Management of Hepatitis C Virus Infection in Patients with Cirrhosis

In this chapter, we review the history of HCV infection in patients with liver cirrhosis. Selection of appropriate regimens for HCV-infected patients with cirrhosis, consistent with approved indications, practice guidelines, and emerging data is presented. Finally, this chapter explains individualization of therapy to maximize SVR rates in HCV-infected patients with cirrhosis and to critically appraise the role of newer agents and regimens in the management of HCV-infected patients with cirrhosis

Ascites: Causes, Diagnosis, and Treatment

Ascites is a pathological accumulation of fluid in the peritoneal cavity. Cirrhosis is the most common cause of ascites, representing for 85% of cases. More than one cause may be responsible for the development of ascites (multifactorial). Development of ascites is a poor prognostic event in the natural history of cirrhosis, with approximately 15 and 44% of patients with ascites succumbing in 1 and 5 years, respectively. Patients with cirrhosis need referral for liver transplantation after development of ascites. Proper history and physical examination are important in diagnosing the cause of ascites. Diagnostic paracentesis and abdominal sonogram should be performed during initial evaluation. Low salt diet and diuretic are the initial treatment option, and large volume paracentesis is an option for non‐responder to diuretics. Transjugular intrahepatic portosystemic stent‐shunt (TIPS) is highly valuable in properly selected patients

Pharmacological Therapy of Ascites

Ascites refer to accumulation of fluids in the peritoneal cavity. Ascites is caused by multiple causes, among which liver cirrhosis is the commonest. Confirming the etiology is the first and most important step toward proper management. Assuming that ascites is always caused by cirrhosis can lead to unnecessarily sending patients with different etiologies for liver transplantation, particularly patients with non-cirrhotic portal hypertension. Calculating serum albumin ascitic gradient is important in differentiating ascites due to portal hypertension from other etiologies. The first-line therapy for ascites in cirrhosis is low salt diet and diuretics. It is important to avoid nonsteroidal anti-inflammatory drugs (NSAIDs) and nephrotoxic medications in these patients

Cirrhotic Ascites: Pathophysiological Changes and Clinical Implications

Liver cirrhosis is associated with a wide range of systemic and pulmonary vascular abnormalities. Cardiac dysfunction also occurs in patients with advanced liver disease (cirrhotic cardiomyopathy). The circulation in cirrhosis is hyperdynamic, which is typically characterized by hypotension resulting from the associated vasodilatation and reflex tachycardia. The circulatory dysfunction in cirrhosis is the proposed pathophysiological mechanism leading to sodium and water retention in patients with liver cirrhosis. Hyperdynamic circulation is triggered by increased intrahepatic resistance due to cirrhosis, leading to a progressive increase in portal venous pressure. As portal hypertension worsens, local production of vasodilators increases due to endothelial activation, leading to splanchnic and systemic arterial vasodilation. Nitric oxide (NO) is considered one of the most important vasodilator molecules in the splanchnic and systemic circulation. The reduction in the effective arterial blood volume results in diminished renal arterial blood flow and subsequently triggers the rennin-angiotensin-aldosterone system (RAAS), antidiuretic hormones (ADHs) and sympathetic nervous system (SNS), leading to renal artery vasoconstriction. All these changes lead to sodium retention and volume expansion, manifested as ascites and peripheral edema. Furthermore, disease progression is associated with various degrees of renal dysfunction

Non-pharmacological Treatment of Ascites

Diuretics are considered the first-line pharmacological treatment option for ascites. Diuretic treatment begins with spironolactone and furosemide. Non-pharmacological options include salt restriction, large-volume paracentesis (LVP), transjugular intrahepatic portosystemic shunt (TIPS), and peritoneovenous shunt. Ascites can be mobilized if renal sodium excretion tops 78 mmol daily (88 mmol–10 mmol daily) after restricting sodium intake to 88 mmol/day (about 2000 mg/day). The majority of patients with cirrhotic ascites respond to a combination of sodium restriction and diuretics such as spironolactone and furosemide (90%). Ascites that does not respond to sodium restriction and high-dose diuretic treatment (400 mg/day of spironolactone and 160 mg/day of furosemide) or following paracentesis is labeled refractory. Refractory ascites can be managed with large-volume paracentesis or transjugular intrahepatic portosystemic shunt. Peritoneovenous shunting is considered as a third-line treatment option after all other measures such as diuretics, large-volume paracentesis, or transjugular intrahepatic portosystemic shunt deemed unsuccessful or contraindicated. It has a high rate of shunt obstruction

Natural products and hepatocellular carcinoma: a review

Hepatocellular carcinoma (HCC) is the fifth commonest cause of malignancy and the third cause of cancer mortality. There are different treatment options for HCC ranging from loco-regional therapy to surgical treatment. Different regimen of systemic chemotherapy has been tried with a poor response. Several studies aimed at discovering more molecules for the management of HCC. Those studies aimed at recognizing and targeting several signalling and molecular pathways that lead to cellular proliferation and tumour formation. In this review, we discussed the role of several agents found in natural and dietary products such as curcumin, resveratrol, flavonoids, Rubus aleaefolious Poir total alkaloids, Livistona chinesis seed, and crocetin. We had used the names of the above-mentioned products as key words in addition to “Hepatocellular Carcinoma” on PubMed to find studies that discussed their roles in HCC. Articles were downloaded for reviewing and discussing natural products that had adequate studies in treating HCC

Glycogenic Hepatopathy: A Rare Hepatic Complication of Poorly Controlled Type 1 DM

Glycogen hepatopathy (GH) is a rare complication of type 1 diabetes mellitus that leads to an abnormal accumulation of glycogen in the hepatocytes. The exact mechanism of GH remains unknown, but fluctuations in blood glucose and insulin levels play important roles in promoting glycogen accumulation. We report a case of a 16-year-old female diagnosed with poorly controlled type 1 diabetes mellitus with hepatomegaly and elevated liver enzymes. The patient experienced multiple admissions for diabetic ketoacidosis, and she also had celiac disease diagnosed 2 years previously based on serology and a duodenal biopsy. The laboratory analyses results were compatible with acute hepatitis, and the celiac serology was positive. Other investigations ruled out viral hepatitis and autoimmune and metabolic liver diseases. Ultrasound and computerized tomography (CT) scans of the abdomen revealed liver enlargement with diffuse fatty infiltration. A liver biopsy revealed the presence of abundant glycogen in the cytoplasm of the hepatocytes. PAS staining was strongly positive, which confirmed the diagnosis of GH. There were no features of autoimmune hepatitis or significant fibrosis. Duodenal biopsy results were consistent with celiac disease. Despite our efforts, which are supported by a multidisciplinary team approach that included a hepatologist, a diabetic educator, a dietitian, and an endocrinologist, we have encountered difficulties in controlling the patient’s diabetes, and she persistently maintains symptomatic hepatomegaly and abnormal liver biochemistry. Given the patient’s age, we assumed that these abnormalities were related to patient noncompliance. In conclusion, GH remains an under-recognized complication of type 1 DM that is potentially reversible with adequate glycemic control. The awareness of GH should prevent diagnostic delay and its implications for management and the outcome

Left-sided portal hypertension with a patent splenic vein: An impossible or a not-so-uncommon scenario?

ABSTRACT Introduction: Left-sided portal hypertension is usually thought to result from a mechanical obstruction of the splenic vein. However, a functional obstruction of a patent splenic vein due to high venous flow can also cause left-sided portal hypertension. Case Report: We report a case of left-sided portal hypertension with a patent splenic vein. Conclusion: The case illustrates that left-sided portal hypertension is a syndrome that results from the variable interactions of different mechanisms and highlights that the selection of suitable treatment is based on understanding the portal pathophysiology and portal venous anatomy in the patient