Role of porta systemic shunt and hepatocellular damage in the genesis of hepatic neuropathy.
A study was undertaken to evaluate the relative role of porta-systemic shunts and hepatocellular damage in the genesis of neuropathy in chronic liver disease. Two of the 14 patients with non-alcoholic cirrhosis showed clinical evidence of neuropathy, whereas none of the patients with idiopathic portal fibrosis had evidence of neuropathy clinically. Decreased motor conduction velocities were present in some cases of idiopathic portal fibrosis as well as non-alcoholic cirrhosis. Subclinical evidence of histopathological neuropathy in the form of segmental demyelination and remyelination as well as myelin fiber loss was seen in 10 out of 11 sural nerves studied in idiopathic portal fibrosis group and in all the 10 patients in the non-alcoholic cirrhosis group. No correlation was found between histological features and various parameters studied. It is postulated that the development of clinical or subclinical neuropathy in chronic liver disease depends on two factors, being collateral shunting and hepatocellular damage or both and probably related to abnormalities of nitrogen metabolism.
D000328:Adult; D003097:Collateral Circulation; D006801:Humans; D008099:Liver / Q000473:pathology*; D008103:Liver Cirrhosis / Q000601:surgery; D008107:Liver Diseases / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D010525:Peripheral Nerves / Q000503:physiopathology; D010523:Peripheral Nervous System Diseases / Q000209:etiology*; D011168:Portal System / Q000503:physiopathology*; D013497:Sural Nerve / Q000473:pathology