Common musculoskeletal disorders in chronic liver disease patients

Chronic liver disease (CLD) is the commonest ailment affecting the hepatobiliary system. Six significant pathologies related to CLD include hepatic osteodystrophy (HO), increased infection susceptibility, sarcopenia, osteonecrosis of the femoral head (OFH), increased risk of periprosthetic complications and fracture. Hepatic osteodystrophy, which comprises osteopenia, osteoporosis, and osteomalacia, refers to alterations in bone mineral metabolism found in patients with CLD. The HO prevalence ranges from 13 to 95%. Low complement levels, poor opsonization capacity, portosystemic shunting, decreased albumin levels, and impaired reticuloendothelial system make the cirrhotic patients more susceptible to developing infectious diseases. Septic arthritis, osteomyelitis, prosthetic joint infection, and cellulitis were common types of CLD-associated infectious conditions. The incidence of septic arthritis is 1.5 to 2-fold higher in patients with cirrhosis. Sarcopenia, also known as muscle wasting, is one of the frequently overlooked manifestations of CLD. Sarcopenia has been shown to be independent predictor of longer mechanical ventilation, hospital stay, and 12-month mortality of post-transplantation. Alcohol and steroid abuse commonly associated with CLD are the two most important contributory factors for non-traumatic osteonecrosis. However, many studies have identified cirrhosis alone to be an independent cause of atraumatic osteonecrosis. The risk of developing OFH in cirrhosis patients increases by 2.4 folds and the need for total hip arthroplasty increases by 10 folds. Liver disease has been associated with worse outcomes and higher costs after arthroplasty. Cirrhosis is a risk factor for arthroplasty complications and is associated with a prolonged hospital stay, higher costs, readmission rates, and increased mortality after arthroplasty. Greater physician awareness of risk factors associated with musculoskeletal complications of CLD patients would yield earlier interventions, lower healthcare costs, and better overall clinical outcomes for this group of patients.

A cross-sectional study of chronic liver disease patients complicating to hepatic osteodystrophy

Background: Hepatic osteodystrophy encompasses the spectrum of metabolic bone diseases in chronic liver disease (CLD) patients. CLD causing changes in BMD is well known. Although BMD evaluation in CLD cirrhosis are recommended by societies of British and American gastroenterology ,very less number of literature exist from India and none from the North-eastern region of India. Aim of the study to determine the association and severity of bone mineral density changes in patients with CLD and to correlate it with different aetiologies and severity of CLD.Methods: This cross-sectional study which included 79 patients with CLD was conducted in RIMS, Manipur from September 2017 to August 2019. All CLD patients of age 18-60 years were included. DEXA scan and other related blood investigations were performed.Results: Chronic alcohol intake (56.9%), viral infection (20.3%) and mixed (17.7%) were the main aetiology of CLD in our study. Seventy three (92.4%) of the total 79 patients had low BMD (Osteopenia in 29 (36.7%) and osteoporosis in 44 (55.7%) patients). Osteoporosis was detected in 53.4% of alcohol related Cirrhosis, 25%of viral liver disease. Majority of the severe CLD patients (Child class C) had osteoporosis (70.6%) as compared to less severe groups (23.5% and 36.4% in class B and A respectively).Conclusions: CLD patients have high prevalence of osteoporosis. Severity of liver disease, alcoholic liver disease, serum calcium and vitamin D deficiency predisposes to osteoporosis in these patients. Hence early screening of BMD is necessary in CLD patients.

Hepatic Osteodystrophy—Molecular Mechanisms Proposed to Favor Its Development

Almost all patients with chronic liver diseases (CLD) show altered bone metabolism. Depending on the etiology, this manifests in a severe osteoporosis in up to 75% of the affected patients. Due to high prevalence, the generic term hepatic osteodystrophy (HOD) evolved, describing altered bone metabolism, decreased bone mineral density, and deterioration of bone structure in patients with CLD. Once developed, HOD is difficult to treat and increases the risk of fragility fractures. Existing fractures affect the quality of life and, more importantly, long-term prognosis of these patients, which presents with increased mortality. Thus, special care is required to support the healing process. However, for early diagnosis (reduce fracture risk) and development of adequate treatment strategies (support healing of existing fractures), it is essential to understand the underlying mechanisms that link disturbed liver function with this bone phenotype. In the present review, we summarize proposed molecular mechanisms favoring the development of HOD and compromising the healing of associated fractures, including alterations in vitamin D metabolism and action, disbalances in transforming growth factor beta (TGF-β) and bone morphogenetic protein (BMP) signaling with histone deacetylases (HDACs) as secondary regulators, as well as alterations in the receptor activator of nuclear factor kappa B ligand (RANKL)–osteoprotegerin (OPG) system mediated by sclerostin. Based on these mechanisms, we give an overview on the limitations of early diagnosis of HOD with established serum markers.