enlarged endothelial pores or by progressive invagination in the endothelial wall followed by outpouching in the sinusoid. In an enlarged Disse space containing amorphous material and collagen fibrils some perisinusoidal cells were transitional cells. These results indicate that pure cholestasis leads not only to hepatocyte injury with intense phagocytic activity but also to some degree of sinusoidal cell damage and extracellular matrix changes.

Adult↗
PubMed1987

"Campylobacter pyloridis" and epigastric pain: endoscopic, histological, and bacteriological correlations.

Campylobacter pyloridis is a newly discovered bacterium which has been implicated in gastric pathology. C. pyloridis was looked for by hematoxylin and eosin staining and culture (chocolate and brucella blood agar) in gastric antral biopsies in 136 unselected patients suffering from epigastric pain. The distribution of C. pyloridis positive cases according to the endoscopic diagnosis was as follows: duodenal ulcer (19 positive/21 tested), duodenitis (6/10), gastric ulcer (9/21), gastritis (13/26), and normal endoscopy (21/58). The association was statistically significant for duodenal ulcers (p less than 0.001). All of the 68 C. pyloridis positive patients showed histologic signs of gastritis as compared to 29 of the 68 C. pyloridis negative patients. The two techniques detection were comparable in sensitivity: 57 were detected by culture only and 63 by microscopy only. We also looked for C. pyloridis in biopsies of the body of the stomach in 71 patients. Bacteria were found in 33 of 36 cases with C. pyloridis positive antral biopsies (15 had histologic lesions) but only in 2 of 35 C. pyloridis antrum negative cases. Therefore, C. pyloridis was tightly associated with histologic signs of antral gastritis and with duodenal ulcers when diagnosed by endoscopy.

Adult↗
PubMed1986

The sinusoidal barrier in alcoholic patients without liver fibrosis. A morphometric study.

Alcohol induces morphological changes in the endothelial and perisinusoidal cells at the fibrotic stage of alcoholic liver diseases. Directly or indirectly, through hemodynamic disturbances linked to the enlargement of steatotic hepatocytes, alcohol may modify this barrier before the onset of fibrosis. Liver biopsies were obtained from control and from alcoholic patients and perfusion-fixed. Volume and surface densities of endothelial cells, perisinusoidal cells and their processes were measured. Liver histology was normal in the 2 groups except for steatosis in the alcoholics. Volume densities represented 8.2%, 4.7% and 3.2% of the sinusoid in controls for endothelial cells, perisinusoidal cells and their processes whereas surface densities represented respectively 0.5, 0.23, 0.21 m2/cm3 of sinusoid. Morphometric values were not significantly different in the alcoholic patients. In none of the alcoholic patients did fine morphological studies of sinusoidal cells give any indication of the possible evolution of the alcoholic disease towards fibrosis. These results indicate that in the group of patients studied, alcohol, before the fibrotic stage, did not significantly alter the sinusoidal barrier.

Adult↗
PubMed1986

The treatment of refractory ascites by the LeVeen shunt. A multi-centre controlled trial (57 patients).

A multi-centre random trial of 57 cases of alcoholic cirrhosis with refractory ascites was carried out; 29 patients received a LeVeen shunt and 28 were treated by conventional medical therapy. The effectiveness of the LeVeen shunt in reducing ascites was good in the first month, but was not different from conventional medical therapy by the end of one year. Complications were significantly more frequent in the surgical group. Of the 29 patients fitted with a LeVeen shunt, 25 developed one or more complications. Of the 28 patients in the medical control group, only 8 developed complications. The mortality rate of the two groups also differed significantly. Twelve patients in the surgical group (41%) died in the course of the first month against only 5 (18%) in the medical control group. By the end of one year, the mortality rate of the two groups was almost identical: 23 (79%) and 21 (75%) respectively. These observations confirm the poor prognosis for refractory ascites in cases of alcoholic cirrhosis and the inadvisability of attempting to treat it by implanting a LeVeen shunt.

Ascites↗
PubMed1986

Perisinusoidal cells in patients with normal liver histology. A morphometric study.

We measured the number and the morphometric characteristics of perisinusoidal cells in perfusion-fixed biopsy samples from 7 control patients with normal liver histology. On 1-micron section, the number of cells was 18 +/- 1.5/0.1 mm2; 25% of cells did not apparently contain lipids. There were no significant zonal differences. The volume density of the cells represented 1 +/- 0.2% of the hepatic parenchyma. On ultrathin sections, the volume and surface densities of processes were 3.2 +/- 0.7% of sinusoid and 0.21 +/- 0.04 m2/cm3 of sinusoid respectively which represented 70% and 90% of total PSC volume and surface densities. Lipid volume density was 20.5 +/- 7.3% of the nucleated cell. More than 30% of cells contained less than 10% of lipids. There was no correlation between lipid volume density and RER surface density.

Adult↗
PubMed1986

Salt or no salt in the treatment of cirrhotic ascites: a randomised study.

To compare the effect of diet, cirrhotic patients with ascites were randomised into two treatment groups: (1) a low sodium diet (21 mmol) per day or (2) an unrestricted sodium intake. Both groups received effective doses of diuretics (spironolactone or, if necessary, spironolactone and furosemide. One hundred and forty patients from 12 liver units were included according to well defined criteria (group 1: 76; group 2: 64). After an initial four to seven day period of bed rest and salt restriction (21 mmol sodium pd), randomisation was done in each centre. We saw no significant difference between the two groups with respect to clinical and biochemical data; mortality or withdrawal (definitive or temporary) because of biochemical disturbances (group 1: 34%, group 2: 22%); the time for complete disappearance of ascites was significantly shorter (p = 0.014) for the salt restricted patients actuarial survival (curves plotted up to the 120th day) was not statistically different (p = 0.18), but division into subgroups using various prognostic factors showed that survival was significantly better for salt restricted patients without previous gastrointestinal bleeding (p = 0.02); hospitalisation time and costs were identical in both groups. We conclude that the advantage of a normal salt diet was not shown in this study.

Adult↗
PubMed1986

Ultrastructure of sinusoids in patients with agnogenic myeloid metaplasia.

Four patients with agnogenic myeloid metaplasia underwent liver biopsies. Under light microscopy, sinusoidal infiltration was very mild or moderate, liver architecture was normal with sinusoids slightly dilated and the perisinusoidal collagen network was increased. Under electron microscopy, in perfusion-fixed sinusoids, the following abnormalities were noticed. a) Presence of hemopoietic cells (erythroid, megakaryocytic, lymphoid, myeloid) at different stages of maturation. More frequently observed in the lumen than in the Disse space, they were usually isolated and never exceeded 2 or 3 cells. In the Disse space, hepatocytes in contact with hemopoietic cells were devoid of microvilli. In the lumen they were close to endothelial cells and Kupffer cells. Kupffer cells were numerous with intense phagocytic activity. b) Numerous collagen bundles encircling sinusoids. c) Transformation of perisinusoidal cells into transitional cells with few lipids, prominent RER, long and thick processes containing filaments sometimes condensed below the plasma membrane. Although only one patient showed clinical evidence of portal hypertension of sinusoidal origin, these results suggest that hepatic vascular resistance might be raised in agnogenic myeloid metaplasia.

Cell Adhesion↗