Trial of Liv.52 in Infectious Hepatitis in Children in Goa
Harish Mazumdar, M.B., F.A.A.P. (U.S.A.), Professor and Head of the Department, and Mira Mazumdar, M.B.,B.S., F.A.A.P. (U.S.A.), Research Officer, Department of Paediatrics, Goa Medical College, Panaji, Goa.
DISCUSSION
Clinical improvement was more rapid and symptoms subsided earlier in the patients treated with Liv.52 than in the control group. This was elicited by the early subsidence of jaundice and return of appetite, the latter being substantiated by the finding of an average weight gain of 0.92 kg. In the control group the appetite remained poor considerably longer and consequently there was hardly any weight gain during the observation period.
Tenderness of the liver seemed to persist longer in the control than in the trial group. It is difficult to conclude if the liver size regressed to "Normal" in any children, since throughout childhood, the liver is normally palpable anywhere upto 2 cm below the costal margin. We did, however, notice that excessive enlargement of more than 5 cm regressed in 4-6 weeks in the trial group, whereas in the control group it took longer.
Liver function tests have shown that Liv.52 brings down the level of serum bilirubin in a great majority of patients much earlier than in patients treated without this drug. It was seen that the rise in serum total proteins after treatment was similar in both groups but in the Liv.52 group the rise in serum albumin was seen in a larger number of patients to definitely higher levels. Lowered serum albumin level has been recognised as an index of hepatocellular damage and in as much as that, Liv.52 seems to stimulate liver cell regeneration. SGPT is the index of hepatic cell destruction and its continued presence at high levels indicates liver function impairment and that the disease has not resolved. There was a large difference in the Liv.52 and the control group of patients who showed continued high SGPT levels indicating that Liv.52 stimulates hepatic cell repair earlier. Without this treatment a number of patients seemed to continue having liver cell damage and it is conceivable that some of them might have gone on to develop further and irreparable damage.
Alkaline phosphatase and zinc turbidity tests convincing returned to normal in a larger number of patients treated with Liv.52 than in the control group. In the latter, 90 to 100% of patients continued to show abnormal levels of one or both tests at the end of 2 weeks. In the trial group this number was reduced to almost 33% indicating the beneficial effects of Liv.52 in reducing inflammation of the liver cells and promoting their regeneration, as well as decreasing bile stasis.
About half the patients in both groups had prolonged prothrombin time. Two weeks of Liv.52 reduced the time to normal in all the 50 cases, whereas in the control group, 20% of cases still showed abnormal values after two weeks, indicating a more serious prognosis.
A noteworthy case, not included in the study, was a 12 day old male infant with neonatal hepatitis who had deep jaundice and hepatosplenomegaly. His LFT were – serum bilirubin – 13 mg%, alkaline phosphatase 20 units, SGPT – 200 i.u., Zinc turbidity – 12 units and Prothrombin time – 100 seconds (19 seconds for control). Urobilinogen was present in urine initially but it disappeared after 5 days of treatment. Liv.52 effected clinical improvement in 5 days and clinical cure in 4 weeks. LFT returned to normal after six weeks. He has remained normal to date after two years of follow-up.
CONCLUSIONS
Liv.52 is beneficial in the treatment of acute infectious hepatitis. It abates the symptoms rapidly, reduces the duration of jaundice and restores appetite. It causes the return of impaired liver function tests to normal indicating its effectiveness in promoting liver cell regeneration and preventing further damage.
Prolonged use of Liv.52 is helpful in cases of severe acute hepatic necrosis by promoting liver cell regeneration.
No untoward side effects of Liv.52 therapy were noted during the course of this study.
ACKNOWLEDGEMENT
We are thankful to the Dean, Goa Medical College for permission to publish this paper.
We are grateful to The Himalaya Drug Co. Pvt. Ltd., for the generous supply of Liv.52 required for the trial.
REFERENCES
1. Ramalingam, V., Sundaravalli, N. and Raju, B., 'Liv.52 Studies in Acute Hepatitis'. Indian Paediatrics (1971): 12, 839.
2. Gupta, S., Khatri, R.L. and Srivastava, G., 'Therapy of Infectious Hepatitis and other Liver Disorders'. Probe (1972): 2, 93.
3. Sheth, S.C., Northover, B.J., Tibrewala, N.S., Warerkar, U.R. and Karande, V.S., 'Therapy of Cirrhosis of Liver and Liver Damage with Indigenous Drugs–Experimental and Clinical Studies'. Indian Journal of Paediatrics (1960): 149, 202.
4. Joglekar, G.V. and Leevy, C.M., 'Effect of an Indigenous Drug on I.C.G. (Indocyanine Green) Clearance and Autoradiographic Patterns in Albino Rats with Experimentally Induced Hepatotoxicity'. Probe (1972): 2, 81.
5. Kulkarni, S.D., Kulkarni, D.S., Vasantgadkar, P.S. and Joglekar, G.V., 'Study on Liv.52 An Indigenous Anabolic Compound'. Probe (1972): 2, 89.
6. Patel, Jal, R. and Sadre, N.L., 'Effect of Liv.52 on Structural and Functional Damage Caused by some Hepatotoxic Agents'. Probe (1963): 1, 19.
Refference: http://www.himalayahealthcare.com/pdf_files/liv223.pdf
Tenderness of the liver seemed to persist longer in the control than in the trial group. It is difficult to conclude if the liver size regressed to "Normal" in any children, since throughout childhood, the liver is normally palpable anywhere upto 2 cm below the costal margin. We did, however, notice that excessive enlargement of more than 5 cm regressed in 4-6 weeks in the trial group, whereas in the control group it took longer.
Liver function tests have shown that Liv.52 brings down the level of serum bilirubin in a great majority of patients much earlier than in patients treated without this drug. It was seen that the rise in serum total proteins after treatment was similar in both groups but in the Liv.52 group the rise in serum albumin was seen in a larger number of patients to definitely higher levels. Lowered serum albumin level has been recognised as an index of hepatocellular damage and in as much as that, Liv.52 seems to stimulate liver cell regeneration. SGPT is the index of hepatic cell destruction and its continued presence at high levels indicates liver function impairment and that the disease has not resolved. There was a large difference in the Liv.52 and the control group of patients who showed continued high SGPT levels indicating that Liv.52 stimulates hepatic cell repair earlier. Without this treatment a number of patients seemed to continue having liver cell damage and it is conceivable that some of them might have gone on to develop further and irreparable damage.
Alkaline phosphatase and zinc turbidity tests convincing returned to normal in a larger number of patients treated with Liv.52 than in the control group. In the latter, 90 to 100% of patients continued to show abnormal levels of one or both tests at the end of 2 weeks. In the trial group this number was reduced to almost 33% indicating the beneficial effects of Liv.52 in reducing inflammation of the liver cells and promoting their regeneration, as well as decreasing bile stasis.
About half the patients in both groups had prolonged prothrombin time. Two weeks of Liv.52 reduced the time to normal in all the 50 cases, whereas in the control group, 20% of cases still showed abnormal values after two weeks, indicating a more serious prognosis.
A noteworthy case, not included in the study, was a 12 day old male infant with neonatal hepatitis who had deep jaundice and hepatosplenomegaly. His LFT were – serum bilirubin – 13 mg%, alkaline phosphatase 20 units, SGPT – 200 i.u., Zinc turbidity – 12 units and Prothrombin time – 100 seconds (19 seconds for control). Urobilinogen was present in urine initially but it disappeared after 5 days of treatment. Liv.52 effected clinical improvement in 5 days and clinical cure in 4 weeks. LFT returned to normal after six weeks. He has remained normal to date after two years of follow-up.
CONCLUSIONS
Liv.52 is beneficial in the treatment of acute infectious hepatitis. It abates the symptoms rapidly, reduces the duration of jaundice and restores appetite. It causes the return of impaired liver function tests to normal indicating its effectiveness in promoting liver cell regeneration and preventing further damage.
Prolonged use of Liv.52 is helpful in cases of severe acute hepatic necrosis by promoting liver cell regeneration.
No untoward side effects of Liv.52 therapy were noted during the course of this study.
ACKNOWLEDGEMENT
We are thankful to the Dean, Goa Medical College for permission to publish this paper.
We are grateful to The Himalaya Drug Co. Pvt. Ltd., for the generous supply of Liv.52 required for the trial.
REFERENCES
1. Ramalingam, V., Sundaravalli, N. and Raju, B., 'Liv.52 Studies in Acute Hepatitis'. Indian Paediatrics (1971): 12, 839.
2. Gupta, S., Khatri, R.L. and Srivastava, G., 'Therapy of Infectious Hepatitis and other Liver Disorders'. Probe (1972): 2, 93.
3. Sheth, S.C., Northover, B.J., Tibrewala, N.S., Warerkar, U.R. and Karande, V.S., 'Therapy of Cirrhosis of Liver and Liver Damage with Indigenous Drugs–Experimental and Clinical Studies'. Indian Journal of Paediatrics (1960): 149, 202.
4. Joglekar, G.V. and Leevy, C.M., 'Effect of an Indigenous Drug on I.C.G. (Indocyanine Green) Clearance and Autoradiographic Patterns in Albino Rats with Experimentally Induced Hepatotoxicity'. Probe (1972): 2, 81.
5. Kulkarni, S.D., Kulkarni, D.S., Vasantgadkar, P.S. and Joglekar, G.V., 'Study on Liv.52 An Indigenous Anabolic Compound'. Probe (1972): 2, 89.
6. Patel, Jal, R. and Sadre, N.L., 'Effect of Liv.52 on Structural and Functional Damage Caused by some Hepatotoxic Agents'. Probe (1963): 1, 19.
Refference: http://www.himalayahealthcare.com/pdf_files/liv223.pdf
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