Time-course changes in nerve conduction velocity (NCV) in type 2 diabetes.

AIM: Changes in NCV were surveyed over 10 years in type 2 diabetes patients to clarify the time-course relationships between NCV and retinopathy stage and between NCV and HbA1c. In addition, the natural course of diabetic sensorimotor polyneuropathy (DSPN) was discussed based on the findings. METHODS: Using a simple NCV measurement device, NCV (MCV and SCV) was measured once a year over 10 years in 474 patients with type 2 diabetes. These patients were grouped based on the retinopathy stage and HbA1c level in the course to investigate the time-course relationships between the retinopathy stage and NCV and between HbA1c and NCV. RESULTS: The retinopathy stage and NCV reduction were strongly correlated, and NCV decreased as retinopathy progressed. On comparison of time-course NCV among the retinopathy stages, continuity of NCV reduction along with the retinopathy progression was noted. Regarding the relationship between HbA1c and NCV, NCV reduction was moderate in the group maintaining HbA1c at a relatively favorable level, but morbid reduction of NCV could not be prevented even though favorable control was maintained. CONCLUSION: NCV reduction is strongly correlated with retinopathy progression from more than 10 years before its manifestation through reaching proliferative retinopathy. It was also suggested that NCV reduction can be attenuated by controlling blood glucose, but the reduction cannot be prevented completely. Based on these findings, DSPN is a progressive complication that starts from an early phase after onset of diabetes and steadily aggravates, keeping step with retinopathy aggravation, and it may be difficult to completely prevent the progression.

Association of an overlap syndrome of autoimmune hepatitis and primary biliary cirrhosis with cytomegalovirus infection.

A 63-year-old woman, who presented with severe jaundice and elevated serum conjugated bilirubin level, denied alcohol and drug use and showed no evidence of viral hepatitis. Based on clinical and laboratory features, she was diagnosed with autoimmune hepatitis with primary biliary cirrhosis. Hematological and immunochemical assays, radiographic imaging, clinical examination, and liver biopsy were conducted. Laboratory results were the following: negative for fluorescence antinuclear antibody, negative for antismooth muscle antibodies but positive for antinuclear antibody (enzyme-linked immunosorbent assay) and antimitochondrial M2 antibody, high titers of serum globulin, and positive for cytomegalovirus IgM. Liver biopsy showed submassive lobular necrosis, inflammation with broad areas of parenchymal collapse, and chronic nonsuppurative destructive cholangitis. The patient responded well to corticosteroid therapy. This case might illustrate an association between cytomegalovirus infection and the occurrence of autoimmune hepatitis.

A case of drug-induced hepatic injury associated with sitagliptin.

A 58-year-old man with a 10-year history of type II diabetes mellitus presented with progressive jaundice that began three days before admission. Thorough history-taking revealed that the patient had started on a new medication, sitagliptin, one month previously for the treatment of diabetes mellitus. Laboratory investigations showed severe liver dysfunction. Ultrasonography detected no extrahepatic biliary duct dilatation or gallstones. Abdominal computed tomography excluded pancreatic and hepatic focal lesions. Liver function improved upon discontinuation of sitagliptin. Drugs are an important, often unrecognized, cause of acute liver injury. This report presents a rare case in which sitagliptin was responsible for acute hepatic damage. As demonstrated, a thorough drug history is helpful in any case of unexplained liver injury.

Acute intrahepatic cholestasis accompanied with Chlamydophila pneumoniae infection.

We report a case of Chlamydophila (C.) pneumoniae infection presenting with fever and rapid intrahepatic cholestasis. A 63-year-old man had a week-long history of intermittent high fever and rapidly progressive jaundice with atypical erythema. The results of liver function tests were recorded. The results of all serological tests were negative; the IgM, IgG, and IgA titers for C. pneumoniae had increased, which indicates a C. pneumoniae infection. The patient's fever and liver dysfunction improved upon administration of minocycline. Light microscopic findings showed the presence of enlarged liver cells with clear cytoplasm, a few mitotic figures, multinucleated cells, and bile cholestasis. The electron microscopic appearance of liver biopsy showed that bile canaliculi exhibited intrahepatic forms of cholestasis. From the results of light and electron microscopy, we inferred atypical intrahepatic cholestasis, probably resulting from the C. pneumoniae infection.