Bone disease in cirrhosis

Patel, Nishita; Muñoz, Santiago J.

doi:10.1002/cld.498

Cited by 28 publications

(35 citation statements)

References 23 publications

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“…Shakibaei et al, observed alteration in trabecular pattern and changes in jaw bone density (16). The frequency of bone disease in cirrhotic patients was reported to be 12% to 55% by Patel et al (17). In the study by Dagistan et al, pathologic defects with ground-glass appearance were seen in the mandible (18).…”

Section: Introductionmentioning

confidence: 97%

Evaluation of mandibular inferior cortex changes in patients candidate for liver and kidney transplantation using panoramic view

Ghapanchi¹,

Haghnegahdar²,

Faghih³

et al. 2017

J Nephropathol

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Section: Introductionmentioning

confidence: 97%

Evaluation of mandibular inferior cortex changes in patients candidate for liver and kidney transplantation using panoramic view

Ghapanchi¹,

Haghnegahdar²,

Faghih³

et al. 2017

J Nephropathol

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“…Major risk factors of bone disease in patients with cirrhosis include all risk factors of osteoporosis in the general population. Thus, female gender, advanced age, previous fragility fracture, poor nutritional status, limited physical activity, oral glucocorticoid therapy, low body mass index (<19), high alcohol intake, maternal history of hip fracture, smoking and malnutrition render particularly probable the diagnosis of osteoporosis in a cirrhotic patient [10][11][12][13] .…”

Section: Discussionmentioning

confidence: 99%

“…vitamin D deficiency, secondary hyperparathyroidism and hypogonadism are risk factors of osteoporosis of great relevance among cirrhotic patients 12,14 . After orthotopic liver transplantation (OLT), osteoporosis is the result of two parameters: preexisting osteopenia at OLT and rapid decline in bone mass in the post-transplantation period.…”

Section: Jrpmsmentioning

confidence: 99%

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Multiple vertebral fractures in a liver transplant recipient with HCV cirrhosis: A case report

Tournis¹

2019

JRPMS

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Cirrhosis is a known major risk factor for osteoporosis. The already compromised bone health of cirrhotic patients tends to deteriorate further after liver transplantation, mainly as a result of immunosuppressive treatment. This case report describes a 63-year-old man who presented with multiple vertebral fractures and severe osteoporosis, one year after orthotopic liver transplantation (OLT) because of end-stage HCV cirrhosis. At his initial consultation, the patient was taking everolimus and mycophenolate, while previously the immunosuppressive regimen included corticosteroids. We present follow-up data of the patient after anti-osteoporotic treatment, including consecutive measurements of bone mineral density, vertebral morphometry, biomarkers of bone turnover and related hormones. Two years after OLT, during which he followed treatment with calcium, vitamin D supplements and zolendronic acid (intravenous infusion of 5mg once a year), the patient showed remarkable improvement in bone densitometry, hormones and biomarkers of bone metabolism, with the exception of persistent secondary hyperparathyroidism. As the survival rates of liver transplant recipients improve, osteoporosis constitutes an important long-term complication among these patients. Consequently, prompt diagnosis and treatment of osteoporosis in cirrhotic and liver transplanted patients is crucial, with biphosphonates, and in particular zolendronic acid, a potent possible first-line therapeutical option.

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“…This observation led us to further explore the pathogenesis of these altered pro‐osteoclastic and anti‐osteoclastic factors in advanced cirrhosis. Activation of inflammatory cells in patients with cirrhosis induces proinflammatory cytokine production, such as TNF‐α, IL‐1, IL‐13, IL‐6, IL‐7, IL‐11, IL‐15, and IL‐17 . These inflammatory mediators have been described to be elevated in advanced cirrhosis and promote osteoclast precursor activation or RANKL production by osteoblasts, which are associated with bone resorption .…”

Section: Discussionmentioning

confidence: 99%

Suboptimal Level of Bone‐Forming Cells in Advanced Cirrhosis are Associated with Hepatic Osteodystrophy

Bihari

Lal

Thakur

et al. 2018

Hepatology Communications

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Bone loss is common in advanced cirrhosis, although the precise mechanisms underlying bone loss in cirrhosis are unknown. We studied the profile and functionality of bone‐forming cells and bone‐building proteins in bone marrow (BM) of individuals with cirrhosis (n = 61) and individuals without cirrhosis as normal controls (n = 50). We also performed dual energy X‐ray absorptiometry for clinical correlation. BM mesenchymal cells (MSCs) were analyzed for colony‐forming units‐fibroblasts and their osteogenic (fibronectin‐1 [FN1], insulin‐like growth factor binding protein 3 [IGFBP3], collagen type 1 alpha 1 chain [COL1A1], runt‐related transcription factor 2 [RUNX2], and alkaline phosphatase, liver [ALPL]) and adipogenic ( adiponectin, C1Q, and collagen domain containing [ADIPOQ], peroxisome proliferator‐activated receptor gamma [PPARγ], and fatty acid binding protein 4 [FABP4]) potentials. Colony‐forming units‐fibroblasts were lower in patients with cirrhosis (P = 0.002) than in controls. Cirrhotic BM‐MSCs showed >2‐fold decrease in osteogenic markers. Compared to controls, patients with cirrhosis showed fewer osteocytes (P = 0.05), osteoblasts, chondroblasts, osteocalcin‐positive (osteocalcin+) area, clusters of differentiation (CD)169+ macrophages (P < 0.001, each), and nestin+ MSCs (P = 0.001); this was more apparent in Child‐Turcotte‐Pugh (CTP) class C than A (P < 0.001). Multivariate logistic regression showed low nestin+ MSCs (P = 0.004) as a predictor of bone loss. Bone‐resolving osteoclasts were comparable among CTP groups, but >2‐fold decreased anti‐osteoclastic and increased pro‐osteoclastic factors were noted in patients with CTP C compared to CTP A. Bone‐building proteins (osteocalcin [P = 0.008], osteonectin [P < 0.001], and bone morphogenic protein 2 [P = 0.001]) were decreased while anti‐bone repair factors (fibroblast growth factor 23 [P = 0.015] and dipeptidyl peptidase 4 [P < 0.001]) were increased in BM and peripheral blood; this was more apparent in advanced cirrhosis. The dual energy X‐ray absorptiometry scan T score significantly correlated with the population of osteoblasts, osteocytes, MSCs, and CD169+ macrophages. Conclusion: Osteoprogenitor cells are substantially reduced in patients with cirrhosis and more so in advanced disease. Additionally, increased anti‐bone repair proteins enhance the ineffective bone repair and development of osteoporosis in cirrhosis. Hepatology Communications 2018;0:0‐0)

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Bone disease in cirrhosis

Cited by 28 publications

References 23 publications

Evaluation of mandibular inferior cortex changes in patients candidate for liver and kidney transplantation using panoramic view

Evaluation of mandibular inferior cortex changes in patients candidate for liver and kidney transplantation using panoramic view

Multiple vertebral fractures in a liver transplant recipient with HCV cirrhosis: A case report

Suboptimal Level of Bone‐Forming Cells in Advanced Cirrhosis are Associated with Hepatic Osteodystrophy

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