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Biomedical subjects

M D Voigt

Publications and source records attributed to M D Voigt.

13 recordsLinked to original sources
PubMed1999

Role of angiotensin in renal sympathetic activation in cirrhotic rats.

Central nervous system (CNS) renin-angiotensin activity influences the basal level of renal sympathetic nerve activity (RSNA) and its reflex regulation. The effect of type 1 angiotensin II (ANG II)-receptor antagonist treatment (losartan) on cardiac baroreflex regulation of RSNA and renal sodium handling was examined in rats with cirrhosis due to common bile duct ligation (CBDL). Basal levels of heart rate, mean arterial pressure (MAP), RSNA, and urinary sodium excretion were not affected by intracerebroventricular administration of either losartan or vehicle to CBDL rats. After acute intravenous isotonic saline loading (10% body wt) in vehicle-treated CBDL rats, MAP was unchanged and the decrease in RSNA seen in normal rats did not occur. However, in losartan-treated CBDL rats, there were significant concurrent but transient decreases in MAP (-20 +/- 2 mmHg) and RSNA (-25 +/- 3%). The natriuretic response to acute volume loading in losartan-treated CBDL rats was significantly less than that in vehicle-treated CBDL rats only at those time points where there were significant decreases in MAP. Antagonism of CNS ANG II type 1 receptors augments the renal sympathoinhibitory response to acute volume loading in CBDL. However, the natriuretic response to the acute volume loading is not improved, likely due to the strong antinatriuretic influence of the concomitant marked decrease in MAP (renal perfusion pressure) mediated by widespread sympathetic withdrawal from the systemic vasculature.

Angiotensin II↗
PubMed1997

Autonomic neuropathy in extra-hepatic portal vein thrombosis: evidence for impaired autonomic reflex arc.

BACKGROUND/AIMS: Autonomic dysfunction is common in cirrhosis, and may be associated with increased mortality and hyperdynamic circulatory changes. Our aim was to investigate whether autonomic disturbances occur in extrahepatic portal vein thrombosis and their correlation with hemodynamic abnormalities. PATIENTS AND METHODS: Heart rate variation in response to standing, deep breathing, and Valsalva maneuver, and blood pressure response to sustained handgrip and to standing, were studied in 16 subjects with portal vein thrombosis (10 males, 30.8+/-2.8 years: mean+/-SE), 12 with cirrhosis (7 males, 52+/-2.3 years), and 10 healthy controls (7 males, 30.8+/-3.0 years). Supine resting, and 10- and 30-min standing epinephrine and norepinephrine levels were measured and results correlated with cardiac output. RESULTS: Autonomic dysfunction occurred in 62% of portal vein thrombosis and 75% of cirrhosis subjects, but in no controls (p<0.02). Similarly, postural hypotension occurred in portal vein thrombosis (-10.25+/-0.65 mmHg, p=0.003) and cirrhosis (-7.42+/-0.82 mmHg, p=0.007) but not in controls. All groups had similar baseline epinephrine and norepinephrine concentrations. Epinephrine increased significantly in controls (45%, p<0.01 and 49%, p<0.02) after 10 of 30 min standing but not in the portal vein thrombosis or the cirrhotic group, and norepinephrine increased after 10 and 30 min standing in cirrhotics (128%, p<0.004 and 130%, p<0.008) and controls (129%, p<0.002 and 116%, p<0.004), but not portal vein thrombosis (34.5% and 39%, NS vs baseline). Portal vein thrombosis and cirrhosis groups had increased cardiac output (4441+/-509 and 3262+/-292) vs controls (1763+/-212 ml/min/m2, p<0.002), but there was no correlation with autonomic neuropathy or with catecholamine levels. CONCLUSIONS: Autonomic dysfunction and impaired catecholamine response to orthostatic stress occur commonly in portal vein thrombosis and suggest an impairment of the autonomic reflex arc, but changes do not correlate with hemodynamic abnormalities.

Adult↗
PubMed1997

Halothane hepatitis in a South African population--frequency and the influence of gender and ethnicity.

AIM: To review post-anaesthetic hepatitis in a South African population, given that halothane use is restricted in other countries because of the high mortality and morbidity of its associated type II (idiosyncratic) hepatitis, even though it is still widely used in South Africa. STUDY DESIGN: Descriptive, retrospective analysis. PATIENTS AND METHODS: Hepatitis cases that occurred after inhalational anaesthetic use were identified by means of a computer search of Groote Schuur Hospital records, 1980-1994. Cases of hepatitis caused by circulatory failure and viral hepatitis were excluded. RESULTS: Twenty-six episodes occurred in 22 patients (mean age 49.05 years, range 32-65 years), of whom 15 were women. This gave an estimated incidence of 3.53/100,000 anaesthetics (95% confidence interval 2.06-5.0/100,000). All had pyrexia (mean 38.7 +/- 0.72 degrees C), malaise, anorexia or nausea and vomiting, with onset a mean of 4.27 +/- 3.5 days after exposure. Jaundice occurred in 86%, rash in 13.6%; 17 patients (77%) were obese. Alanine and aspartate aminotransferase levels were raised 47.49 +/- 61.8 and 55.9 +/- 54.5 times the upper limit of normal. Seven patients died and 1 underwent liver transplantation. Hepatitis occurred after the first exposure in only 2 patients (9%). Men and women had a similar risk, but the estimated relative risk for whites v. black or coloured patients was 3.33 (95% confidence interval 1.45-7.23; P = 0.003) controlling for gender. Awareness of the condition was suboptimal, and in 3 patients re-exposure to halothane occurred after an initial episode of typical halothane hepatitis. CONCLUSION: Halothane hepatitis remains a major cause of morbidity and mortality in South Africa. It is more common in whites, but there was no gender-related excess risk.

Adult↗
PubMed1996

Threshold effect of liver iron content on hepatic inflammation and fibrosis in hepatitis B and C.

BACKGROUND/AIMS: In hepatitis C, iron depletion may improve serum aminotransferases and the response to interferon, but it is not known whether inflammation and fibrosis correlate with hepatic iron content. Our aim was to establish whether hepatic iron content correlates with histological and serum indices of hepatic inflammation and fibrosis in hepatitis B and C. METHODS: Total hepatic iron was measured using computerized histomorphometry, and hepatic inflammation and fibrosis using a modified Knodell score, on histological slides from 31 patients with chronic hepatitis B and 38 with hepatitis C. RESULTS: Total hepatic iron was similar in the hepatitis B and C groups (0.82 +/- 1.72% and 0.56 +/- 1.12%; mean +/- SD). No iron was detectable in 11 patients with hepatitis B and 13 with hepatitis C. Alanine aminotransferase (85.96 +/- 67.1 vs 44.2 +/- 39.7 p < 0.05), aspartate aminotransferase (93.8 +/- 75.6 vs 47 +/- 33.5 IU/ml p < 0.05) and histological inflammatory score (9.33 +/- 3.51 vs 7.79 +/- 3.3 p = 0.07) were increased in those with stainable hepatic iron compared to those without. However, where iron was present, no association was found between the amount of hepatic iron and inflammatory or fibrosis scores. In hepatitis C, fibrosis was minimal in 77% of patients if iron was absent vs 24% with iron present, while marked fibrosis was present in 56% with iron vs 15% without iron (p < 0.01, Fisher's exact test). CONCLUSION: Hepatic iron is associated with increased hepatic inflammation in chronic hepatitis B and hepatitis C and with high fibrosis scores in hepatitis C. There is a threshold effect, and once present, increasing iron does not correlate with increasing inflammation or fibrosis.

Adolescent↗
PubMed1994

Pulmonary hypertension associated with non-cirrhotic portal hypertension in systemic lupus erythematosus.

A case of non-cirrhotic portal hypertension in a patient with systemic lupus erythematosus, the first of our knowledge, is described. Severe pulmonary hypertension was associated with the portal hypertension and with markers of active auto-immunity. Pulmonary hypertension has not previously been associated with non-cirrhotic portal hypertension. The coexistence of vasculopathy of the portal and pulmonary vascular beds in this patient with active autoimmunity supports the postulate that portal-pulmonary hypertension may be immunologically mediated.

Adult↗
PubMed1994

Distribution of hepatic nerve fibers in liver diseases.

Autonomic hyperactivity with increased cardiac output and other manifestations occurs in patients with both cirrhosis and noncirrhotic portal hypertension. The role of the disordered hepatic autonomic innervation in the mediation of these abnormalities is unknown. We have studied the hepatic nerve network and associated extracellular matrix proteins in patients with portal hypertension (alcoholic cirrhosis, extrahepatic portal vein obstruction, idiopathic portal hypertension), and in patients without portal hypertension (alcoholic hepatitis, psoriasis before and after treatment with methotrexate, a potentially hepatotoxic drug) by immunohistochemical methods. Histologically normal liver biopsies from patients undergoing abdominal surgery served as normal controls. Hepatic parenchymal nerves were absent in cirrhotic nodules and were depleted in the fibrotic strands of alcoholic cirrhotic livers. In alcoholic hepatitis, where clinical and histological features associated with portal hypertension were absent, nerve fibers were increased around the portal vein branches. Similar increase was also noted in liver biopsies from patients with noncirrhotic portal hypertension. Increased numbers of nerve fibers around portal veins were demonstrated in psoriatics, particularly those treated with methotrexate. Immunohistochemical studies of extracellular matrix proteins revealed apparent inverse relationships between innervation and fibronectin deposition with direct relationships to laminin staining. The association of nerve network with portal hypertension and cellular inflammation was inconsistent.

Autonomic Nervous System↗
PubMed1992

Orthotopic liver transplantation at Groote Schuur Hospital.

We present data on 10 patients (5 men and 5 women, aged 21-56 yrs) with end-stage liver disease or tumour who underwent orthotopic liver transplantation at Groote Schuur Hospital between October 1988 and June 1991. Standard surgical techniques were used for procuring the donor liver, the recipient hepatectomy and the implantation of the liver. The venovenous bypass method was used in all but 2 patients. Postoperative immunosuppression was usually achieved with cyclosporin, azathioprine and low-dose steroids. Six patients were treated with prophylactic OKT3. Rejection episodes were treated with bolus doses of intravenous steroids. The indications for liver transplantation included chronic active hepatitis progressing to cirrhosis (5), biliary cirrhosis in association with inflammatory bowel disease (1), sclerosing cholangitis (2), alpha 1-antitrypsin deficiency (1), and tumour (1). All patients with chronic liver disease had experienced at least one complication, examples of which included encephalopathy, bacterial peritonitis, ascites, variceal bleeding and septicaemia. Serious postoperative complications included acute rejection of the transplanted liver, renal and liver failure that responded to intensive care support and medical management. One patient died on the 11th postoperative day with complications of bleeding oesophageal ulcer, shock and fungaemia. The remaining patients are alive and well 1-31 months after transplantation.

Adult↗
PubMed1989

Diagnostic value of ascites adenosine deaminase in tuberculous peritonitis.

The value of ascitic fluid adenosine deaminase activity in distinguishing tuberculosis from other causes of ascites was examined in a retrospective study of 41 patients with bacteriologically confirmed tuberculous peritonitis and 41 control patients, matched for age and sex, with ascites of other causes (12 alcoholic cirrhosis, 5 cryptogenic cirrhosis, 12 malignant disorders, 3 pancreatitis, and 9 miscellaneous causes). The mean ascites adenosine deaminase activity was 99.8 (SD 49.1) in tuberculous patients and 14.8 (8.4) U/l in control patients (p less than 0.0001). A cutoff of 32.3 U/l had a sensitivity of 95% and specificity of 98% in distinguishing between the two groups. In a subsequent prospective study of 64 patients with ascites, 11 were found to have tuberculosis. Of the others, 23 had cirrhosis (18 alcoholic, 5 cryptogenic), 17 malignant disorders, 3 pancreatitis, 5 cor pulmonale, 3 congestive cardiac failure, 1 systemic mastocytosis, and 1 renal failure and hypothyroidism. The mean ascites adenosine deaminase activity was 112.6 (45.0) U/l in the patients with tuberculous ascites and 16.3 (36.7) U/l (p less than 0.0001) in those with ascites of other causes. In this study, adenosine deaminase had a sensitivity of 100% and specificity of 96% in discriminating tuberculosis from other causes of ascites. These findings suggest that the ascitic fluid adenosine deaminase activity may be used to identify patients in whom the diagnosis of abdominal tuberculosis must be pursued.

Adenosine Deaminase↗
PubMed1986

Tuberculous perforation of the bowel. A report of 8 cases.

Eight patients with tuberculous perforation of the bowel, representing 15% of all cases of intestinal tuberculosis, were seen over a 13-year period. A wide spectrum of presentations was encountered. A history of acute abdominal pain was not always obtained, but it could be the first indication of the presence of associated intestinal involvement in a patient receiving treatment for pulmonary tuberculosis. Free subdiaphragmatic air was detected radiologically in only 2 cases (25%). It is suggested that emergency surgery should be limited to dealing with only the perforated and any obviously obstructed bowel, and the advantages of delaying additional procedures are stressed. Despite the invariable accompanying suboptimal nutritional status and associated medical problems found in this group of patients, only 2 died.

Adolescent↗