Hepatic osteodystrophy(HO)is a common and frequently untreated complica-tion,manifested as osteoporosis or osteopenia,encountered in the evolution of chronic liver diseases(CLD).In addition to patients with chronic ch...Hepatic osteodystrophy(HO)is a common and frequently untreated complica-tion,manifested as osteoporosis or osteopenia,encountered in the evolution of chronic liver diseases(CLD).In addition to patients with chronic cholestasis and cirrhosis,patients with CLD from other etiologies may be affected.Several studies have reported an increased prevalence of osteoporosis/osteopenia in patients with CLD.The pathogenesis varies according to etiology and is multifactorial,involving genetic factors,vitamin deficiencies,proinflammatory cytokines,hypo-gonadism,hyperbilirubinemia,antiviral therapy,corticosteroids,and lifestyle fa-ctors.The approach to management should include individualized assessment for fracture risk factors and bone mineral density.Prevention of osteoporosis in CLD relies on the mitigation of risk factors,treatment of underlying hypogonadism,and encouraging a healthy diet and weight-bearing exercise.Treatment trials specific to HO are small,and the primary medical intervention for the treatment of osteoporosis in CLD remains bisphosphonates although the benefit in fracture reduction has not consistently been shown.Further research is necessary to better define the management and specific treatment of HO for the prevention of fragility fractures and to improve the quality of life.This article provides an updated review of HO covering all these aspects.展开更多
AIM: To investigate the correlation between hepatic osteodystrophy and osteoporosis in patients with liver cirrhosis. METHODS: Bone mineral density of the patients (n = 55) and that of the control group (n = 30) were ...AIM: To investigate the correlation between hepatic osteodystrophy and osteoporosis in patients with liver cirrhosis. METHODS: Bone mineral density of the patients (n = 55) and that of the control group (n = 30) were measured by dual-energy X-ray absorptiometry. All the women in the study were premenopausal. Deoxypyridinoline, pyridinoline and urinary Ca 2+ were measured as bone destruction markers, while alkaline phosphatase (ALP), osteocalcin and insulin-like growth factor-1 (IGF-1) were measured as bone formation markers. Furthermore, interleukin-1 (IL-1), IL-6, tumor necrosis factor α (TNF-α), vitamin D3, direct bilirubin, albumin, cortisol and parathyroid hormone (PTH) levels were measured. The independent Student t test and χ 2 test were employed in comparing both groups, and the Pearson correlation test was used to determine associations. RESULTS: Comparing cirrhosis and control groups, lumbar total T-score (-1.6 ± 1.2 g/cm 2 vs -0.25 ± 1.3 g/cm 2 , P < 0.001), lumbar total Z-score (-1.2 ± 1.23 g/cm 2 vs -0.6 ± 1.3 g/cm 2 , P < 0.001), total femur T-score (-0.05 ± 1 g/cm 2 vs -0.6 ± 0.9 g/cm 2 , P = 0.003) and total femur Z-score (-0.08 ± 1.5 g/cm 2 vs 0.7 ± 0.9 g/cm 2 , P =0.003) showed significantly lower values in the cirrhosis group. Blood ALP level (109.2 ± 57 U/Lvs 62.6 ± 32.5 U/L, P < 0.001), IL-6 level (27.9 ± 51.6 pg/mL vs 3.3 ± 3.1 pg/mL, P = 0.01), TNF-α level (42.6 ± 33.2 pg/mL vs 25.3 ± 12.3 pg/mL, P = 0.007) and direct bilirubin level (0.9 ± 0.7 mg/dL vs 0.3 ± 0.2 mg/dL, P < 0.001) were significantly higher in the cirrhosis group. IGF-1 level (47.7 ± 26.2 ng/mL vs 143.4 ± 53.2 ng/mL, P < 0.001), osteocalcin level (1.05 ± 2.5 ng/mL vs 7.0 ± 13 ng/mL, P = 0.002) and 24 h urinary Ca 2+ (169.6 ± 227.2 mg/dL vs 287 ± 168.6 mg/dL, P = 0.003) were significantly lower in the cirrhosis group. Urinary deoxypyridinoline/creatinine (9.4 ± 9.9 pmol/μmol vs 8.1 ± 5.3 pmol/μmol, P = 0.51), urinary pyridinoline/creatinine (51.3 ± 66.6 pmol/μmol vs 29 ± 25.8 pmol/μmol, P = 0.08), blood IL-1 level (3.4 ± 8.8 pg/mL vs 1.6 ± 3.5 pg/mL, P = 0.29), vitamin D3 level (18.6 ± 13.3 μg/L vs 18.4 ± 8.9 μg/L, P = 0.95), cortisol level (11.1 ± 4.8 μg/dL vs 12.6 ± 4.3 μg/dL, P = 0.15) and PTH level (42.7 ± 38 μg/dL vs 34.8 ± 10.9 μg/dL,P = 0.27) were not significantly different. CONCLUSION: Hepatic osteodystrophy is an important complication encountered in patients with liver cirrhosis and all patients should be monitored for hepatic osteodystrophy.展开更多
AIM： To estimate the prevalence and identify the risk factors for metabolic bone disease in patients with cirrhosis. METHODS： The study was performed on 72 Indian patients with cirrhosis （63 male, 9 female; aged 〈...AIM： To estimate the prevalence and identify the risk factors for metabolic bone disease in patients with cirrhosis. METHODS： The study was performed on 72 Indian patients with cirrhosis （63 male, 9 female; aged 〈 50 years）. Etiology of cirrhosis was alcoholism （n = 37）, hepatitis B （n = 25） and hepatitis C （n = 10）. Twenty-three patients belonged to Child class A, while 39 were in class B and 10 in class C. Secondary causes for metabolic bone disease and osteoporosis were ruled out. Sunlight exposure, physical activity and dietary constituents were calculated. Complete metabolic profiles were derived, and bone mineral density （BMD） was measured using dual energy X ray absorptiometry. Low BMD was defined as a Z score below -2. RESULTS： Low BMD was found in 68% of patients. Lumbar spine was the most frequently and severely affected site. Risk factors for low BMD included low physical activity, decreased sunlight exposure, and low lean body mass. Calcium intake was adequate, with unfavorable calcium： protein ratio and calcium： phosphorus ratio. Vitamin D deficiency was highly prevalent （92%）. There was a high incidence of hypogonadism （41%）. Serum estradiol level was elevated significantly in patients with normal BMD. Insulin-like growth factor （IGF） 1 and IGF binding protein 3 levels were below the age-related normal range in both groups. IGF-1 was significantly lower in patients with low BMD. Serum osteocalcin level was low （68%） and urinary deoxypyridinoline to creatinine ratio was high （79%）, which demonstrated low bone formation with high resorption. CONCLUSION： Patients with cirrhosis have low BMD. Contributory factors are reduced physical activity, low lean body mass, vitamin D deficiency and hypogonadism and low IGF-1 level.展开更多
Given that the liver is involved in many metabolic mechanisms,it is not surprising that chronic liver disease(CLD)could have numerous complications.Secondary osteoporosis and increased bone fragility are frequently ov...Given that the liver is involved in many metabolic mechanisms,it is not surprising that chronic liver disease(CLD)could have numerous complications.Secondary osteoporosis and increased bone fragility are frequently overlooked complications in CLD patients.Previous studies implied that up to one-third of these individuals meet diagnostic criteria for osteopenia or osteoporosis.Recent publications indicated that CLD-induced bone fragility depends on the etiology,duration,and stage of liver disease.Therefore,the increased fracture risk in CLD patients puts a severe socioeconomic burden on the health system and urgently requires more effective prevention,diagnosis,and treatment measures.The pathogenesis of CLD-induced bone loss is multifactorial and still insufficiently understood,especially considering the relative impact of increased bone resorption and reduced bone formation in these individuals.It is essential to note that inconsistent findings regarding bone mineral density measurement were previously reported in these individuals.Bone mineral density is widely used as the“golden standard”in the clinical assessment of bone fragility although it is not adequate to predict individual fracture risk.Therefore,microscale bone alterations(bone microstructure,mechanical properties,and cellular indices)were analyzed in CLD individuals.These studies further support the thesis that bone strength could be compromised in CLD individuals,implying that an individualized approach to fracture risk assessment and subsequent therapy is necessary for CLD patients.However,more well-designed studies are required to solve the bone fragility puzzle in CLD patients.展开更多
文摘Hepatic osteodystrophy(HO)is a common and frequently untreated complica-tion,manifested as osteoporosis or osteopenia,encountered in the evolution of chronic liver diseases(CLD).In addition to patients with chronic cholestasis and cirrhosis,patients with CLD from other etiologies may be affected.Several studies have reported an increased prevalence of osteoporosis/osteopenia in patients with CLD.The pathogenesis varies according to etiology and is multifactorial,involving genetic factors,vitamin deficiencies,proinflammatory cytokines,hypo-gonadism,hyperbilirubinemia,antiviral therapy,corticosteroids,and lifestyle fa-ctors.The approach to management should include individualized assessment for fracture risk factors and bone mineral density.Prevention of osteoporosis in CLD relies on the mitigation of risk factors,treatment of underlying hypogonadism,and encouraging a healthy diet and weight-bearing exercise.Treatment trials specific to HO are small,and the primary medical intervention for the treatment of osteoporosis in CLD remains bisphosphonates although the benefit in fracture reduction has not consistently been shown.Further research is necessary to better define the management and specific treatment of HO for the prevention of fragility fractures and to improve the quality of life.This article provides an updated review of HO covering all these aspects.
文摘AIM: To investigate the correlation between hepatic osteodystrophy and osteoporosis in patients with liver cirrhosis. METHODS: Bone mineral density of the patients (n = 55) and that of the control group (n = 30) were measured by dual-energy X-ray absorptiometry. All the women in the study were premenopausal. Deoxypyridinoline, pyridinoline and urinary Ca 2+ were measured as bone destruction markers, while alkaline phosphatase (ALP), osteocalcin and insulin-like growth factor-1 (IGF-1) were measured as bone formation markers. Furthermore, interleukin-1 (IL-1), IL-6, tumor necrosis factor α (TNF-α), vitamin D3, direct bilirubin, albumin, cortisol and parathyroid hormone (PTH) levels were measured. The independent Student t test and χ 2 test were employed in comparing both groups, and the Pearson correlation test was used to determine associations. RESULTS: Comparing cirrhosis and control groups, lumbar total T-score (-1.6 ± 1.2 g/cm 2 vs -0.25 ± 1.3 g/cm 2 , P < 0.001), lumbar total Z-score (-1.2 ± 1.23 g/cm 2 vs -0.6 ± 1.3 g/cm 2 , P < 0.001), total femur T-score (-0.05 ± 1 g/cm 2 vs -0.6 ± 0.9 g/cm 2 , P = 0.003) and total femur Z-score (-0.08 ± 1.5 g/cm 2 vs 0.7 ± 0.9 g/cm 2 , P =0.003) showed significantly lower values in the cirrhosis group. Blood ALP level (109.2 ± 57 U/Lvs 62.6 ± 32.5 U/L, P < 0.001), IL-6 level (27.9 ± 51.6 pg/mL vs 3.3 ± 3.1 pg/mL, P = 0.01), TNF-α level (42.6 ± 33.2 pg/mL vs 25.3 ± 12.3 pg/mL, P = 0.007) and direct bilirubin level (0.9 ± 0.7 mg/dL vs 0.3 ± 0.2 mg/dL, P < 0.001) were significantly higher in the cirrhosis group. IGF-1 level (47.7 ± 26.2 ng/mL vs 143.4 ± 53.2 ng/mL, P < 0.001), osteocalcin level (1.05 ± 2.5 ng/mL vs 7.0 ± 13 ng/mL, P = 0.002) and 24 h urinary Ca 2+ (169.6 ± 227.2 mg/dL vs 287 ± 168.6 mg/dL, P = 0.003) were significantly lower in the cirrhosis group. Urinary deoxypyridinoline/creatinine (9.4 ± 9.9 pmol/μmol vs 8.1 ± 5.3 pmol/μmol, P = 0.51), urinary pyridinoline/creatinine (51.3 ± 66.6 pmol/μmol vs 29 ± 25.8 pmol/μmol, P = 0.08), blood IL-1 level (3.4 ± 8.8 pg/mL vs 1.6 ± 3.5 pg/mL, P = 0.29), vitamin D3 level (18.6 ± 13.3 μg/L vs 18.4 ± 8.9 μg/L, P = 0.95), cortisol level (11.1 ± 4.8 μg/dL vs 12.6 ± 4.3 μg/dL, P = 0.15) and PTH level (42.7 ± 38 μg/dL vs 34.8 ± 10.9 μg/dL,P = 0.27) were not significantly different. CONCLUSION: Hepatic osteodystrophy is an important complication encountered in patients with liver cirrhosis and all patients should be monitored for hepatic osteodystrophy.
基金Supported by Corpus generated by Department of Endocrinology, KEM Hospital, Mumbai, India
文摘AIM： To estimate the prevalence and identify the risk factors for metabolic bone disease in patients with cirrhosis. METHODS： The study was performed on 72 Indian patients with cirrhosis （63 male, 9 female; aged 〈 50 years）. Etiology of cirrhosis was alcoholism （n = 37）, hepatitis B （n = 25） and hepatitis C （n = 10）. Twenty-three patients belonged to Child class A, while 39 were in class B and 10 in class C. Secondary causes for metabolic bone disease and osteoporosis were ruled out. Sunlight exposure, physical activity and dietary constituents were calculated. Complete metabolic profiles were derived, and bone mineral density （BMD） was measured using dual energy X ray absorptiometry. Low BMD was defined as a Z score below -2. RESULTS： Low BMD was found in 68% of patients. Lumbar spine was the most frequently and severely affected site. Risk factors for low BMD included low physical activity, decreased sunlight exposure, and low lean body mass. Calcium intake was adequate, with unfavorable calcium： protein ratio and calcium： phosphorus ratio. Vitamin D deficiency was highly prevalent （92%）. There was a high incidence of hypogonadism （41%）. Serum estradiol level was elevated significantly in patients with normal BMD. Insulin-like growth factor （IGF） 1 and IGF binding protein 3 levels were below the age-related normal range in both groups. IGF-1 was significantly lower in patients with low BMD. Serum osteocalcin level was low （68%） and urinary deoxypyridinoline to creatinine ratio was high （79%）, which demonstrated low bone formation with high resorption. CONCLUSION： Patients with cirrhosis have low BMD. Contributory factors are reduced physical activity, low lean body mass, vitamin D deficiency and hypogonadism and low IGF-1 level.
文摘Given that the liver is involved in many metabolic mechanisms,it is not surprising that chronic liver disease(CLD)could have numerous complications.Secondary osteoporosis and increased bone fragility are frequently overlooked complications in CLD patients.Previous studies implied that up to one-third of these individuals meet diagnostic criteria for osteopenia or osteoporosis.Recent publications indicated that CLD-induced bone fragility depends on the etiology,duration,and stage of liver disease.Therefore,the increased fracture risk in CLD patients puts a severe socioeconomic burden on the health system and urgently requires more effective prevention,diagnosis,and treatment measures.The pathogenesis of CLD-induced bone loss is multifactorial and still insufficiently understood,especially considering the relative impact of increased bone resorption and reduced bone formation in these individuals.It is essential to note that inconsistent findings regarding bone mineral density measurement were previously reported in these individuals.Bone mineral density is widely used as the“golden standard”in the clinical assessment of bone fragility although it is not adequate to predict individual fracture risk.Therefore,microscale bone alterations(bone microstructure,mechanical properties,and cellular indices)were analyzed in CLD individuals.These studies further support the thesis that bone strength could be compromised in CLD individuals,implying that an individualized approach to fracture risk assessment and subsequent therapy is necessary for CLD patients.However,more well-designed studies are required to solve the bone fragility puzzle in CLD patients.
