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mmol/l (p<0.002). Total cholesterol was reduced capsule from 6.6±1.9 to capsule 5.7±1.1 mmol/l (p<0.005), and HDL-C levels increased from 0.96±0.2 to 1.1±0.2 mmol/l (p<0.002). During the follow-up period, liver enzyme levels were reduced to some degree in all but two patients (46/48, 96%). In 25 patients (52%) they were reduced back to the normal range. The two patients who did not improve their LFTs were a 48-year-old obese male with diabetes (diagnosed by fasting hyperglycaemia) and dyslipidaemia with liver biopsy showing fatty infiltration (+2), and capsule a 55-year-old obese woman with IGT and dyslipidaemia who refused a liver biopsy. Both patients did not lose weight and did not receive hypoglycaemic or lipid-lowering medications. None of the patients developed symptoms or laboratory features suggestive of liver function deterioration. The improvement in liver enzymes was not associated with initial anthropometric or metabolic findings. The six patients who had fibrosis in their liver biopsies had a similar response as the patients who had only steatosis.
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