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Biomedical subjects

O Epstein

Publications and source records attributed to O Epstein.

At least 73 records · Page 4Linked to original sources
PubMed1984

Recurrent bacteriuria and primary biliary cirrhosis: ABO blood group, P1 blood group, and secretor status.

Patients with primary biliary cirrhosis have an abnormally high incidence of urinary tract infection (35%). Susceptibility to urinary infection and other infectious diseases has been linked with certain blood group antigens and secretor status. We have therefore studied these characteristics in patients with primary biliary cirrhosis. We were unable to show any abnormal distribution in blood groups or secretor status in patients with primary biliary cirrhosis (compared with a normal population) which might reflect their predisposition to urinary infection. The distribution of blood groups and secretor status in patients with primary biliary cirrhosis with a history of urinary infections was not significantly different from patients without such a history. Escherichia coli strains isolated from patients with primary biliary cirrhosis did not bind in any greater numbers to the uroepithelial cells of primary biliary cirrhosis patients than to the cells of a normal healthy control. We therefore conclude that blood group distribution, abnormal secretor status, and epithelial cell type are not important factors in the predisposition of primary biliary cirrhosis patients to urinary infections.

ABO Blood-Group System↗
PubMed1984

Effect of prolonged fasting on heme metabolism in the rat.

It is known that fasting may provoke an acute attack in patients with latent hepatic porphyrias. We examined the influence of fasting on some aspects of heme synthesis in rats. Urinary excretion of both uroporphyrin and coproporphyrin, as well as fecal elimination of protoporphyrin and coproporphyrin, were increased on fasting. These biochemical aberrations resemble those found in subjects with latent porphyria variegata, suggesting that fasting rats may constitute an experimental model for latent variegate porphyria. The administration of phenobarbitone had a pronounced, synergistic effect on the urinary excretion of porphyrins. The activity of delta-aminolevulinic acid synthase (ALAS) and the concentration of cellular heme were determined in homogenates and subcellular fractions of the livers of fasting rats. A marked increase in the concentration of heme in the homogenate, the nuclei and the postmicrosomal supernatant fractions was observed. ALAS activity in the homogenate and the supernatant fraction increased while that in the mitochondria decreased. The possible relationship of these results to the human disease is discussed.

5-Aminolevulinate Synthetase↗
PubMed1983

Erythrocyte uroporphyrinogen synthase activity as a possible diagnostic aid in the diagnosis of lymphoproliferative diseases.

Patients with active lymphoproliferative diseases were shown to have high activity of erythrocyte uroporphyrinogen synthetase (URO-S), the enzyme which converts porphobilinogen to uroporphyrinogen. In a few patients examined the lymphocyte URO-S was markedly increased. No correlation was found between the high URO-S activity and the degree of anemia, reticulocytosis, or the presence of hemolysis. Patients with epithelial malignancies and with some common viral diseases had normal erythrocyte URO-S values. Three patients with nonalcoholic cirrhosis also had high erythrocyte URO-S activities. The determination of erythrocyte and lymphocyte URO-S activity may be of aid in the diagnosis of lymphoproliferative diseases. It may also indicate whether remission has been achieved and whether treatment should be continued or reinstituted. These preliminary observations justify the investigation of a larger patient and control material.

Adult↗
PubMed1982

The effects of succinylacetone (4,6-dioxoheptanoic acid) on delta-aminolevulinate synthase activity and the content of heme in monolayers of chick embryo liver cells.

Succinylacetone was shown to inhibit aminolevulinate dehydratase (5-aminolevulinate hydro-lyase (adding 5-aminolevulinate and cyclizing), EC 4.2.1.24) to reduce cellular heme and porphyrins and to induce delta-aminolevulinate synthase (succinyl-CoA:glycine C-succinyltransferase (decarboxylating), EC 2.3.1.37) in monolayers of chick embryo liver cells. Marked synergistic effects on delta-aminolevulinate synthase activity were obtained by combining succinylacetone with levulinate and porphyrogenic drugs. The time course of delta-aminolevulinate synthase activity showed a delayed synergistic response.

5-Aminolevulinate Synthetase↗
PubMed1982

Radiological patterns of cortical bone modelling in women with chronic liver disease.

The pattern of cortical bone modelling in healthy and diseased populations can be derived from simple measurements taken from radiographs of tubular bones. To determine the pattern of bone modelling in women with chronic cholestatic and parenchymal liver diseases, these parameters have been measured in 83 women with primary biliary cirrhosis (PBC), 34 with steroid-treated chronic active hepatitis (CAH) and 27 with parenchymal liver disease (PLD) not treated with corticosteroids. Bone modelling profiles have been compared in these groups with expected pattern in healthy females. Abnormal bone modelling occurs in all three groups. In PBC, cortical thinning is progressive from the fourth decade onwards. In steroid-treated CAH, an initial increase in cortical thickness is observed in the third and fourth decades, after which cortical thinning occurs. In the PLD group, progressive loss of bone cortex is present from the fourth decade onwards. In all forms of liver disease, cortical thinning results from widening of the medullary cavity rather than resorption of the cortical surface.

Bone Diseases↗
PubMed1982

The influence of propranolol on the concentration of heme and on the activity of delta aminolevulinate synthase in monolayers of chick embryo liver cells.

The addition of propranolol to monolayers of chick embryo liver cells caused a rapid increase in cellular heme, followed by an equally rapid decrease. Subsequently the concentration of heme rose at a relatively slower rate. About 10 hr after addition of propranolol to the medium a plateau level was reached at +/- 35% above control values. Changes in the activity of delta-aminolevulinate synthase (ALAS) were negatively correlated with those of cellular heme. Cycloheximide prevented the above phenomenon. ALAS activity was not clearly correlated with the rapid, partial inhibition of protein synthesis, caused by propranolol. These observations are related to the beneficial influence of administration of hemin or of propranolol to patients with acute attacks of hepatic porphyria.

5-Aminolevulinate Synthetase↗
PubMed1982

The effect of oral copper loading and portasystemic shunting on the distribution of copper in the liver, brain, kidney, and cornea of the rat.

In Wilson's disease, redistribution of copper from the liver to extrahepatic tissue coincides with the development of liver disease and cirrhosis. We have considered the possibility that portasystemic shunting may be a factor determining the organ distribution of copper in patients with liver disease. Thirty-two Sprague-Dawley rats were randomized into a sham-operated group, and a group subjected to partial occlusion of the portal vein (PPVO). Half the rats in each group were fed on normal diet and the remainder had copper added to the drinking water. Rats subjected to PPVO developed large portasystemic shunts. Over a 3-month period, none of the groups showed an increase in serum copper concentrations, or copper oxidase levels. Liver and kidney copper concentrations were similarly increased in copper supplemented sham-operated and PPVO rats, but brain copper content in both groups was similar to the unsupplemented controls. In neither unsupplemented nor copper supplemented rats subjected to PPVO, was the organ distribution of copper different from sham-operated controls. This study suggests that portasystemic shunting does not alter the organ distribution, or tissue concentration of copper.

Animals↗
PubMed1982

Vitamin D, hydroxyapatite, and calcium gluconate in treatment of cortical bone thinning in postmenopausal women with primary biliary cirrhosis.

Women with primary biliary cirrhosis malabsorb calcium, phosphate and vitamin D, and develop accelerated cortical bone thinning. We have assessed the value of parenteral vitamin D, oral hydroxyapatite (HA), and calcium gluconate (CG) in the treatment of cortical bone thinning in primary biliary cirrhosis. Sixty-four postmenopausal women with primary biliary cirrhosis were assigned randomly into three groups: one group receiving no mineral supplements (control), one group receiving HA, and one group receiving CG. All patients received parenteral vitamin D2 (100,000 IU monthly). Eleven patients withdrew from the study and 10 withdrew due to poor compliance (six HA, four CG). Over a 14-month follow-up period, none of the groups showed a significant change in serum calcium or inorganic phosphate levels. Pre- and posttreatment hand radiographs were used to assess changes in metacarpal cortical thickness using the technique of caliper radiogrammetry. Cortical bone loss occurred in the control group (p less than 0.01). The HA group showed a significant gain in cortical bone thickness (p less than 0.01), while no significant change occurred in the CG group. This study indicated that vitamin D2 does not halt metacarpal cortical bone thinning in primary biliary cirrhosis. The addition of CG prevents bone thinning, and HA promotes positive cortical bone balance.

Bone Diseases, Metabolic↗
PubMed1982

Immunocytochemical identification of caeruloplasmin in hepatocytes of patients with Wilson's disease.

Decreased serum caeruloplasmin levels in patients with Wilson's disease have been attributed to decreased caeruloplasmin synthesis in the hepatocyte. An immunoperoxidase procedure was used to identify caeruloplasmin in liver biopsies. The pattern of staining in biopsies from patients with Wilson's disease did not differ from the pattern seen in normal adult or neonatal liver. This indicates that immunoreactive caeruloplasmin is synthesized by the liver cell in Wilson's disease. Low serum levels of caeruloplasmin may reflect an abnormality of copper incorporation into the apoprotein or an abnormality of holocaeruloplasmin export.

Adolescent↗
PubMed1982

T cell subsets in autoimmune and HBV-induced chronic liver disease, HBs antigen carriers with normal histology and primary biliary cirrhosis: a review of the abnormalities and the effects of treatment.

Review of the limited data currently available on the ratios of helper (OKT4+) to suppressor (OKT8+) T cells in autoimmune liver disease (primary biliary cirrhosis and chronic active lupoid hepatitis) and virally induced liver disease indicates that this OKT4+:OKT8+ ratio is elevated in autoimmune liver disease manifesting hyperglobulinemia. This ratio was decreased in patients with chronic hepatitis B virus infection during the HBe antigen-positive phase of viral replication but reverts to normal in the majority of patients in whom HBV replication has ceased (HBe antibody-positive) and these individuals exhibit normal liver histology. Patients with HBV infection who continue to show elevated ratios after the appearance of HBe antibody also continue to exhibit signs of active hepatitis. The implications of these findings for further research in the management of these disorders is discussed.

Antibodies, Monoclonal↗
PubMed1982

The effect of porta-systemic shunting on liver, brain and kidney zinc concentrations in the rat.

Patients with alcoholic cirrhosis have subnormal liver zinc concentrations, and excessive urinary zinc excretion. It has been suggested that diversion of dietary zinc into the systemic circulation through porta-systemic shunts may be a major factor influencing the organ distribution of zinc in these patients. To test this hypothesis, we randomized Sprague-Dawley rats into a sham-operated group, and a group subjected to partial portal-vein occlusion (PPVO), which induces the formation of extensive porta-systemic collaterals. Three months after the operation, liver, brain and kidney zinc concentrations were measured in 8 sham-operated and 8 PPVO rats. Mean liver zinc concentrations were significantly higher in the PPVO group when compared to sham-operated controls (P less than 0.05). Brain and kidney zinc concentrations were similar in the 2 groups. This short-term study indicates that liver zinc concentrations are maintained and even increased in rats with porta-systemic shunting, and that diversion of portal blood into the systemic circulation is not a major cause of the low liver zinc concentration observed in alcoholic cirrhosis.

Animals↗
PubMed1982

The pancreas in primary biliary cirrhosis and primary sclerosing cholangitis.

In patients with primary biliary cirrhosis, the chronic cholestasis, salivary, and lacrimal hyposecretion suggest that the disease is a "dry gland" syndrome. To determine whether or not pancreatic damage occurs in primary biliary cirrhosis and other forms of chronic cholestasis, we have studied pancreatic structure and function in primary biliary cirrhosis, and primary sclerosing cholangitis. In a retrospective study, retrograde pancreatograms were abnormal in 43% of 35 patients with primary biliary cirrhosis and 15% of 20 patients with primary sclerosing cholangitis (p less than 0.02). In a prospective study, serum pancreatic isoamylase was abnormal in 56% of 41 patients with primary biliary cirrhosis and 36% of 22 patients with primary sclerosing cholangitis (NS), indicating pancreatic damage in both diseases. After secretin-pancreozymin stimulation, patients with primary biliary cirrhosis, but not patients with primary sclerosing cholangitis, showed a significant reduction in duodenal juice flow rate (p less than 0.01) and immunoreactive trypsin output (p less than 0.01). The reduced trypsin output in patients with primary biliary cirrhosis indicates pancreatic hyposecretion. In neither patients with primary biliary cirrhosis nor patients with primary sclerosing cholangitis was the immunoreactive trypsin concentration, or tryptic activity in duodenal juice, significantly different from controls. Pancreatic involvement in primary biliary cirrhosis is closely associated with Sjogrens syndrome, and it is likely that the pancreatic hyposecretion is a component of the sicca complex. This association was not obvious in primary sclerosing cholangitis.

Cholangitis↗
PubMed1981

D-penicillamine treatment improves survival in primary biliary cirrhosis.

The copper-chelating, immunological, and antifibrotic effects of D-penicillamine indicated that it might be suitable for the treatment of primary biliary cirrhosis (PBC). In a randomised clinical trail, 55 PBC patients received penicillamine (600 mg daily), and 32 received a placebo. Drug reactions developed in 16 patients on penicillamine. All deaths occurred in patients with stage 3 or 4 (late stage) liver histology on entry to the study. 5 (14%) of 37 penicillamine-treated patients and 10 (43%) of 23 placebo patients have died (p less than 0.01). Improvement in survival only became evident after 18 months. Survivors in the penicillamine group demonstrated a significant fall in serum aspartate transaminase, serum immunoglobulins, and liver copper concentrations. On follow-up liver biopsy 12-72 months (median 33) after joining the study, 21% of penicillamine-treated patients had less pronounced inflammation and piecemeal necrosis, whereas there had been no improvement in patients on placebo (p less than 0.02). Penicillamine did not retard the histological evolution of the liver disease from the early prefibrotic stages to the late fibrotic or cirrhotic stages. Both the copper-chelating and immunological effects of penicillamine are probably important in improving survival. The excellent prognosis of patients with PBC in its early histological stages, and the failure of penicillamine to prevent histological progression from early to late stages, suggests that penicillamine treatment should not be given to patients with PBC in the early (stage 1 or 2) histological phase of the disease. Penicillamine treatment is recommended in patients once liver biopsy has demonstrated histological results typical of late stage 3 or 4 PBC.

Antigen-Antibody Complex↗