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Biomedical subjects

J K Boitnott

Publications and source records attributed to J K Boitnott.

At least 55 records · Page 3Linked to original sources
PubMed1981

The effects of heparin treatment on hypertension and vascular lesions in stroke-prone spontaneously hypertensive rats.

Stroke-prone spontaneously hypertensive rats (SPSHRs) were used to test the theory that heparin treatment may prevent the development of "malignant" hypertension and fibrinoid vascular lesions in the kidney. Subcutaneous injections of heparin (100 units/100 g body weight) were given every 8 hours over a 5-week period to 12 young (10-week-old) SPSHRs. A control group of 12 SPSHRs was injected with saline. Both heparin-treated and control animals showed an incremental rise in mean systolic pressure, but the pressure was significantly lower (P less than 0.05) in the heparin-treated animals during weeks 1-4 of treatment. There were significantly fewer fibrinoid vascular lesions (P less than 0.03) in the heparin-treated group. In 7 additional heparin-treated and 7 control SPSHRs plasma and blood volumes were determined for assessment of the effects of heparin treatment. There was no significant difference in total blood volume or plasma volume between the two groups, but heparin-treated animals had lower hematocrit levels. In 8 SPSHRs direct arterial pressures were recorded for 1 hour after a single heparin injection, and no acute changes in blood pressure were observed. The results suggest that heparin treatment prevents the development of severe fibrinoid vascular lesions and also attenuates the rate of the rise in systolic blood pressure; moreover, this reduction in blood pressure is not caused by a significant reduction in blood volume or an acute hypotensive effect of heparin.

Animals↗
PubMed1980

Enhancement by cholera toxin of IgA secretion from intestinal crypt epithelium.

Studies of the effects of cholera toxin on the intestine have produced conflicting results regarding stimulation of IgA secretion. In the present study rabbit ileal loops were perfused with saline, and the IgA content of the perfusate was assessed by immunoradiometric assay. Crypt epithelial IgA content in biopsies was studied by immunofluorescence. Cumulative loop fluid IgA production 300 minutes after exposure to cholera toxin was 6216 +/- 993 microgram/cm compared with 4646 +/- 953 microgram/cm in controls (P < 0 . 20). However, rate of fluid IgA production above baseline at 300 minutes was 1742 +/- 181 microgram/h/cm in cholera loops and 1049 +/- 310 microgram/h/cm in controls, and the mean difference between the cholera and control loops was statistically significant (P < 0 . 05). In biopsies, mean rank of crypt epithelial IgA at 300 minutes was decreased compared with controls (P < 0 . 05). The findings of increased rate of fluid IgA production and decreased epithelial IgA suggest that a single dose of cholera toxin enhanced secretion of IgA from crypt epithelium into the intestinal lumen, although the magnitude of the enhancement was not great.

Animals↗
PubMed1980

Pathology of the liver with bone marrow transplantation. Effects of busulfan, carmustine, acute graft-versus-host disease, and cytomegalovirus infection.

The morphologic changes in the livers of autopsy specimens from recipients of 62 allogeneic bone marrow transplants were reviewed and characterized in specimens from patients who had had apparent drug toxicity, graft-versus-host disease (GVHD), and disseminated cytomegalovirus (CMV) infection. Two conditioning protocols were associated with significant hepatic toxicity. Two of 3 recipients on whom autopsies were performed who had been prepared with high doses of carmustine, cyclophosphamide, and total body irradiation had undergone acute hepatic failure and submassive necrosis with periportal sparing. Seven of 9 patients prepared with busulfan (16 or 20 mg/kg) and cyclophosphamide had moderate to marked centrilobular sinusoidal fibrosis and associated hepatocellular atrophy and necrosis. Twenty of the patients had acute cutaneous GVHD with associated hepatic dysfunction, including 8 with disseminated CMV infection. Of the 12 patients without concomitant CMV infection, 5 had an early onset of GVHD and had predominantly periportal and focal midzonal hepatocellular necrosis, and 7 had acute GVHD with later onset with predominantly bile duct injury. Fifteen patients had evidence of disseminated CMV infection. Whereas CMV infection alone was associated with both hepatocellular and bile duct injury, detectable virus infection was not a requirement for hepatocellular or bile duct injury associated with GVHD.

Anemia, Aplastic↗
PubMed1979

Perforation of the colon associated with cytomegalovirus infection.

Cytomegalovirus (CMV) inclusions were found at colonic perforation sites in three patients with clinical settings suggesting a compromised immunologic status. This could be interpreted as: (1) CMV was an etiologic agent in these perforations; or (2) CMV was an opportunistic superinfection in areas of preexisting inflammation. To determine which interpretation was more likely, we examined material from these three and ten similar patients with colonic perforations, identifying any potential causative factors present. Eleven of the 13 patients had an identifiable cause of perforation, either tumor, diverticulitis, arteritis, or pancreatic pseudocyst, while two remained unexplained. If the presence of CMV merely represented an opportunistic superinfection, then all 13 should have been at equal risk of infection. However, CMV was present in only one of the 11 cases with another identifiable cause of perforation but was present in both of the cases without another cause. This is consistent with the hypothesis that CMV was in fact an etiologic or contributing factor in those cases where it was present. Other cases of CMV infection of the gastrointestinal tract were studied to determine the mechanism by which this infection could lead to perforation of a viscus. In our three cases with perforation, four additional cases of CMV infection of the colon which we have studied, and 30 other cases in the literature, CMV inclusions were found only in areas of ulceration or perforation, never in undamaged mucosa. Thus there is as yet no evidence that CMV can be a primary cause of colonic mucosal injury. It remains likely, however, that a mucosal injury due to another cause may be followed by CMV infection of the granulation tissue which then may lead to further injury and perforation.

Adult↗
PubMed1979

Ischemic hepatitis.

Seven patients with cardiovascular disease had clinical episodes and marked transaminase elevations that suggested viral hepatitis, but all had morphologic evidence (from liver biopsy or autopsy specimens) that documented centrilobular necrosis (ischemic hepatitis) with no evidence of viral or drug injury. Several also had moderate or marked passive congestion of the liver so the liver biopsies of 15 additional patients were retrospectively reviewed. In this latter group congestion alone was associated with normal or minimal elevation in transaminases while all patients with notable (greater than 5 times normal) transaminase elevations had centrilobular necrosis. Congestion alone, no matter how severe or prolonged, seems to do little if any damage to the liver. Centrilobular necrosis, or ischemic hepatitis, correlates with significant hypertransaminasemia, appears to result from failure of hepatic perfusion (with or without preceding hypotension), and presents with clinical and laboratory manifestations that suggest viral hepatitis.

Adolescent↗
PubMed1979

Lipoprotein X and alkaline phosphatase as indicators of cholestasis.

Lipoprotein X is considered to be an indicator of cholestasis, but its clinical usefulness is unclear owing to different methods of measurement in use and varying definitions of cholestasis. We investigated the reliability of the qualitative determination of lipoprotein X in predicting cholestasis, defined here as the presence of stainable bile in tissue sections. Liver tissue and serum were collected from 42 patients. Patients were divided into those who did and those who did not have stainable bile in tissue sections. Lipoprotein X was demonstrated by electrophoresis and polyanion precipitation. Lipoprotein X in serum correlated with the presence of stainable bile (p = 0.0006). A normal range of alkaline phosphatase values correlated with the absence (p = 0.04), but elevated values did not correlate with the presence of stainable bile. In patients known to have elevated alkaline phosphatase, the presence of lipoprotein X still correlated with the presence of bile (p = 0.008). We conclude that lipoprotein X is a reliable indicator of cholestasis and that it is more useful than alkaline phosphatase in this application.

Alkaline Phosphatase↗
PubMed1978

Atypical mycobacterial infection complicating mineral oil pneumonia.

Two patients had pulmonary infections with atypical mycobacteria superimposed on mineral oil pneumonia. In both cases, long-standing laxative use and neurological disorders led to development of the lipid pneumonia. The pathogenicity of the rapidly growing mycobacteria causing infection in the two patients is apparently enhanced by the presence of mineral oil, a relationship supported by experimental studies. The clinical diagnosis of both atypical mycobacterial infection and mineral oil pneumonia may be difficult, but the presence of one should suggest the possibility of occurrence of the other.

Aged↗
PubMed1978

Bridging hepatic necrosis. Etiology and prognosis.

The probable etiology and outcome of bridging hepatic necrosis found on a liver biopsy performed within three months of the onset of clinical illness was evaluated in 42 consecutive patients with this finding. Eighteen of the patients (43%) had a probable drug etiology for their hepatitis. Ten patients had HBSAG-positive acute hepatitis. Fourteen patients had neither drug-induced disease nor proven HBSAg-positive hepatitis. One patient from the drug-induced group died, but the other 17 had complete clinical recovery. Eight of ten in the hepatitis B antigen-postive group cleared their antigen and had complete clinical recovery. Chronic hepatitis developed in two who remained persistently HGSAg positive. Eight of the patients in the group with unknown etiology recovered, while six developed evidence of active chronic liver disease. This incidence of active chronic liver disease is significantly greater than that found in the drug-induced group (P less than 0.02). We conclude that drug-induced hepatitiis accounts for a significant proportion of patients of acute hepatitis who have bridging hepatic necrosis on liver biopsy. However, in these drug-induced cases the finding of bridging hepatic necrosis does not appear to be associated with an increased risk of development of active chronic liver disease.

Acute Disease↗
PubMed1978

Aprindine hepatitis.

We have seen two patients whose hepatitis was due to the administration of aprindine, a new antiarrhythmic agent. In both patients evidence of hepatitis appeared within 3 weeks of initiating aprindine therapy and resolved rapidly when the drug was withdrawn. The reintroduction of aprindine in one patient was associated with the reappearance of hepatitis, which resolved despite continued administration of the drug.

Aprindine↗
PubMed1978

Corticosteroid therapy of alcoholic hepatitis.

Fifty-five patients with alcoholic hepatitis were studied in a 28- to 32-day randomized double blind treatment trial comparing prednisolone (40 mg per day) with placebo therapy. Of 31 placebo-treated patients, 4 died during the study interval and 2 more died within 5 days of study completion. Only 1 of 24 prednisolone-treated patients died during the same interval (Fisher exact test; P = 0.10). Stepwise discriminant analysis of laboratory factors associated with death revealed independently significant associations with prolongation of prothrombin time and height of serum bilirubin at the initiation of the study. When treatment was included as a variable in this discriminant analysis, it was found that corticosteroid therapy significantly decreased mortality (P less than 0.05). The corrected wedged hepatic venous presure decreased to a similar extent in the two groups. These studies suggest that corticosteroid therapy does decrease early mortality in patients with severe alcoholic hepatitis, but has no short term effect on the development of portal hypertension.

Adult↗
PubMed1978

Hepatic bilirubin UDP-glucuronyltransferase in patients with sickle cell anemia.

In sickle cell anemia the shortened survival of red blood cells presents the liver with an augmented load of bilirubin for hepatic clearance. To determine the effects of this excessive bilirubin load on the microsomal conjugating enzyme, hepatic bilirubin UDP-glucuronyltransferase, levels of this enzyme were measured in liver biopsies from patients with sickle cell anemia and several comparison groups. UDP-glucuronyltransferase activity in 14 patients with sickle cell anemia was 2-fold greater (P less than 0.005) than in 14 nonjaundiced comparison patients without liver disease. The elevated UDP-glucuronyltransferase activity in sickle cell anemia was similar to that found in 10 patients who chronically ingested drugs (barbiturates or estrogens) known to increase UDP-glucuronyltransferase activity. These observations suggest enhanced conjugation of bilirubin in patients with sickle cell anemia may result from substrate (bilirubin) induction of UDP-glycuronyltransferase.

Adolescent↗
PubMed1977

Effect of oral amino acid supplementation on liver disease after jejunoileal bypass for morbid obesity.

Previous work in our laboratory and others suggests that protein malnutrition plays an important role in the pathogenesis of hepatic steatosis and dysfunction which characteristically appears after jejunoileal bypass for morbid obesity. Postoperative protein-calorie malnutrition is at least in part a consequence of diminished intestinal absorption of free amino acids. In an attempt to prevent liver disease, six morbidly obese patients were orally supplemented with essential amino acids for 4 months after surgery. Oral amino acid supplementation only partially influenced protein malnutrition and had no effect on deterioration of hepatic morphology and dysfunction. Although this mode of therapy appears to be ineffective in preventing postoperative liver abnormalities, other studies suggest that oral oligopeptide supplementation and parenteral administration of amino acids are beneficial. In addition to protein deificiency, other factors which may contribute to the development of liver disease are reviewed.

Amino Acids↗
PubMed1977

Dantrolene-associated hepatic injury. Incidence and character.

Hepatic injury during long term dantrolene sodium therapy occurred in 19 of 1044 patients (1.8%) monitored for at least 60 days. Six had icteric hepatitis (0.6%) and 3 died (0.3%). After the marketing of the drug, an additional 31 cases of dantrolene-associated liver disease were available for analysis. Of these 16 had icteric hepatitis with a favorable outcome, whereas 11 died. The injury was mainly hepatocellular with a pattern of acute or subacute hepatic disease or chronic active hepatitis. Analysis of total of 50 cases showed a 28% case fatality rate. All the fatalities occurred in patients above 30 years of age and after at least 2 months of therapy, with 57% cases exposed for at least 6 months. Eleven of the 14 fatalities occurred in females (P is less than 0.05). No cases of hepatic disease occurred in patients exposed for less than 1 month or under the age of 10. The majority of adverse reactions (71%) occurred between 1 and 6 months of therapy. Daily dosage of 300 mg or more is associated with higher incidenceof hepatotoxic reactions and with the majority (85%) of the fatalities. The idiosyncratic hepatic injury does not appear to involve hypersensitivity to the drug. A careful assessment of the benefit-risk ratio in the therapeutic use of dantrolene sodium is proposed.

Adolescent↗
PubMed1976

Vessel caliber and branch-angle of human coronary artery branch-points.

Measurements were made of parent and branch vessel diameters and of the included angles of branch-points from postmortem human coronary arteriograms to determine the usefulness of theoretical equations predicting the relationships between parent and branch vessel caliber and between arterial caliber and branch-angle. The formulas were based on the concept that blood vessel size and arrangement provided for blood flow with minimum energy loss. Size relationships between parent vessel and its branches were determined for 42 left main and 53 other epicardial coronary artery branch-points in hearts with angiographically normal arteries. Left main coronary artery branch-points were studied in 68 hearts with various degrees of angiographically defined coronary artery disease. Measured diameters (D) of parent and branch vessels corresponded well to the theoretical formula: (DParent)3 = (DBranch1)3 + (DBranch2)3....,in angiographically normal coronary arteries. The exponent, on the average, is less with increasing grades of vascular disease for left main coronary artery branch-points. Mean area ratio, the sum of the cross-sectional area of the branches divided by the area of parent vessel, decreased with greater arteriographic disease. Area ratio varies with changes in the relative calibers of branch vessels. Fifty-seven branch-angles were determined by graphic analysis of postmortem biplane coronary arteriograms. No relationship could be found between branch-angle and vessel caliber. The included angle between branches varied from 32 degrees to 124 degrees without respect to relative or absolute vessel calibers. The results of these postmortem measurements on human coronary arteriogram suggest that coronary artery caliber may adjust to minimize energy loss at the branch-point but that branch-angle is determined by other factors. Restudy of arteriograms suggests that branch-angle may be determined by branch vessel destination.

Adaptation, Physiological↗