Living Donor Liver Transplantation Following Transcatheter Aortic Valve Implantation for Aortic Valvular Disease.

Over the last few decades, outcomes with living donor liver transplantation (LDLT) have improved significantly. This has resulted in patients who were denied liver transplantation previously, due to various comorbidities and high risk, now being considered for LDLT. This includes patients with severe valvular heart disease such as aortic stenosis. These patients require aortic valve replacement to help cope with significant perioperative hemodynamic changes. High-risk cardiac procedures like aortic valve replacement are associated with serious perioperative morbidity and mortality in patients with end-stage liver disease. Since the advent of transcatheter aortic valve implantation (TAVI) in 2002, there have been a few case reports of its successful use prior to deceased donor liver transplantation, but there is no literature on this procedure before LDLT. In this article, we report our experience with 2 patients, the first patient with infective endocarditis-induced acute aortic regurgitation and the second patient with bicuspid aortic stenosis who underwent uneventful TAVI followed by successful LDLT. In conclusion, with the increasing expertise and experience in this procedure, an increasing number of potential recipients, previously considered as high-risk transplant candidates, can now be offered liver transplantation by performing pretransplant TAVI.

Hepatopulmonary syndrome - past to present.

Hepatopulmonary syndrome (HPS) is the one of the complication of liver cirrhosis with portal hypertension, irrespective of etiology, age and sex. It has also been observed in non cirrhotic portal hypertension and in acute hepatic conditions. Presence of hypoxemia or abnormal alveolar arterial oxygen tension with intrapulmonary vasodilation in liver cirrhosis is termed as HPS. Contrast echocardiogram is the better screening tool to demonstrate intrapulmonary shunt. Clinicians should be aware of other common chronic pulmonary and cardiac comorbid conditions, in particular COPD, tuberculosis, bronchial asthma and idiopathic pulmonary fibrosis, etc. which may coexist with HPS. There is no specific clinical finding to diagnose but digital clubbing, cyanosis, dyspnoea, platypnoea, and spider naevi are more common among cirrhosis with HPS. The presence of HPS independently worsens prognosis of cirrhosis. Even though number of mechanisms have been proposed to explain arterial hypoxemia in HPS, role of nitric oxide is the major one along with cytokines. Liver transplantation is the choice of treatment though mortality is comparatively high. There is no still effective recommended medical therapy to reverse this condition and anti cytokine/ nitric oxide inhibitors, etc are under preliminary stage.

Alcoholic chronic pancreatitis and alcoholic liver cirrhosis: differences in alcohol use habits and patterns in Indian subjects.

OBJECTIVES: Alcohol abuse is a risk factor for both liver cirrhosis and chronic pancreatitis. However, less than 15% of heavy drinkers develop these complications. Coexistence of cirrhosis and pancreatitis in the same patient is considered uncommon. We compared drinking patterns and related patient factors in patients with alcoholic liver cirrhosis and alcoholic chronic pancreatitis. METHODS: A prospective evaluation of 307 patients (all men: 188 with alcoholic liver cirrhosis and 119 with alcoholic chronic pancreatitis) was conducted over a 7-year period using a detailed alcohol assessment proforma. Assessment of demographic features, diet, and other habits like tobacco smoking were recorded. RESULTS: Patients with alcoholic liver cirrhosis were older. The mean ± SD age in alcoholic liver cirrhosis was 52.4 ± 9.16 years and 47.1 ± 9.78 years (P < 0.001) in alcoholic chronic pancreatitis. The mean ± SD age when they started drinking was similar in both groups (22.8 ± 5.32 years and 24.3 ± 6.94; P > 0.05). The mean ± SD duration of drinking was higher in the cirrhosis group (29.5 ± 10.25 years) than in the pancreatitis group (21.5 ± 9.61 years) (P < 0.001). Fifty-nine percent of cirrhosis and 75% of pancreatitis were heavy tobacco smokers (P = 0.004). CONCLUSIONS: There are distinct differences in drinking patterns and related patient factors between alcoholic liver cirrhosis and alcoholic chronic pancreatitis, suggesting the need to orient different interventional strategies.

Assessment of allograft fibrosis by transient elastography and noninvasive biomarker scoring systems in liver transplant patients.

BACKGROUND: This prospective, monocentric study was designed to assess the efficacy of transient elastography (TE), biochemical tests, and more complex scores in determining fibrosis stage in 157 patients transplanted for hepatitis C virus (HCV) infection or non-HCV-related liver diseases. METHODS AND RESULTS: The optimal TE cutoff values for HCV patients and non-HCV patients were 4.7 and 5.0 kPa for F> or =1, 7.1 and 7.3 kPa for F> or =2, 10.9 kPa and 9.9 kPa for F> or =3, and 17.3 and 12.6 kPa for F=4, respectively. The corresponding area under the receiver operating characteristic (AUROC) curves for F> or =1, F> or =2, F> or =3, and F=4 were 0.95 and 0.86, 0.89 and 0.85, 0.97 and 0.88, and 0.99 and 0.97 for HCV and non-HCV patients, respectively. On the basis of the logistic regression equation, we created a model (FibroTransplant score) to identify advanced fibrosis (F> or =3). The accuracy of this model was tested in a validation group (n=74). AUROCs for diagnosis of F> or =3 in HCV patients and non-HCV patients of the training group were 0.89 and 0.83 (FibroTransplant score), 0.86 and 0.66 (Benlloch score), 0.81 and 0.71 (aspartate aminotransferase-to-platelet ratio index), 0.80 and 0.77 (Hepascore), 0.79 and 0.70 (FibroTest), 0.78 and 0.71 (FIB-4), 0.75 and 0.60 (Forns index), 0.73 and 0.69 (FibroIndex), and 0.70 and 0.59 (Lok score). Among the validation group, AUROCs of the FibroTransplant score for F> or =3 were 0.90 and 0.91, respectively. CONCLUSIONS: TE and the FibroTransplant score can be reliably used for diagnosing advanced fibrosis in transplanted patients.

Muscle cell membrane damage by very low serum sodium.

A 63-year-old male was admitted with complaints of upper gastrointestinal symptoms with fatigue and myalgia. Investigations revealed severe hyponatremia with elevated creatine phosphokinase levels. Following further workup, it was diagnosed as a case of hyponatremia induced rhabdomyolysis. Because of prompt correction of hyponatremia, his renal function was preserved and myoglobinuria induced renal failure was avoided. The importance of early recognition of this potentially dangerous condition is emphasized.