A consensus integrated care pathway for patients with primary biliary cholangitis: a guideline-based approach to clinical care of patients.

INTRODUCTION: Primary biliary cholangitis (PBC) is an infrequent, immune-mediated cholestatic liver disease, which can lead to liver fibrosis, cirrhosis and complications of end-stage liver disease. The established goals of treatment of PBC are prevention of end-stage liver disease and amelioration of associated symptoms. The European Association for the Study of the Liver (EASL) management guidelines provide extensive recommendations on the diagnosis and management of PBC. AREAS COVERED: This article describes the development by expert consensus of a 'PBC Integrated Patient Care Pathway' to simplify and standardize the management of PBC for clinicians based on current practice. EXPERT OPINION: Guideline adoption is potentially poor in practice since most patients with PBC in the community are seen by general gastroenterologists or hepatologists without a special interest in autoimmune liver disease. The PBC Integrated Patient Care Pathway is a best practice tool for clinicians designed to complement the EASL Clinical Practice Guidelines for the diagnosis and management of PBC patients. It gives clinicians a practical decision tree of the key steps in PBC management, thereby providing a simplified framework and an opportunity for more uniform practice that supports the safe and timely adoption of varied models of care provision to patients with PBC.

HIV infection, viral hepatitis and liver fibrosis among prison inmates in West Africa.

BACKGROUND: Prisoners represent a vulnerable population for blood-borne and sexually transmitted infections which can potentially lead to liver fibrosis and ultimately cirrhosis. However, little is known about the prevalence of liver fibrosis and associated risk factors among inmates in sub-Saharan Africa. METHODS: Screening of liver fibrosis was undertaken in a randomly selected sample of male inmates incarcerated in Lome, Togo and in Dakar, Senegal using transient elastography. A liver stiffness measurement ≥9.5 KPa was retained to define the presence of a severe liver fibrosis. All included inmates were also screened for HIV, Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) infection. Substances abuse including alcohol, tobacco and cannabis use were assessed during face-to-face interviews. Odds Ratio (OR) estimates were computed with their 95 % Confidence Interval (CI) to identify factors associated with severe liver fibrosis. RESULTS: Overall, 680 inmates were included with a median age of 30 years [interquartile range: 24-35]. The prevalence of severe fibrosis was 3.1 % (4.9 % in Lome and 1.2 % in Dakar). Infections with HIV, HBV and HCV were identified in 2.6 %, 12.5 % and 0.5 % of inmates, respectively. Factors associated with a severe liver fibrosis were HIV infection (OR = 7.6; CI 1.8-32.1), HBV infection (OR = 4.8; CI 1.8-12.8), HCV infection (OR = 52.6; CI 4.1-673.8), use of traditional medicines (OR = 3.7; CI 1.4-10.1) and being incarcerated in Lome (OR = 3.3; CI 1.1-9.8) compared to Dakar. CONCLUSIONS: HIV infection and viral hepatitis infections were identified as important and independent determinants of severe liver fibrosis. While access to active antiviral therapies against HIV and viral hepatitis expands in Africa, adapted strategies for the monitoring of liver disease need to be explored, especially in vulnerable populations such as inmates.

[Managing comorbidities in hepatology: toward a more holistic medicine]. / Comment gérer les comorbidités en hépatologie? Vers une médecine plus globale.

Approximately 20% of patients infected with the hepatitis B or C virus (HBV and HCV) develop cirrhosis of the liver. It is essential, especially for preventive purposes, to test for related etiological factors, especially excess alcohol consumption, metabolic syndrome, and obesity. The frequency of these health problems and their hepatic tropism explain these frequent associations. In patients with chronic HBV and HCV, alcohol consumption and metabolic syndrome increase the risk of fibrosis; in those with HCV, they also reduce the likelihood of treatment response. In patients with alcoholic hepatitis, overweight increases cirrhotic risk. If cytolysis persists after the identified factor is controlled, another etiologic factor must be sought and treated. For patients with excess alcohol consumption and similarly those with metabolic syndrome, it is essential to differentiate between dependency, which is more difficult to treat, and other risk situations, for which the efficacy of a brief intervention by the physician has been demonstrated. In this more holistic approach, the physician treats a person with liver disease, rather than just a diseased liver.

Hepatic hydrothorax associated with vitamin a toxicity.

We report the first case of an adult presenting with respiratory symptoms caused by hepatic hydrothorax secondary to vitamin A intoxication. The patient was a 52-year-old woman who presented to the hospital with progressive dyspnea. Evaluation demonstrated mild elevation of her liver function tests, ascites, and a right pleural effusion. The patient consumed a variety of vitamins, including vitamin A. Her estimated vitamin A intake was at least 162,300,000 international units (IU) during 18 years. She dramatically escalated her dose the year before admission for a total acute dose of 98,550,000 IU, with a daily intake of 270,000 IU. The recommended daily allowance is 4,000 IU. A transjugular liver biopsy revealed histopathologic changes consistent with vitamin A toxicity: hypertrophy and hyperplasia of hepatic stellate cells, focal pericellular fibrosis, mild perivenular fibrosis, and minimal, predominantly microvesicular steatosis. Despite the absence of cirrhosis, pressure readings demonstrated portal hypertension. During her hospitalization, the patient's symptoms and biochemical profile improved. As the large and generally unregulated United States dietary supplement industry continues to grow, it is increasingly likely that individuals will present with the signs and symptoms of vitamin excess rather than vitamin deficiency. Physicians need to remain alert to the varied presentations and toxic manifestations of excessive vitamin use.