School of Clinical Medicine (ETDs)

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Subject: search.filters.subject.Metabolic syndrome

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    The effect of medical castration on lipid levels in black South African men with Prostate cancer
    (University of the Witwatersrand, Johannesburg, 2024) Minkowitz, Shaul
    Background In South Africa, androgen deprivation therapy (ADT) is commonly given as primary therapy for prostate cancer (PCa) due to many patients presenting with advanced disease. The metabolic adverse effects of ADT on lipid profile and weight gain have been reported mainly in Caucasian populations but few studies have been performed in African populations. Men of African descent generally have favorable lipid profiles compared to other populations and our study looked to analyze the effect of medical castration on lipid levels in black South African men with PCa. Methods The aim of this study is to describe the changes in blood total cholesterol, triglycerides, LDL and HDL at 6 months and at 1 year in men with prostate cancer newly initiated on ADT. Changes to BMI, waist circumference and HbA1c were also measured after 1 year of ADT. Our study was conducted at Chris Hani Baragwanath Academic Hospital which is a teaching hospital affiliated with the University of the Witwatersrand. It is located in Soweto, South of Johannesburg and serves the 1.3 million local residents who are predominantly black and of the lower income bracket. This study enrolled 38 black South African men who were starting to receive ADT for PCa. Subjects were evaluated at baseline and at 6 and 12 months. Lipid profiles and HbA1C levels were measured using blood samples and body composition was measure using BMI and waist circumference. Results In this prospective single center study we found that ADT resulted in a significant rise in triglyceride levels and weight gain in black South African men reaching mean levels of obesity using ethnic specific definitions. High density lipoproteins levels decreased significantly particularly in the first 6 months of treatment and thereafter began to rise. ADT also resulted in an increased HbA1C level which is a marker for insulin resistance. Conclusions Androgen deprivation therapy unfavorably changed the body habitus and lipid profile of men with PCa. It was demonstrated that even black South Africans who generally have favorable lipid profiles compared to their counterparts are at risk of developing metabolic syndrome while being treated with ADT
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    The role of increased gastrointestinal alcohol production in patients with the metabolic syndrome: Implications for the pathogenesis of non-alcoholic fatty liver disease
    (University of the Witwatersrand, Johannesburg, 2006) Menezes, Colin Nigel; Immelman, Ronnie; Raal, Derick
    Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease with hepatic histology that resembles alcoholic liver disease. It is a frequent cause of chronic liver disease and is attracting increasing scientific attention worldwide. I explored the possibility that increased gastrointestinal alcohol production may have a role as a “second hit” in the pathogenesis of NAFLD in study subjects with the metabolic syndrome. In an attempt to investigate this hypothesis, this study looked at blood, urine and breath levels of alcohol in patients with the metabolic syndrome versus matched age and ethnic group healthy controls. Of the twenty study subjects, 80% had dyslipidaemia, 60% had hypertension and 70% had type 2 diabetes mellitus. Their mean BMI was 35.1±8.2 kg/m² (mean ± SD, P < 0.0001 versus controls). The serum aminotransferases were significantly elevated in the study subjects, their ALT levels being 57.4±44.79 U/L versus 17.4±4.60 U/L in the controls (95% CI 18.02 – 61.42, P < 0.001), and their AST levels 52.5±36.21 U/L versus 23.4±4.86 U/L in the controls (95% CI 11.99 – 46.20, P < 0.01). Seventy five percent of the study group had sonar features suggestive of fatty liver disease. Two adipocytokines, adiponectin and leptin, mediators of insulin resistance, an important factor in the development and progression of NAFLD, were also measured. Adiponectin levels were significantly lower (6875 ng/L versus 15475 ng/L; median value, P < 0.01), and leptin concentration levels significantly higher (13.56 ng/L versus 3.05 ng/L; median value, P < 0.05) in the study subjects than in the control group. Alcohol was detected in 60% of the study subjects, of which 35% tested positive for ethanol, 55% tested positive for methanol, and 30% tested positive for both ethanol and methanol. This was a statistically significant result, as none of the control group tested positive for any of the alcohols. The ethanol concentration in the study subjects’ blood was 7.14±3.28 mg% (mean ± SD), in their urine 3.71± 12.87 mg% (mean ± SD) whilst none was detected in their breath. The methanol concentration in the study subjects’ blood was 16.17±17.95 mg% (mean ± SD), in their urine 6.8± 13.58 mg% (mean ± SD) while their breath level was 2.05±3.19 mg (mean ± SD). This study therefore suggests that endogenous alcohol production may be indeed be involved in the pathogenesis of NAFLD in subjects with the metabolic syndrome. Not only ethanol but also methanol was detected in the subjects tested. endogenous alcohol may therefore be responsible for the ‘second hit’ theory in the pathogenesis of NAFLD, and it is likely that formaldehyde, the metabolite of methanol may be a more potent toxin of the patocyte injury as opposed to acetaldehyde, the metabolite of ethanol. The most likely source of the alcohol is from intestinal bacterial flora. These findings provide further insight into the pathogenesis of NALFD, suggesting other therapeutic alternatives such as the use of antibiotics and probiotics as a potential treatment strategy for NAFLD.