BIOCHEMISTRY OF SERUM AND BILE CHOLELITHIASIS

Dear Editor,

Reference is made to the article “Study of serum and bile from patients of cholelithiasis in north eastern India” (MJAFI 1995; 51 : 9–12). Being a keen student of cholelithiasis I will like to highlight a few points.

• 1.In discussion authors have quoted Krishnan et al [1] as stating that incidence of cholelithiasis is as high as 15–20 per cent of general population. However the said article does not say so. In fact in Kashmir, where cholelithiasis is reported to be rampant [2] the incidence is only 6.12 per cent of the population [3].
• 2.It is an erroneous assumption that no prior study has reported the incidence of cholelithiasis in north east India. See Malhotra et al [4].
• 3.Authors have stated that their controls were 25 healthy individuals hailing from non-lithogenic areas of the country. There is no area in India which can be considered as non-lithogenic. Even in Kerala it is reported to be “not an uncommon problem” [5] and sufficient number of cases have been reported from Tamil Nadu [6].
• 4.Were the controls matched in relation to age, sex and weight?
• 5.Comparison among the same population was warranted. Lack of comparative data pertaining to scrum and bile studies from normal population of north eastern India has vitiated the study.
• 6.As far as cholelithiasis is concerned, the most crucial components of bile are cholesterol, phospholipids and bile salts. Authors have reported the former two and totally ignored the bile salts, which are responsible for solubility of cholesterol in bile.
• 7.It has been repeatedly stressed by authors that gall bladder bile showed increased concentration of cholesterol and phospholipids in relation to hepatic bile. It is the normal physiological function of gall bladder to concentrate bile, a fact known to every student of physiology [7].
• 8.What is the relevance of biliary LCAT activity, ALP and bilirubin vis-a-vis cholelithiasis?
• 9.Mean phospholipid level as shown in Table 2 are 2.55 mg/dL for hepatic bile and 19.75 mg/dL for gall bladder bile. Wani et al reported 815 mg per cent and 1723 mg per cent correspondingly [2]. What is the significance of the findings that phospholipid level was 1/300 to 1/80 lower that other regions?
• 10.Significance of esterified cholesterol in relation to cholelithiasis has been brought out. It has been stated that in liver diseases these levels are lower. Are we dealing with liver diseases or gall bladder diseases?
• 11.In how many cases were CBD stones present in the study? CBD obstruction itself may raise the level of various liver enzymes and lower the LCAT activity leading to erroneous conclusion that subclinical hepatic dysfunction is responsible for altered enzyme levels in cholelithiasis.
• 12.LCAT deficiency has been described as a rare autosomal recessive disorder of lipid metabolism. It is associated with variable levels of total plasma cholesterol, marked decrease in esterified cholesterol but nowhere it is mentioned that these patients are more prone to cholelithiasis [8].
• 13.To sum up, the authors have failed to substantiate their projected pointers for lithogenicity of bile e.g. first pointer that serum phospholipids are raised in patient was negated by their own study as the level in patients were lower than controls. Other pointers e.g. decrease in LCAT activity is not associated with cholelithiasis. Remaining may be incidental to normal variations in the population for which no data has been supplied,