Alcohol, HIV/AIDS, and Liver Disease

Background:Liver disease related to Hepatitis B (HBV) and C (HCV) infection has become a major cause of morbidity and mortality in HIV/AIDS patients. Data on the prevalence of HBV and HCV in Cameroon remains inconclusive.Objective:We aimed to determine the sero-prevalence and correlates of Hepatitis markers in HIV/AIDS patients in two Regional Hospitals.Methods:A cross-sectional study carried out from December 2014 to March 2015. HIV/AIDS patients aged 21 were included and above, receiving care at HIV treatment centres. Data was collected using a structured questionnaire. Blood samples were collected to screen for Hepatitis with HBsAg and anti HCV antibody rapid immunochromatographic test kits. Correlates of hepatitis were investigated by logistic regression. STATA was used for data analysis.Results:We included 833 HIV/AIDS patients,78.8% (657) were female. Mean age was 44(SD 11) years. Prevalence of Hepatitis in general (total of two viral markers tested) was 8.9% (74/833), with 6.1% for HBsAg and 2.8% for Anti-HCV antibodies. From multivariate analysis, the likelihood of having hepatitis was independently increased by a history of surgical interventions [OR: 1.82(1.06-3.14)], and of sexually transmitted infections [OR: 2.20(1.04-4.67)].Conclusion:Almost one in ten participants with HIV/AIDS attending the BRH and LRH tested positive for either HBsAg or anti HCV antibodies. Screening for HBV and HCV should therefore be integrated to the existing guidelines in Cameroon as it can influence management. More studies are needed to evaluate the extent of liver disease and magnitude of HIV suppression in hepatitis and HIV coinfection in this setting.

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Crystalloid Inclusions in Hepatocyte Mitochondria and Their Similarity to Cytoplasmic Crystalloids

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100051001 ◽

1974 ◽

Vol 32 ◽

pp. 198-199

Author(s):

Odell T. Minick ◽

Hidejiro Yokoo

Keyword(s):

Liver Disease ◽

Alcoholic Liver Disease ◽

Special Interest ◽

Structural Variations ◽

Mitochondrial Alterations ◽

The Matrix ◽

Crystalloid Inclusions ◽

Liver Biopsies

Mitochondrial alterations were studied in 25 liver biopsies from patients with alcoholic liver disease. Of special interest were the morphologic resemblance of certain fine structural variations in mitochondria and crystalloid inclusions. Four types of alterations within mitochondria were found that seemed to relate to cytoplasmic crystalloids.Type 1 alteration consisted of localized groups of cristae, usually oriented in the long direction of the organelle (Fig. 1A). In this plane they appeared serrated at the periphery with blind endings in the matrix. Other sections revealed a system of equally-spaced diagonal lines lengthwise in the mitochondrion with cristae protruding from both ends (Fig. 1B). Profiles of this inclusion were not unlike tangential cuts of a crystalloid structure frequently seen in enlarged mitochondria described below.

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Healing gone wrong: convergence of hemostatic pathways and liver fibrosis?

Clinical Science ◽

10.1042/cs20191102 ◽

2020 ◽

Vol 134 (16) ◽

pp. 2189-2201

Author(s):

Jessica P.E. Davis ◽

Stephen H. Caldwell

Keyword(s):

Wound Healing ◽

Liver Disease ◽

Hepatic Fibrosis ◽

Cell Activation ◽

Stellate Cell ◽

Factor Xa ◽

Clinical Trial Data ◽

Chronic Liver ◽

Healing Response ◽

Wound Healing Response

Abstract Fibrosis results from a disordered wound healing response within the liver with activated hepatic stellate cells laying down dense, collagen-rich extracellular matrix that eventually restricts liver hepatic synthetic function and causes increased sinusoidal resistance. The end result of progressive fibrosis, cirrhosis, is associated with significant morbidity and mortality as well as tremendous economic burden. Fibrosis can be conceptualized as an aberrant wound healing response analogous to a chronic ankle sprain that is driven by chronic liver injury commonly over decades. Two unique aspects of hepatic fibrosis – the chronic nature of insult required and the liver’s unique ability to regenerate – give an opportunity for pharmacologic intervention to stop or slow the pace of fibrosis in patients early in the course of their liver disease. Two potential biologic mechanisms link together hemostasis and fibrosis: focal parenchymal extinction and direct stellate cell activation by thrombin and Factor Xa. Available translational research further supports the role of thrombosis in fibrosis. In this review, we will summarize what is known about the convergence of hemostatic changes and hepatic fibrosis in chronic liver disease and present current preclinical and clinical data exploring the relationship between the two. We will also present clinical trial data that underscores the potential use of anticoagulant therapy as an antifibrotic factor in liver disease.

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