Bone disease in patients awaiting liver transplantation. Has the situation improved in the last two decades?

In recent years, there has been speculation about the possibility of a reduction in the incidence of fractures after liver transplantation (LT) because of changes in the characteristics of candidates and the use of different immunosuppressive therapies. We analyzed the characteristics of LT candidates (CTC) and compared them with historical data from a group of LT candidate patients (HTC). Data from 60 CTC patients consecutively included in a screening program of metabolic bone disease were compared with data from 60 HTC patients prospectively evaluated between 1992 and 1993. In all patients, we analyzed the clinical and laboratory characteristics, bone mineral density (BMD) dual-energy X-ray absorptiometry, and skeletal fractures. Patients in the CTC group were older than patients in the HTC group. The CTC group had lower femoral neck T scores. No differences were observed between groups in the proportion of patients with osteoporosis (22 vs. 30 %, p = ns) or fractures (36 vs. 33 %, p = ns). The percentage of patients with normal BMD decreased from 38 to 20 %. 25(OH)D values were low in both groups. Only 7.5 % of the CTC patients received calcium and/or vitamin D supplementation. The prevalence of fractures among CTC patients was similar to that seen two decades ago. At present, candidates for LT are older and have lower femoral bone mass. Vitamin D deficiency remains frequent; however, calcium and/or vitamin D supplementation is uncommon.

[Treatment of liver fibrosis]. / Tratamiento de la fibrosis hepática.

Liver fibrosis is the progressive deposition of extracellular matrix in the liver parenchyma that precedes the development of cirrhosis. In the last few years, knowledge of the cellular and molecular bases of liver fibrosis has increased considerably. Environmental and genetic factors have been described that influence the progression of liver fibrosis, while non-invasive methods have been developed that allow the grade of fibrosis to be estimated without the need for liver biopsy. Currently, the only clearly effective treatment to attenuate or reverse liver fibrosis is elimination of the causative agent. When this is not feasible, fibrogenic factors (such as insulin resistance, obesity, alcohol intake, cannabis consumption, etc.) should be identified and treated. However, several agents are able to reduce liver fibrosis in experimental models of chronic liver damage. Few controlled clinical trials have been performed that evaluate the efficacy and safety of these agents and consequently the level of evidence supporting their use as anti-fibrogenic therapy is still low. The efficacy of the anti- fibrogenic drugs, renin-angiotensin system inhibitors, is currently being evaluated.

Tratamiento de la fibrosis hepática / Treatment of liver fibrosis

La fibrosis hepática (FH) es el depósito progresivo de matriz extracelular en el parénquima hepático que precede al desarrollo de cirrosis. El conocimiento de las bases celulares y moleculares de la FH ha aumentado considerablemente en las dos últimas décadas. Se han descrito factores ambientales y genéticos que influyen en su progresión, así como métodos no invasivos que permiten estimar el grado de fibrosis sin necesidad de realizar una biopsia hepática. En la actualidad, el único tratamiento claramente efectivo para atenuar o revertir la FH es la eliminación del agente causal. En los casos en los que esto no es posible, se recomienda identificar y tratar factores profibrogénicos (como la resistencia a la insulina, la obesidad, el consumo de alcohol, el consumo de cannabis, etc.). Se han descrito diversos agentes capaces de reducir la FH en modelos experimentales de daño hepático crónico. No obstante, apenas existen estudios clínicos controlados que evaluen la eficacia y la seguridad de estos agentes, por lo que no existe suficiente evidencia científica para indicarlos como tratamiento antifibrogénicos. La eficacia de los inhibidores del sistema renina-angiotensina como fármacos antifibrogénicos se está evaluando en la actualidad(AU)

Liver fibrosis is the progressive deposition of extracellular matrix in the liver parenchyma that precedes the development of cirrhosis. In the last few years, knowledge of the cellular and molecular bases of liver fibrosis has increased considerably. Environmental and genetic factors have been described that influence the progression of liver fibrosis, while non-invasive methods have been developed that allow the grade of fibrosis to be estimated without the need for liver biopsy. Currently, the only clearly effective treatment to attenuate or reverse liver fibrosis is elimination of the causative agent. When this is not feasible, fibrogenic factors (such as insulin resistance, obesity, alcohol intake, cannabis consumption, etc.) should be identified and treated. However, several agents are able to reduce liver fibrosis in experimental models of chronic liver damage. Few controlled clinical trials have been performed that evaluate the efficacy and safety of these agents and consequently the level of evidence supporting their use as anti-fibrogenic therapy is still low. The efficacy of the anti- fibrogenic drugs, renin-angiotensin system inhibitors, is currently being evaluated(AU)