Diagnostic parameters of minimal hepatic encephalopathy: clinical, electrophysiological, and neuroimaging study

Cirrhotic patients with minimal hepatic encephalopathy [MHE] have subtle cognitive deficits that can be detected by neuropsychometric tests, P300 event related potential, EEG, and increased signal on T1-weighted brain Magnetic Resonance Imaging. The present study was designed to assess the magnitude of cognitive dysfunction, a marker of minimal hepatic encephalopathy [MHE];to evaluate diagnostic usefulness of neuropsychological cognitive tests, EEG, P300 ERP latency, and MRI brain signs; and to investigate the clinical outcome of patients with MHE in terms of progression to overt encephalopathy. A total of 43 well-compensated cirrhotic patients without signs of encephalopathy were studied by neuropsychological cognitive test battery, P300 ERP latency, EEG, conventional MRI brain. The patients were followed-up for 2 yrs. to monitor subsequent episodes of overt encephalopathy. Child-Pugh classification was done throughout the study to assess severity of liver cirrhosis. Forty-six healthy subjects, age, sex, and education matched, served as a control group. Minimal HE was diagnosed in 21[48.8%], out of 43 cirrhotic patients. Inverted sleep rhythm was reported in 85.7%, of cirrhotic with MHE. Delayed P3ERP latency were seen in 38.1% of cirrhotic patients with MHE, while Number Connection Test [NCT-A and B] time were prolonged in 71.4% of the patients. EEG abnormality was detected in 47.6%, while MRI signs were reported in 80.9% of cirrhotic with MHE. Out of 43 patients, 18[41.8%] developed overt encephalopathy, 66.7% of the patients with MHE progressed to overt encephalopathy within a mean duration of 9 months, while only 13. 6% of the non-mHE patients did so. Of the patients who developed overt encephalopathy, 83.3% had abnormal EEG, 77. 8% had abnormal NCT, while 59. 3% had P3ERP latency prolongations. The results of the present study suggest that inverted sleep rhythm, abnormal NCT, slow EEG activity, and delayed P300 latency are valid tools for the screening of MHE in cirrhotic patients as there is a greater likelihood of overt encephalopathy development in patients with an abnormality detected by these tests than in patients without such abnormality. EEG is useful for follow-up screening and prediction of the development of overt hepatic encephalopathy

Evaluation of the antibilharzial activity of mirazid versus praziquantel against S. haematobium: an experimental study

Mirazid [myrrh] is a new herbal extract [oleo gum resin from the stem of the plant Commiphora molmol with claimed antibilharzial activity. LD16, LD50, and LD84 of Mirazid were determined in albino mice and were found to be 1984, 3138, and 4963 mg/kg respectively. The antibilharzial efficacy of Mirazid, administered orally at a dose of 250X5 mg/kg, in comparison to the schistosomicidal drug of choice praziquantel [PZQ], administered orally at a dose of 250X2 mg/kg, was evaluated in S. haematobium infected hamsters. Treatment was conducted 90 days post infection. Parasitological parameters expressing cure and hepatic histopathological changes were evaluated 4 weeks after treatment. Praziquantel treatment completely eradicated S.haematobium worms, caused disappearance of immature and mature egg stages, with 100% dead eggs. Hepatic and intestinal tissue egg loads were reduced by 79.2% and 99.7% respectively. Mirazid failed to induce any significant change in total number of worms, but induced significant reduction in the 1[st], 2[nd], and 3[rd] immature egg stages with increase in the number of the fourth stage, but this change was not reflected on the total number of immature eggs. Mirazid did not affect tissue egg load. The hepatic histopathological changes induced by S. haematobium infection were improved in praziquantel treated hamsters with reduction in granuloma number and size. Ova degeneration with regression of granulomatous inflammatory reaction was more manifested when compared to infected untreated controls. Mirazid did not results in evident regression of hepatic schistosomal pathology. In conclusion, praziquantel is still the drug of choice for treatment of S. haematobium, while Mrazid cannot substitute PZQ in the treatment of S. haematobium. Further trials using modified preparations may result in better antibilharzial efficacy of this novel herbal extract preparation