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Inadequate dietary intake but not renal tubular acidosis is associated with bone demineralization in primary biliary cirrhosis
Author(s) -
ALLOCCA M.,
CROSIGNANI A.,
GRITTI A.,
BENETTI A.,
ZUIN M.,
PODDA M.,
BATTEZZATI P. M.
Publication year - 2007
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1111/j.1365-2036.2006.03181.x
Subject(s) - medicine , demineralization , primary biliary cirrhosis , gastroenterology , dentistry , enamel paint
Summary Background Metabolic bone disease associated with primary biliary cirrhosis (PBC) is inadequately characterized. Renal tubular acidosis (RTA) may lead to bone loss through chronic mobilization of skeletal calcium salts to buffer increased acid load. Aim To evaluate the prevalence of RTA in PBC and establish the relationships among bone mineral density (BMD), renal function and nutritional status. Methods We enrolled 69 female patients with compensated PBC and 35 control patients with chronic hepatitis C. RTA was searched in all patients, and 24‐h dietary recalls were collected at enrolment. BMD was measured by dual‐energy X‐ray absorptiometry at the femur neck, lumbar spine and radius ultradistalis sites. Results No patients received a diagnosis of RTA. BMD values ( Z ‐scores) showed only little deviation from normal population with no difference between PBC and controls. Osteopoenic PBC patients ( T ‐score < 1) showed significantly lower daily phosphorus intake [median: 672 (288–1374) vs. 921 (253–1923) mg/day; P = 0.037], with a trend towards lower caloric intake than their nonosteopoenic counterparts. Conclusions Renal tubular acidosis is uncommon in compensated PBC. Cholestasis is not associated with an increased risk of bone demineralization. Inadequate dietary intake may be a preventable factor contributing to bone loss in PBC.