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Bone disease in primary biliary cirrhosis and renal tubular acidosis

SIRS , The article by Allocca et al., focused on the relationship between inadequate dietary intake, renal tubular acidosis (RTA) and metabolic bone disease in primary biliary cirrhosis (PBC), which was recently published in Alimentary Pharmacology & Therapeutics, concluded that chronic buffering of low-grade metabolic acidosis originating from defective urinary acidification is not responsible for bone disease in PBC. Different from that stated by the authors, the likely relationship between RTA and bone demineralization in PBC had already been previously addressed by a specifically designed study, that also failed to demonstrate significant correlation. Using the same criteria for RTA, we performed a urinary acidification test in 23 non-selected PBC patients, all of them with compensated liver disease (Child A and B) and assessed bone mineral density (BMD) by dual energy X-ray absorptiometry. Factors that could interfere with the result of the urinary acidification test were ruled out. We also excluded patients with de-compensated liver disease because the diagnostic criteria for RTA are not clearly defined in those subset of patients, inasmuch as associated acid-basic disturbances are common and impaired sodium metabolism may lead to deficient sodium delivery to distal tubules resulting in disturbance of acidification (pseudo RTA), in spite of the normal proton secretory capacity. Different from the paper of Alloca that found no case of RTA or osteoporosis, in our study eleven subjects were found to have RTA and densitometric signs of osteoporosis were detected in 82% of RTA cases and 83% of patients without RTA (difference not significant). In addition, there were no significant differences neither in BMD measurements, T and Z scores and history of complications of bone disease of patients with and without RTA nor in duration of disease, age, severity of liver histology, duration of therapy with ursodeoxycholic acid, vitamin D or calcium and dietary intake history.