Osteoporosis is an important and common complication in patients with chronic liver disease. The goal of this study was to determine the bone mineral density (BMD) in different subgroups among pretransplant cirrhotic patients. BMD of the lumbar vertebrae (L) and femoral neck (F) were obtained in 104 consecutive cirrhotic patients. Descriptive and inferential statistics were used to compare the BMD among various groups. The mean BMD in males (n ‫؍‬ 54) and females (n ‫؍‬ 50) at L were 1.28 ؎ 0.25 g/cm 2 and 1.13 ؎ 0.20 g/cm 2 , respectively (P ‫؍‬ .001); at F they were 1.03 ؎ 0.14 and 0.91 ؎ 0.17, respectively (P < .0001). Among males, BMD at L in Child-Turcotte-Pugh class B and C were 1.40 ؎ 0.21 and 1.13 ؎ 0.20, respectively (P ‫؍‬ .001); at F they were 1.11 ؎ 0.10 and 0.93 ؎ 0.13, respectively (P < .0001).

Aging is characterized by a progressive decline of cellular functions. The aging liver appears to preserve its function relatively well. Aging is associated in human liver with morphological changes such as decrease in size attributable to decreased hepatic blood flow. Ultrastructural analysis of the human liver has revealed that the integrity of mitochondria and enzymatic activity remain mostly unchanged with aging. Reactive oxygen species (ROS) are involved in the aging process and result mainly from nonenzymatic processes in the liver. Endogenous free radicals are generated within mitochondria and suspected to cause severe injury to mitochondrial DNA. This damaged DNA accumulates with aging. In addition, polyunsaturated fatty acids, highly sensitive to ROS, decrease in liver mitochondria from human centenarians, a feature acquired during evolution as a protective mechanism to favor longevity. Diet is considered the main environmental factor having effect on lifespan. It has a major impact on aging liver, the central metabolic organ of the body. The ubiquitin proteolytic pathway in the liver serves to destroy many proteins, among them p21 which is encoded by abundant mRNA in senescent cells, can inhibit cell proliferation and favors DNA repair. Drug therapy in the elderly may be complicated by several factors such as decline in body weight, renal function, liver mass and hepatic blood flow, making adverse drug reactions more frequent. Hepatic drug metabolism is mainly mediated by the cytochrome P₄₅₀ system and drug interactions in the elderly are likely related to the progressive decline of this system after the fifth decade of life and another decrease in individuals aged >70. Antihypertensive therapy in the elderly depends upon either hepatic or renal function and should be adjusted accordingly. Finally, telomerases are the biological clocks of replicative lifespan. Shortening of telomeric ends of chromosomes correlates with aging and decline in the replicative potential of the cell: replicative senescence. Telomere DNA of human somatic cells shortens during each cell division thus leading to a finite proliferation. Transfection of the telomerase reverse transcriptase gene results in elongation of telomeres and extension of lifespan. This also applies to humans. Replicative senescence in human cells evolved as a mechanism to protect them from continuous divisions leading to multiple mutations. Longer-lived species such as humans had to develop replicative senescence to ensure that they would have the increased protection that their longevity necessitates.

The SR rate achieved by intravenous drug abusers to high-dose, daily IFN is similar to that in a non-drug-abusing HCV positive population. Recent use of illicit drugs within a 6-month period of starting IFN therapy or continued methadone use during treatment does not seem to impair the response to IFN when the results are compared with those of a matched cohort of non-drug-abusing controls.

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Small intestinal bacterial overgrowth (SIBO) is one of the causes of malabsorption syndromes. The prevalence of metabolic bone disease in patients with SIBO is unknown, but a recent prospective case-control study indicated significant contribution of SIBO to the development of metabolic bone disease. We review this and other reports in the literature and discuss the possible mechanisms causing metabolic bone disease in patients with SIBO.