Background: The milk alkali syndrome has always been suspected when patients present with hypercalcemia, renal impairment and metabolic alkalosis. Nowadays, the occupational exposure to carbonate salts at the workplace is considered an environmental problem that seems to increase the possibility of the appearance of more cases
of the syndrome.Objective: investigating the effects of exposure to lime stone dust among working population in the petrochemical industry and determining the importance of interpreting the unexplained abnormal kidney functions in the diagnosis of chronic form of milk alkali syndrome.Methods: Detailed assessment questionnaire and thorough clinical examination were used to study the health condition of 24 workers exposed to sodium and calcium carbonate during the processing of limestone and of 21 matched non-exposed workers. The cardiovascular changes were further evaluated using the electrocardiogram. The blood gases as well as sodium, potassium and chloride were estimated by the utomated
analyzer. Laboratory tests investigated the serum levels of ionized calcium and phosphorus calorimetrically and the 1,25-dihydroxyvitamin D (1,25-(OH)2-D) by chromatography. As for the intact parathyroid hormone (PTH) and parathormone
hormone related peptides (PTH-rP) in serum, estimation was carried out using the two-site immunoassay technique.
Results: Urinary frequency was detected among exposed workers as sign of isotoni polyuria caused by increased stimulation of calcium-sensitive receptors in the collecting tubules. Elevation of ionized calcium levels (mean values 8.32 ± 0.72 mg/ dl) among exposed workers resulted in lowered glomerular filtration rate as evidenced by azotemia. A positive linear association was detected between urea and the ionized levels of calcium. At the renal tubules, hypercalcemia induced bicarbonate absorption that led to metabolic alkalosis as evidenced by elevation in blood pH
(7.46 ± 0.03) and bicarbonate equivalent above 28 mEq/L, and by the positive correlation of calcium and PTH with blood gas parameters. The resulting decreased kidney activity appeared to be a major factor in derangement of the vitamin D metabolism and lowering of phosphorus levels. Deficiency of vitamin D stimulated the release of parathyroid hormone highly significantly to maintain calcium level via decreasing urinary excretion and increasing renal calcium re-absorption. PTH and calcium, which were positively associated together highly significantly, both showed negative correlations with the 1,25-(OH)2-D level. The PTH-rP was significantly low among exposed workers excluding the possibility of any active role in the development of hypercalcemia. Age and smoking were not considered confounding factors in the study compared to the exposure duration which was significantly playing a positive role in the development of alkalemia and hypercalcemia.Conclusion: The obtained data suggested the presence of a relationship between the exposure to limestone and renal affection. The milk alkali syndrome which was a familiar entity might therefore be considered an occupational disorder that is manifesting in an unfamiliar way. The important element in diagnosis is the initial consideration
of milk alkali syndrome as potential cause of symptoms seen among workers with hypercalcemia.