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| Year : 1982 | Volume
: 28
| Issue : 4 | Page : 218-20 |
Serum phosphorus levels in Indian childhood cirrhosis.
Chahar CK, Sharma SS, Gupta BD, Chaudhary AA, Miglani NN
How to cite this article:
Chahar C K, Sharma S S, Gupta B D, Chaudhary A A, Miglani N N. Serum phosphorus levels in Indian childhood cirrhosis. J Postgrad Med 1982;28:218 |
How to cite this URL:
Chahar C K, Sharma S S, Gupta B D, Chaudhary A A, Miglani N N. Serum phosphorus levels in Indian childhood cirrhosis. J Postgrad Med [serial online] 1982 [cited 2023 Sep 29];28:218. Available from: https://www.jpgmonline.com/text.asp?1982/28/4/218/5596 |
Indian childhood cirrhosis is a disease of unknown etiology, which has figured in the present era as one of the most dreadful clinical conditions, which the Indian pediatrician faces in his day-today practice.[10]
Several contributory factors have been enlisted in the etiology of Indian childhood cirrhosis, out of which various metabolic disorders have been blamed to play some role. Serum electrolyte disturbances have been reported in liver diseases by many workers.[1], [2], [8], [11] The present study has been aimed to see the alteration of serum phosphorus levels in Indian childhood cirrhosis.
Twenty five children of Indian childhood cirrhosis and 10 normal healthy age matched children constituted the subject of the present study.
The diagnosis of Indian childhood cirrhosis was established according to the criteria laid down by the Liver Disease Sub-committee, I.C.M.R.,[7] which was further confirmed by relevant biochemical tests and histopathological examination of the liver tissues. The blood was collected from the femoral vein with all aseptic precautions in glass tubes free from electrolytes. Serum was separated and the estimation of inorganic phosphorus was done by the method of Fiske and Subbarow.[3]
None of the patients received electrolyte therapy in any form before being subjected to collection of blood.
In the present study, out of 25 cases of Indian childhood cirrhosis, 22 (88%) were males and 3 (12%) females. The patients were between the age of six months to three years.
The mean serum phosphorus level in 10 normal subjects was found to be 4.94 ± 0.60 (S.D.) mg/dl with a range of 3.6 to 5.8 mg/ dl. In 25 patients with Indian childhood cirrhosis, the phosphorus level was only 2.4 ± 1.30 (S.D.) mg/dl with a range of 0.8 to 5.0 mg/dl. This difference in the levels of phosphorus of the two groups was highly significant (p<0.001).
In the present study, the mean phosphorus level was 4.94 ± 0.60 mg/dl in normal healthy controls. This finding is in conformity with the values reported by Hawk et al,[6] who reported the level of phosphorus as 5 mg/dl in infants and children. Harvey et al" reported serum phosphorus levels in the range of 4 to 7 mg/dl in the first year of life and further observed a gradual decline in the levels to adult values by the age of twenty years.[5]
In the present series, the mean phosphorus level in patients of ICC was 2.4 ± 1.30 mg/dl. The decline in the level was statistically highly significant when compared with control (p < 0.001). Amatuzio et all in their study on serum phosphorus levels in adult patients of chronic alcoholism with portal cirrhosis, have recorded low levels as compared to normal healthy controls.
Chaudhary et al[2] in an uncontrolled study have reported low levels of serum phosphorus in some patients of ICC.
Phosphate metabolism is related to liver in several ways, specially through its role in energy transfer and carbohydrate metabolism. In experimental carbon tetrachloride intoxication, the levels of acid soluble phosphates and the fat content in the liver increase simultaneously and to the same extent. Exact reasons for decreased serum phosphorus levels in Indian childhood cirrhosis are not known. This disease is more common among vegetarians.[9] The vegetarian diet contains phytates which interfere with the absorption of phosphorus from the gut, leading to low serum phosphorus levels.
Recently, low zinc levels have been reported and blamed for causation of liver damage in ICC.[4] Just as zinc is related with nucleic acid metabolism, phosphorus is also linked with it and may induce regeneration and repair of hepatic cells. Hence phosphorus deficiency may be a possible factor in the causation of the disease. However, more work is needed before a cause and effect relationship between ICC and phosphorus levels can be established.
| 1. | Amatuzio, D. S., Stutzman, F., Shrifter, N. and Nesbitt. S.: Study of serum electrolytes (Na, K, Ca, P) in patients of severely decompensated portal cirrhosis of liver. J. Lab. & Clin. Med., 39: 26-29, 1952.  |
| 2. | Chaudhari, A., Chaudhari, K. C. and Nag-Chaudhari, J.: Some observations on infantile cirrhosis. Ind. J. Paediatr., 25: 555-565, 1958. |
| 3. | Fiske, C. H. and Subbarow, Y.: Colorimetric determination of phosphorus. J. Biol. Chem., 66: 375-400, 1925. |
| 4. | Gupta, B. D. and Miglani, N.: Zinc in Indian childhood cirrhosis. I-Assessment of serum zinc. Indian Paediatr., 14: 175-179, 1977. |
| 5. | Harvey, D. R., Cooper, L. V. and Stevens, J. F.: Plasma calcium and magnesium in newborn babies. Arch. Dis. Childhood, 45: 506-509,1970. |
| 6. | Hawk, P. B., Oser, B. L. and Summerson, W. H.: "Practical Physiological Chemistry". 13th Edition, The Blackiston Division, McGraw Hill Book Company, New York, 1954, pp. 497-677. |
| 7. | Liver Diseases Sub-Committee, I.C.M.R. (1955): Infantile cirrhosis of liver in India. Ind. J. Med. Res., 43: 723-747, 1955. |
| 8. | Moor-, E. W.: Studies with ion exchange calcium electrode. III-The state of serum calcium in patients with cirrhosis. Gastro-enterology, 60: 43-54, 1971. |
| 9. | Parekh, S. R. and Patel, B. D.: Epidemiological survey of Indian childhood cirrhosis. Indian Paediatr., 9: 431-439, 1972. |
| 10. | Prasad, L. S. and Mallick, S.: Some observations on Indian childhood cirrhosis and infantile hepatitis. India Paediatr., 5: 241-251, 1968. |
| 11. | Talso, P. J., Strub, J. H. and Kirsner, J. B.: The metabolism of water and eleotrolytes in patients with cirrhosis of liver. J. Lab. & Clin. Med., 47: 210-216, 1956. |
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