Elevation of serum globulin levels in Chelidonium majus 6c provers

Elevation of serum globulin levels in Chelidonium majus 6c provers

British HomoeopathicJournal April 1989. Vol. 78. pp. 97-99 Elevation of serum globulin levels in Chelidonium majus 6c provers A. E. VAKIL, Y. E. VAKI...

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British HomoeopathicJournal April 1989. Vol. 78. pp. 97-99

Elevation of serum globulin levels in Chelidonium majus 6c provers A. E. VAKIL, Y. E. VAKIL, A. S. NANABHAI

9 Abstract

Ten healthy volunteers were administered orally 0.04 ml. of Chelidonium majus 6c t.d.s. for 21 days. Seven healthy volunteers were kept as controls and administered orally 0.04 ml. of 90% ethanol t.d.s. The trial was single blind. Fasting venous samples were collected before and after the trial. Serum samples were analysed for total bilirubin, albumin, globulin, total cholesterol, prothrombin time and GPT. Serum globulins registered an increase of 58%, while the other parameters showed no changes.

using a kit supplied by Sigma Chemical Co. USA and cholesterol was estimated by the Liebermann-Burchard method. Both bilirubin and GPT were estimated on a spectrophotometer while proteins and cholesterol were estimated colorimetrically. All glassware used for prothrombin time was siliconized.5

Introduction

A clinical trial of Chelidonium majus 6c was undertaken on healthy humans to study its action on the liver. 1,2,3Chelidonium has marked action on the liver, this is clearly demonstrated by most authors of the homoeopathic materia medica. It was possible to measure the extent of action of the drug on the liver of the provers by performing liver function tests.

Observations

Except for serum globulins, none of the other parameters showed any significant change. Globulins registered an increase by 58% after treatment with Chelidonium majus 6c. The normal serum values are as follows: total bilirubin 0.2-1mg%, total protein 6 - 8 g m % , albumin 3.8-5gm%, globulin 2.3-3.7gm%, total cholesterol 150-250mg%, prothrombin time 10.5-13 sec, SGPT 0-21 Sigma-Frankel units/ml. The mean values observed and their standard deviation are given in Table 1, whereas Table 2 shows their significance.

Materials and methods

A proving of Chelidonium majus 6c was conducted on ten healthy student volunteers of both sexes. A control group of seven students was also set up. The provers were administered orally 0.04 ml. of Chelidonium majus 6c (W. Schwabe, W. Germany) three times daily. On the other hand, the controls were given 0.04 ml. of 90% ethyl alcohol (Fluka, W. Germany) orally, three times daily. The entire trial was single blind. Fasting venous samples were collected before and after the trial. The serum collected was stored frozen in plastic ampoules. Serum was estimated for total bilirubin, albumin, globulin, total cholesterol and GPT. Prothrombin time was estimated on day of collection using citrated plasma. Total serum bilirubin was done by the method of Malloy & Evelyn,4 using freshly prepared reagents in the laboratory. Serum proteins were estimated using a kit prepared by SPAN Diagnostics, Surat. Thrombokinase by Solco was used for prothrombin time. SGPT was estimated

Discussion

The changes in total protein concentration observed are of limited value. In disease there is usually an increase in total globulins, more often y-globulins, albumin being normal or reduced to a lesser extent. Changes can occur in plasma protein levels in response to certain acute illnesses such as acute infection, acute inflammation, trauma, necrosis, infarction, burns and chemical injury. The same changes may occur in focal episodes associated with malignant tumours. This acute reaction protein pattern 97

British HomoeopathicJournal

98 TABLE1 Serum values

Total bilirubin Total protein Albumin Globulin Cholesterol Prothrombin time GPT

Cheldonium majus 6c treated

Control, 90% ethanol treated

Previous

Post

Previous

0.60__.0.21 6.92+--0.57 4.30_+0.31 2.62_+0.73 200_+33.54 11.75_+1.31 19.2_+1.04

0.60_+0.91 8.52_+1.36 4.38_+0.35 4.14_+1.34 200+-37.86 11.29+-1.36 19.06+-0.74

Post

0.60_+0.18 6.60_+0.41 4.49_+0.13 2.11_+0.39 206_+36.9 11.0+-1.53 19.2_+0.9

0.58_+0.18 6.68_+0.33 4.58_+0.29 2.11+-0.29 208_+20.94 10.92__.1.35 19.5_+0.77

TABLE2 Statistical analysis of serum values Previous/post chelidonium

Bilirubin Protein Albumin Globulin Cholesterol PT GPT

Previous/post ethanol 90%

Mean Difference

DF

t

p (two tailed)

Mean Difference

DF

t

p (two tailed)

0.001 2.32 0.08 1.52 0.3 -0.44 -0.08

10 10 10 10 10 10 10

0.012 3.81 0.046 2.446 0.019 - 1.041 -0.682

NS ~<0.01 NS ~<0.05 NS NS NS

-0.02 0.078 0.09 -0.001 2.0 -0.08 0.3

7 7 7 7 7 7 7

-0.353 0.35 0.822 -0.004 0.112 -0.085 0.873

NS NS NS NS NS NS NS

which may be characterized by electrophoresis is called the 'acute phase protein pattern'. U n d e r such conditions there is an increase in fibrinogen, cx-l-antitrypsin, haptoglobulin, caeruloplasmin, C-reactive protein, C3 of complement and c~-l-glycoprotein. There may be an associated decrease in albumin. The present increase could not be due to any such acute illness. In sub-acute and chronic illness this acute reaction pattern is found to exist to a lesser degree. A l b u m i n may return to normal but 7-globulins continue to increase.6 Such a picture would be very similar to our observations. Variations have been observed of the globulin fractions in liver disorders. [3-globulin is usually, but not always, elevated in obstructive jaundice. It may be elevated to some extent in cases of hepatitis and cirrhosis, y-globulins also show marked increase in hepatitis and advanced cases of cirrhosis. 7 A diffuse, polyclonal increase of immunoglobulins is usually observed in chronic liver diseases, with total globulin as high as 3.57 g m % , mainly due to increase of IgG but occasionally accompanied by a smaller increase in [3-globulins. It is noted that except for the rise in globulins none of the other parameters, which are also

indicative of liver dysfunction, registered any change. O n e might infer that the cause for increase in globulins was extra-hepatic. A serum albumin value of less than 3 g% and globulins greater than 4 g% usually connote a chronic or progressive form of liver disease or both, 8 O n the whole, protein analysis by itself is of limited usefulness in liver disorders. In the first place, it is not a sensitive indicator of liver disease. Secondly, it has little value in differential diagnosis because of frequent alterations in serum protein during liver dysfunction. Thirdly, protein changes, as observed, are not specific for liver disease.

Conclusions A tentative inference would be: If Chelidonium related to liver dysfunction that came to expression in the form of globulin increase, there would have been a simultaneous increase in the other parameters. Chelidonium 6c could possibly be a selective stimulus for some fraction of the globulins. The globulin increase may be extra-hepatic in origin, which would explain the absence of change in the other parameters.

Volume 78, Number2, April 1989

The stimuli on the liver may be so minute that the effect could be manifested only by increase in certain globulins. Acknowledgement I wish to thank Dr Panchal, Head of the Dept of Physiology, CMPHMC, Dr Bhatnagar, Head of the Dept. of Anatomy, CMPHMC, and Dr F. R. Binimoria, Head of the Dept. of Biochemistry, LTMMC, for all their help and encouragement.

References 1 Allen TF. The Encyclopedia of Pure Materia Medica Vol III. pp. 141-9. New Delhi: Jain 1986. 2 Hering C. The Guiding Symptoms of our Materia Medica Vol IV. pp. 16-21. New Delhi: Jain 1986.

99 3 Clarke HJ. A Dictionary of Practical Materia Medica Vol I. pp. 462-7. New Delhi: Jain 1982. 4 Varley H, Gowenlock A, Bell M. Practical Clinical Biochemistry Vol I, p. 1018-19. London: William Heinemann Medical Books 1980. 5 Dacie JV, et al. Practical Hematology, p. 437. Singapore: Churchill Livingstone 1984. 6 Ravel R. Clinical Laboratory Medicine, pp. 245-7. Chicago: Year Book Medical 1984. 7 Martin HN. An electrophoretic study of the components of serum proteins in cirrhosis of the liver. Br J Exp Pathol 1959; 30: 231. 8 Combes B, Schenker S. Diseases of the Liver, p. 280-2. Philadelphia: JB Lippincott 1963.