Evaluation of Folate Metabolism in patients with Idiopathic Non-cirrhotic Intra-hepatic Portal Hypertension.

Madhu, K (2009) Evaluation of Folate Metabolism in patients with Idiopathic Non-cirrhotic Intra-hepatic Portal Hypertension. Masters thesis, Christian Medical College, Vellore.

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Abstract

INTRODUCTION : Idiopathic non-cirrhotic intra-hepatic portal hypertension (NCIPH) is a term that defines one or more entities characterized by intra-hepatic portal hypertension and good to excellent liver function.(See references inserted on the previous page) This definition encompasses a number of entities including non-cirrhotic portal fibrosis (NCPF) and idiopathic portal hypertension (IPH) and is sometimes difficult to differentiate from well compensated cirrhosis. By definition this excludes causes like extra-hepatic portal vein obstruction and Budd Chiari Syndrome. The etio-pathogenesis of NCIPH is poorly understood with a number of hypotheses proposed in the past. Arsenic toxicosis from contaminated drinking water is a possible etiological factor for NCIPH in India. Infective hypothesis was put forward with the possibility of umbilical sepsis, bacterial infection and diarrhoeal episodes in infancy and early childhood leading to portal pyemia, pylephlebitis resulting in thrombosis, sclerosis and obstruction of small and medium sized portal vein radicals. AIMS & OBJECTIVES : The hypothesis is that non-cirrhotic intrahepatic portal hypertension (NCIPH) occurs secondary to a defect in folate metabolism, that leads to a procoagulant status and vascular occlusion. The aims of the present study were to evaluate the serum levels of folate, vitamin B12 and homocysteine and to evaluate methylene tetrahydrofolate reductase (MTHFR) gene mutations in patients with NCIPH spectrum disease and to compare them with cirrhosis of known cause and matched healthy controls. CONCLUSIONS : The median serum level of vitamin B12 was significantly higher in patients with cirrhosis when compared with Idiopathic Non cirrhotic Portal hypertension (NCIPH) and the prevalence of vit B12 deficiency was 30% in NCIPH compared to 36% in healthy controls(36%). Inference : This reflects the parenchymal damage in cirrhosis causing release of vit B12 into the circulation and that there is no parenchymal (hepatocyte) injury in NCIPH. Among the NCIPH patients with low vitamin B12, MCV was low or normal in the majority with concomitant iron deficiency seen in the majority of the patients (7 out of 11 tested). Fasting serum Homocysteine was elevated in 12 out the 19 patients of NCIPH in whom it was tested ,but there was no correlation with vitamin B12 deficiency. There was no difference in serum folate levels in the NCIPH group when compared to Cirrhosis patients or Healthy controls. MTHFR C677T Polymorphism (both mutant alleles and mutant genotypes) was more prevalent in healthy controls than NCIPH with a P value of 0.02 (Fisher’s exact test),Relative risk of 0.78(95% CI 0.67-0.92) and Odd’s ratio of 0.25(95%CI 0.07-0.86).

Item Type: Thesis (Masters)
Uncontrolled Keywords: Folate Metabolism ; patients ; Idiopathic ; Non-cirrhotic ; Intra-hepatic Portal ; Hypertension.
Subjects: MEDICAL > Gastroenterology
Depositing User: Kambaraman B
Date Deposited: 14 Jul 2017 04:11
Last Modified: 14 Jul 2017 04:11
URI: http://repository-tnmgrmu.ac.in/id/eprint/1626

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