Liv.52 Therapy in Infective Hepatitis
Khetarpal, S.K., M.D., D.C.H., Professor of Paediatrics, II Unit and Veera Kumar, E., M.B.,B.S., Research Scholar, Department of Paediatrics, Medical College, Amritsar, India.
| Table V: Showing results of liver function tests | |||
| Sr. No. | L.F.T. | Range | Average |
| 1. | S. bilirubin | 3.2 mg% - 6 mg% | 4.37 mg% |
| 2. | Thymol turibidity | 4 - 9 units | 5.95 units |
| 3. | Cephalin cholesterol | 1 + to 3+ (after 48 hours) | 2+ |
| 4. | Alkaline phosphatase | 7 - 10.5 B.U. | 9.25 B.U. |
| Table VI: Showing liver biopsy reports | ||
| Group | Biopsy report | No. of cases |
| 1st group | Mild to moderate degeneration of the liver cells with mild to moderate infiltration by chronic inflammatory cells in the portal areas | 8 |
| 2nd group | Features of first group and in addition, cholestasis | 4 |
| 3rd group | Features of second group with added necrosis of liver cells | 3 |
| Table VII: Showing the average period for the improvement of symptom/sign | |||||||||
| Sr.No. | Symptom or sign | Average period for the improvement of symptom./sign | |||||||
| Group A Liv.52 group | Group B (Control) without Liv.52 | ||||||||
| 1. | Disappearance of nausea | 6.0 days | 19.0 days | ||||||
| 2. | Control of vomiting | 1.4 days | 2.2 days | ||||||
| 3. | Improvement of appetite | 9.4 days | 23.7 days | ||||||
| 4. | Disappearance of fever | 3.6 days | 5.2 days | ||||||
| 5. | Disappearance of jaundice | 10.0 days | 22.6 days | ||||||
| 6. | Disappearance of hepatic tenderness | 12.6 days | 24.3 days | ||||||
| 7. | Clearance of urine | 11.0 days | 24.6 days | ||||||
Liver biopsy was done in 15 cases. In the rest of the patients it was considered unsafe or was not permitted. All the biopsies showed the findings consistent with histopathological picture caused by acute viral hepatitis. The biopsy results were classified into three groups.
An attempt was made to estimate liver function tests at least once in a week. But this was not possible due to practical difficulties like—(1) Patients (patient’s-attendants) were not prepared for giving repeated blood samples. (2) Parents of the diseased frequently felt that their children were “obviously normal” after few days of treatment and refused to give blood for L.F.T. studies.
DISCUSSION
Patro (1957) and Mathur (1957) reported that Liv.52 helps in improving the outlook in severe hepatic damage. Sheth (1963) observed that it has a salutary effect on anorexia of infective hepatitis. Qazi (1965) stated that in animal experiments Liv.52 has a good influence on biochemical and functional abnormalities of the liver. He reported that the drug has a protective action against hepatotoxicity of tetracyclines in rats. Arora (1969) reported that Liv.52 adds “materially to patient’s comfort and accelerates recovery”. According to the study of Prasad and Tripathi (1969) Liv.52 brought an immense increase in appetite and power to assimilate without bowel disturbances in cases of infective hepatitis and malnutrition. As for the work of Jaffari and Shyam Raj (1969)
Liv.52 clears jaundice earlier, improves appetite and gives a sense of well-being. Liv.52 is reported to offer quite considerable protection against carbon tetrachloride and many other toxic agents (Sheth et al., 1960; Joglekar et al., 1963; Joglekar and Leevy 1970). Microscopic examination of the liver of animals treated with Liv.52 and carbon tetrachloride showed that the peripheral cells of the liver parenchyma escape necrosis and definitely show less deglycogenation but the central cell necrosis cannot be prevented. Further, the drug prevents deglycogenation of the peripheral part of the liver lobule to synthesise serum albumin. Liv.52 markedly improves the functional activity of the liver by acting as a powerful hepatic stimulant (Mukerjee and Dasgupta, 1970). Dayal et al. (1971) reported improvement in general condition, regression in jaundice and improvement in liver function tests. Ramalingam et al. (1971) reported that in infective hepatitis with the therapy of Liv.52, symptoms improved earlier than in the Vitamin C plus B-complex group, better weight gain was recorded and earlier restoration of liver function to normal observed.
Table VII clearly shows that the improvement in symptomatology was remarkable as compared to the control group. After Liv.52 therapy patients had a subjective sense of well-being, appetite improved earlier, nausea disappeared more rapidly, jaundice and urine cleared earlier. Regarding the liver, size of the liver decreased much earlier than in controls and hepatic tenderness persisted for many days in the controls unlike in the Liv.52 given group.
These observations are in accordance with the earlier studies (Mukerjee and Dasgupta, 1970; Patel et al., 1971;
Deshpande et al., 1971 and Ramalingam et al., 1971). Liv.52 was also tried in malnutrition in this part of the state by Khetarpal et al., (1972), and they have found marked improvement of appetite and weight gain in cases on Liv.52 besides increase in total serum protein and haemoglobin percentage.
It is also felt from this trial that the shift of deranged L.F.T. to normal was earlier in group A although much emphasis cannot be laid on this aspect due to irregularities in L.F.T. study for reasons beyond our control.
Regarding control of vomiting and absence of fever, little difference between the two groups is noted.
Prasad and Prasad (1971) reported 85% cure rate while poor response in 15% of cases with Liv.52 in infective hepatitis. In this study, all the thirty cases showed better response with Liv.52. Liv.52 was given for two months and no side-effect or toxicity was noted. CONCLUSIONS
1. The symptoms improved earlier in the Liv.52 group than in the B-complex and Vitamin C group.
2. No side effect was noticed. REFERENCES
1. Arora, J.K., Armed Forces med. J. (1969): 3, 362.
2. Captain, S.R. and Syed, A.H., The Indian Veterinary Journal (1966): 43, 11.
3. Dayal, R.S., J. Ind. med. Prof. 91970): 9, 7768.
4. Deshpande, R.S., Sheth, S.C. and Joykutty, M.D., Curr. med. Pract. (1971): 6, 810.
5. Jaffari, S.M.H. and Shyam Raj, Antiseptic (1969): 5, 353.
6. Joglekar, G.V. et al, Acta pharmacol. et toxicol. (1963): 20, 73.
7. Joglekar, G.V. and Leevy, C.M., J. Ind. med. Prof. (1970): 12, 7480.
8. Karandikar, S.M. et al, Acta pharmacol. et toxicol, (1963): 20, 274.
9. Khetarpal, S.K., Ramakumar, Leela and Lubhaya, Ram, Curr. med. Pract. (1972): 16, 481.
10. Mathur, P.S., Curr. med. Pract. (1957): 2, 107.
11. Mukerjee, A.B. and Dasgupta, M., Indian Practitioner (1970): 6, 357.
12. Mukhibhavi, G.R. and Sheth, U.K., Indian Veterinary Journal (1957): 4, 276.
13. Patel, J.R. and Sadre, N.L., Probe (1963): 1, 19.
14. Patrao, S., J. Ind. med. Prof. (1957): 8, 1878.
15. Prasad, L.S. and Prasad, K., Probe, (1969): 3, 114.
16. Prasad, L.S. and Tripathi, D., Probe (1969): 1, 1.
17. Qazi, I.H., Probe (1965): 5, 1.
18. Ramalingam, V. et al, Ind. Paed. (1971): 12, 839.
19. Sheth, S.C., Northover, B.J., Tibrewala, N.S., Warerkar, U.R. and Karande, V.S., Ind. J. Paed. (1960): 149, 204.
20. Sheth, S.C., Tibrewala, N.S., Warerkar, U.R. and Karande, V.S., Probe (1963): 4, 137.
21. Sule, C.R. et al, Ind. Practit. (1956): 4, 357.
Refference: http://www.himalayahealthcare.com/pdf_files/liv221.pdf
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