Primary biliary cirrhosis and osteoporosis: a case-control study

Abstract

Osteoporosis is a common complication of chronic liver disease, from cholestatic disorders to autoimmune, alcoholic, and posthepatitic cirrhosis. Osteoporosis appears more striking in patients with primary biliary cirrhosis (PBC) because the disease usually affects elderly women, who are naturally prone to osteoporosis. Our aims were (1) to compare the prevalence of osteoporosis (T-score <-2.5 SD) between PBC patients and a group of age-and sex-matched controls consisting of healthy subjects from the general population; and (2) to identify the main risk factors for the development of bone loss. Thirty-three women with PBC (mean age, 47.3 +/- 10.4 years) and 66 healthy subjects were enrolled in the study. Bone mineral density (BMD) was assessed at the lumbar spine by dual-photon X-ray absorptiometry. Bone metabolism was evaluated by measuring serum calcium corrected for serum albumin, 25-hydroxyvitamin D (25-OH vit D), parathyroid hormone, and osteocalcin. Vertebral fractures were analyzed using vertebral fracture assessment (VFA). The mean T-score was lower in the PBC group compared to healthy controls, with a significant statistical difference (-2.39 +/- 0.93 and -1.47 +/- 0.99 in lumbar spine and total hip, respectively, in the PBC group versus -0.99 +/- 0.51 and -0.56 +/- 1.14 in healthy controls (P < 0.001). The prevalence of osteoporosis was 51.5% in the PBC group versus 22.7% in healthy controls with a statistically significant difference (P = 0.004). BMD of the PBC group was significantly correlated positively with body mass index (BMI) and 25-OH vit D, and negatively with menopausal status, duration of disease, and parathyroid hormone (PTH) levels. Vertebral fractures were present in 9% of the patients. We found that osteoporosis is more prevalent in women with PBC than in the general population. BMI, menopausal status, duration of the disease, and vitamin D deficiency are the main risk factors for osteoporosis in this liver disease.

An observational study of glucocorticoid-induced osteoporosis prophylaxis in a national cohort of male veterans with rheumatoid arthritis

“…Specifically, loop diuretics [34], anticonvulsants [35], and thyroid replacement medications (especially when taken in excess) [36] have been linked to skeletal compromise. The same may be said of depression [37], diabetes [38], malignancies [39,40], alcohol abuse [41], renal disease [42,43], and hepatic dysfunction [44,45].…”

Immune complexes regulate bone metabolism through FcRγ signalling

“…IC-induced osteoclastogenesis may contribute to both osteoporosis and the local bone erosion that occurs in various autoimmune diseases including RA and SLE, chronic inflammatory diseases 39,40 , multiple myeloma 41 and monoclonal gammopathy of undetermined significance 42 , which are all characterized by a high IgG production. The direct effect of the ICs on osteoclasts may also explain, at least in part, the bone-protective effect of the B-cell-depleting anti-CD20 antibody rituximab in RA patients 43,44 .…”

Body Composition Changes in Patients with Chronic Hepatitis C

“…Chronic cholestasis (such as in primary biliary cirrhosis) [7], low levels of insulin-like growth factor-1 [8,9], impairment of J Gastrointestin Liver Dis, September 2016 Vol. 25 No 3: 323-329 receptor activator of nuclear factor κappa B ligand (RANKL) and osteoprotegerin system [10], vitamin D deficiency [11,12], low body mass index (BMI) [13], chronic alcoholism [14] and sedentary lifestyle [15] were implicated in HO pathogenesis. In CHC, the main mechanism seems to be an inflammatory response that increases release of cytokines with bone resorption due to osteoclast activation [16,17].…”