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Biomedical subjects

E L Krawitt

Publications and source records attributed to E L Krawitt.

At least 55 records · Page 3Linked to original sources
PubMed1982

Effects of testosterone, oestradiol and progesterone on immune regulation.

Clinical observations on differences in the sexual incidence of diseases associated with defects of immune regulation, and of the occasional beneficial effects of pregnancy on disease course suggest that endocrine mechanisms may be important in the immuno-pathogenesis of these disorders. To investigate this possibility the in vitro effects of testosterone, oestradiol and progesterone on selected aspects of immune regulation were studied in normal adults. We observed the effects of these hormones on a mitogen-induced suppressor T-cell system and a monocyte mediated prostaglandin-producing suppressor cell system. The addition of progesterone but not oestradiol or testosterone to the Concanavalin A (Con A) generation of T lymphocyte suppressor cells produced significantly increased suppressor cell activity (P less than 0.005). Pre-incubation of lymphocytes with testosterone but not oestradiol or progesterone in the absence in the absence of Con A resulted in the generation of modest, but highly significant suppressor cell activity (P less than 0.005) No effect on the prostaglandin-producing suppressor cell activity was observed. These findings suggest that certain endocrine changes may alter immunoregulatory function and account for some of the clinical observations previously noted in diseases associated with defects of immune regulation.

Adult↗
PubMed1982

Studies on lymphocyte hyporesponsiveness in cirrhosis: the role of increased monocyte suppressor cell activity.

We investigated the possibility that monocyte suppressor cells play a role in the peripheral lymphocyte hyporesponsiveness of chronic liver disease by utilizing assays of monocyte-mediated suppressor activity in 46 patients with chronic liver disease and 46 controls. The percent change achieved by the addition of indomethacin to a PHA-induced proliferative response was significantly increased in patients with cirrhosis compared with controls (p less than 0.001). The increase was seen in cirrhosis regardless of etiology but was not found in patients with chronic hepatitis without cirrhosis. The effects of indomethacin were abolished by monocyte depletion and were greater in autologous serum than in pooled AB serum (p less than 0.02). Monocyte depletion in cirrhotic patients significantly increased the lymphocyte response to PHA (p less than 0.005) but made no significant difference in controls. There was a significant correlation between the indomethacin-induced changes and the changes in lymphocyte response to PHA on monocyte depletion (r = 0.6583, p less than 0.01). Our initial results led us to study the mode of action of the inhibitory effect of cirrhotic serum on lymphocyte response to PHA. Cirrhotic serum significantly reduced the response of normal lymphocytes compared with control serum (p less than 0.02), but the difference was abolished by adding indomethacin and by monocyte depletion. These results suggest that monocyte suppressor cells may play a role in the depressed cellular immunity seen in some patients with cirrhosis. The inhibitory effect of cirrhotic serum appears to be in part monocyte mediated and prostaglandin dependent.

Adult↗
PubMed1981

HLA A and B locus antigens in patients with unexplained hepatitis following halothane anaesthesia.

HLA A and B locus antigens were determined in 17 patients who had recovered from unexplained hepatitis following halothane anaesthesia. The greatest deviations from expected frequencies were observed with A1, A11 and BW22, but these differences were not statistically significant when the P values were corrected for the number of antigens tested. Although a larger series might show such deviations to be significantly different, HLA typing is of no predictive value in determining those at risk to hepatitis following repeated halothane exposure.

Adult↗
PubMed1981

Increased suppressor cell activity in inflammatory bowel disease.

We studied the in vitro effect of indomethacin, hydrocortisone, sulphasalazine, and its metabolites sulphapyridine (SP) and 5-amino salicylic acid (5-ASA) on peripheral blood mononuclear cells (PBMC) from 49 patients with inflammatory bowel disease and 34 controls. Indomethacin caused a highly significant increase in the PBMC response to the mitogen PHA-P compared with controls (P less than 0.01), indicating increased activity of a prostaglandin-producing suppressor cell system. On the contrary, sulphasalazine resulted in a reduced response which was significantly greater for the group with inflammatory bowel disease than the control group (P less than 0.05). This reduction was also produced by 5-ASA (P less than 0.05) but not by sulphapyridine. Addition of indomethacin to PBMC incubated with sulphasalazine significantly reduced the effect of sulphasalazine (P less than 0.001). Hydrocortisone resulted in a reduced response which was similar to that of controls and was not altered by the addition of indomethacin. The response to indomethacin, hydrocortisone, sulphasalazine, sulphapyridine, and 5-ASA was not dependent on the HLA type of the patients, disease activity, or drug therapy. The results suggest that increased suppression by a population of prostaglandin-producing suppressor cells plays a role in the immunopathology of inflammatory bowel disease, but that sulphasalazine does not exert its therapeutic effect by acting on this step of the immunoregulatory system. Any trials of indomethacin therapy in inflammatory bowel disease should take into account that, in vitro, sulphasalazine and indomethacin have opposing mechanisms of action in this system.

Aminosalicylic Acids↗
PubMed1980

Ischemic gastritis and duodenitis.

Erosive gastritis and duodenitis resulting from chronic ischemia were seen at endoscopy in a 69-year-old woman with classical abdominal angina and severe atheromatous disease of all three splanchnic arteries.

Aged↗
PubMed1980

25-hydroxy vitamin D absorption test in patients with gastrointestinal disorders.

To evaluate the relationships of a 25-hydroxy vitamin D absorption test to intestinal fat absorption and to the absorption of radioactively labeled vitamin D and 25-hydroxy vitamin D, an investigation was undertaken in 19 patients with gastrointestinal disorders. A correlation was noted between the results of the 25-hydroxy vitamin D absorption test and baseline 25-hydroxy vitamin D levels. No correlation was found between results of the 25-hydroxy vitamin D absorption test and quantitative fecal fat excretion. Peak values of the 25-hydroxy vitamin D absorption test correlated with net absorption of 14C vitamin D. No correlation existed between the values obtained in the 25-hydroxy vitamin D absorption test and 3H-25-OH D absorption. These studies indicate that the 25-hydroxy vitamin D absorption test probably does not serve as an effective screening test for intestinal fat malabsorption. The results of the test probably most accurately reflect the body stores of vitamin D at the time of testing, but there appears to be little advantage to performing a 25-hydroxy vitamin D absorption test in lieu of a single determination of the serum level of 25-hydroxy vitamin D as a method of evaluating vitamin D nutritional status.

Carbon Radioisotopes↗
PubMed1980

Comparative absorption of vitamin D3 and 25-hydroxyvitamin D3 in intestinal disease.

The absorption of simultaneously administered equimolar doses of 14C vitamin D3 and 3H 25 hydroxyvitamin D3 (25-OH-D3) has been studied in controls and patients with a variety of gastrointestinal disorders. As assessed from peak radioactivity in the serum and from faecal excretion of radioactivity, malabsorption of both vitamin D3 and 25-OH-D3 occurred in patients with steatorrhoea. Malabsorption of vitamin D3 was greater than 25-OH-D3. The magnitude of malabsorption of these compounds was related to the severity of the steatorrhoea but was moderate enough to suggest that replacement therapy in patients with intestinal malabsorption should be accomplished with relatively small doses of vitamin D. The more potent vitamin D metabolites are probably unnecessary in this situation.

Adult↗
PubMed1977

Absorption, hydroxylation, and excretion of vitamin D3 in primary biliary cirrhosis.

Oral vitamin D3 was poorly absorbed by 4 out of 6 patients with primary biliary cirrhosis; absorption was negatively correlated with faecal fat excretion. 25-hydroxylation of vitamin D3 given by mouth or intravenously was not impaired in the patients compared with controls of similar vitamin-D nutritional status. Urinary radioactivity derived from the intravenous dose of vitamin D3 was significantly greater in patients than in controls and was positively correlated with the serum-bilirubin concentration. Excretion in the urine may lead to loss of administered and endogenous vitamin D and thus contribute to vitamin-D deficiency in patients with primary biliary cirrhosis.

Administration, Oral↗
PubMed1977

Effect of folate deficiency and ethanol ingestion on intestinal folate absorption.

The effects of folate deficiency, generalized malnutrition, and alcohol ingestion on jejunal transport, mucosal uptake, and reduction of folic acid were evaluated in rats. As measured by an everted gut sac technique, a folate-deficient diet fed ad libitum did not alter transport or mucosal uptake of folate. Partial starvation, which was produced in rats pair-fed with animals ingesting ethanol, increased jejunal folate transport and mucosal uptake in animals ingesting either a folate-deficient or control diet. A 20% ethanol ingestion by rats consuming folate-deficient or control diets resulted in transport and mucosal uptake rates intermediate in value compared to those from ad libitum fed and pair-fed groups. No differences in reduction of folic acid were found. These results suggest that folate depletion and ethanol ingestion, alone or in combination, do not affect the ability of the rat jejunal to transport folate but that partial starvation results in an increase in folate transport activity.

Animals↗
PubMed1977

Effect of hypophysectomy on calcium transport by rat duodenum.

To examine the effect of hypophysectomy on intestinal calcium absorption, studies were performed on immature rats 7, 14, and 21 days after hypophysectomy. Duodenal calcium transport was measured in vitro utilizing everted gut sacs and in vivo by a luminal perfusion technique. Hypophysectomy produced no differences in the ability of everted gut sacs to transport calcium. Similarly, when in vivo transport data were expressed on the basis of intestinal length, no significant differences were noted. However, when transport data were expressed on the basis of mucosal weight, increases in absorption and lumen-to-plasma fluxes were apparent in hypophysectomized animals. No differences were seen in plasma-to-lumen fluxes. The results indicate that when the transport data are corrected for mass of intestinal mucosa, the duodenum from hypophysectomized animals absorbs calcium more avidly due to an increase in lumen-to-plasma flux.

Animals↗
PubMed1977

Ethanol and development of disease and injury to tha alimentary tract.

Effects of ethanol on the gastrointestinal tract are reviewed, and an overview of possible mechanisms of ethanol damage to the alimentary tract is presented. Ethanol toxicity most commonly results in metabsorption. Mechanisms contributing to ethanol-induced calcium malabsorption are considered in detail as a prototype for problems encountered in evaluating effects of toxicants on intestinal function. Effects at the local level in the intestine must be differentiated from systemic effects. The mechanism of suppression of calcium absorption by chronic ethanol ingestion differs from that produced by acute administration. Effects of acute administration appear to be due to local mucosal damage and are reversed in 18 hr. Such damage is not present with chronic administration, which affects only duodenal transport. Treatment with vitamin D and its metabolites does not reverse the inhibition of calcium transport. The overall findings suggest that ethanol inhibition of calcium transport is mediated at the intestinal level, probably affecting vitamid D independent mechanisms.

Animals↗
PubMed1976

A morphometric investigation of the duodenal mucosa of normal, vitamin D-deficient, and vitamin D-replete rats.

Light and electron microscopy were utilized to determine differences in morphology and size in duodenal villi and microvilli from normal, vitamin D-deficient, and vitamin D-replete rats. An increase in villus diameter and surface area was observed in vitamin D-deficient rats. Administration of vitamin D reversed the increase in diameter but the height of villi increased resulting in longer, thinner villi without a significant change in surface area. A decrease in microvillus surface area seen in vitamin D-deficient animals was reversed by the administration of vitamin D.

Animals↗
PubMed1976

Intestinal mitochondrial calcium uptake during adaptation to dietary calcium restriction.

In order to evaluate the role of mitochondrial calcium uptake in intestinal calcium absorption, the effect of adaptation to dietary calcium deficiency on the in vitro uptake of calcium by isolated duodenal mitochondria was studied. Experiments were performed utilizing 28-day-old cockerels which had received a diet adequate in vitamin D3 and phosphate and containing either 0.08% or 1.20% calcium. Mitochondrial 45Ca uptake from chicks deprived of dietary calcium was not significantly different from controls. These results suggest that increased calcium uptake by intestinal mitochondria is not crucial for adaptation to a low calcium diet.

Animals↗
PubMed1976

Calcium absorption in Crohn's disease.

Calcium absorption and endogenous loss of calcium were measured in a group of patients with Crohn's disease, using a simultaneous metabolic balance and calcium isotope regimen. Calcium malabsorption resulting in negative calcium balance was found in only 4 of 31 patients with Crohn's disease. No elevation of endogenous fecal calcium or total secreted intestinal calcium was observed in 10 patients studied, regardless of the level of net or true calcium absorption. Correlation between calcium balance and serum protein loss was observed, but no association was noted with intestinal fat excretion, d-xylose absorption, bacterial colonization of the jejunum, or glucocorticosteroid therapy. The results indicate that in this group of patients with Crohn's disease involving different areas of the intestine, calcium malabsorption occurred infrequently and that the levels of calcium excretion correlated best with enteric protein loss.

Adolescent↗
PubMed1975

Effect of 1,25-dihydroxycholecalciferol on ethanol mediated suppression of calcium absorption.

Rats raised on laboratory diet and given 20% ethanol in water as a sole source of fluid for 12 days were given 0.2 mug of 1,25-dihydroxycholecalciferol 24 h before measuring duodenal calcium transport by an in vitro everted gut sac technique. This vitamin D metabolite did not reverse the ethanol-induced inhibitiom of transport capacity. Ultrastructural studies of intestinal epithelial cells from animals ingesting ethanol demonstrated changes in mitochondria and other subcellular organelles as well as accumulation of electron-dense, calcium-containing granules in microvilli and a paucity of granules in mitochondria. The results suggest that the inhibition is mediated at the intestinal level, affecting mechanisms which are probably independent of Vitamin D, and in part by an interference in transport of calcium from microvilli to other intracellular sites.

Animals↗
PubMed1975

Limitations of the usefulness of the d-xylose absorption test.

The results of the conventional 5-hour d-xylose absorption test were surveyed in 38 subjects with disease of the jejunal mucosa, giardiasis or bacterial overgrowth, or no small-bowel disorder. The test was in error in 20-40% of cases, depending on the disease category, and the error for the entire group was 30%. We conclude that the test yields little guidance for diagnosis or therapy of clinical problems and is superfluous when a jejunal biopsy can be obtained.

Administration, Oral↗