View clinical trials related to Liver Cirrhosis.
Filter by:The aim of this work is to study the role of long non-coding RNAs WRAP53 and urothelial carcinoma-associated 1 (UCA1) as potential biomarkers in diagnosis of hepatocellular carcinoma.
In this study, treatment-naïve HBV-related cirrhosis patients were retrospectively enrolled at the first episode of decompensation (ascites or variceal hemorrhage). Patients were followed up every 6 months until death /liver transplantation or for 5 years. Clinical data from medical records about past history, first decompensated events, second /further decompensated events, HCC, and death/ liver transplantation were retrospectively collected. In this retrospective study, the incidence of re-compensation and its clinical characteristics were mainly explored.
Refractory ascites is seen in 17% of cirrhotic patients with the 1year mortality rate being high, upto 20-50% [1]. The pathogenesis of cirrhotic ascites includes release of vasodilatory molecules like nitric oxide, damage associated molecular pathogens (DAMPs) and pattern associated molecular pathogens (PAMPs) secondary to bacterial translocation, which causes splanchnic bed vasodilation resulting in activation of renin-angiotensin and aldosterone axis causing sodium and water retention. The standard medical therapy for the treatment of ascites includes sodium restriction to 2mEq/kg/day with diuretics (Spirinolactone 3-6mg/kg/day and furosemide 0.5-2 mg/kg/day) and therapeutic paracentesis (>50ml/kg/day) with albumin replacement at 8g/L of ascitic fluid tapped. Refractory ascites is defined as ascites that cannot be mobilized by sodium - restricted diet (maximum upto 2mEq/kg/day- 88meq=2gm of salt) and high-dose diuretic treatment (6 mg/kg/day of spironolactone and 2 mg/kg/day of furosemide) or optimum doses of diuretics cannot be given due to development of diuretic-induced complications (Sodium <130mEq, AKI as per KDIGO, hypovolemia, hypo (<3.5meq)/hyperkalemia (>5meq); new onset HE) and recurrent ascites as ascites that has recurred within a 12 weeks period despite standard treatment. All the children and adolescents upto 18 years of age with refractory or recurrent ascites will be included in the study and randomized into 2 groups. One group will receive only standard medical therapy and other group will receive midodrine and standard medical therapy for 12 weeks. Mean arterial pressure will be monitored at every OPD visit. At the end of 12 weeks, plasma renin activity, number of therapeutic paracentesis done, change in serum sodium, estimated glomerular filtration rate and complications will be assessed. If there is complete resolution of ascites, liver transplantation or death before 12 weeks, midodrine will be stopped.
1-to identify the prognostic value of serum bicarbonate and serum electrolytes at time of admission and their association with development of complications ,length of hospital stay ,prognosis and mortality in hospitalized cirrhotic patient
This is a study to assess safety and preliminary clinical activity of treatments of liver cirrhosis in patients with caused by Hepatitis C and Hepatitis B or Nonalcoholic Steatohepatitis of Mesenchymal stem cell. Patients who will be enrolled in the study will be under supervision and monitoring to ensure clinical significance
This trial is being completed to evaluate whether a crystallized form of lactulose (Kristalose) will improve quality of life, sleep and cognitive function in patients with cirrhosis that have not been diagnosed with Hepatic Encephalopathy (HE), but report reduced quality of life.
The study will compare two forms of advice regarding physical activity for patients hospitalized with cirrhosis that are preparing for leaving the hospital. One arm consists of current standard of care: simple oral advice on exercise. One arm instead gives patients a structured but simple paper template on physical activity.
In this randomized controlled trial , The patients who satisfy the below inclusion and exclusion criteria will be included and they will be randomised, according to 2 groups ( in total 110patients in each group) to receive either Midodrine+Tolvaptan or tolvaptan+placebo for 7 days followed by follow up for 1 month. These patients will be admitted to the hospital from OPD or emergency. In patients with cirrhosis with Patients with cirrhosis -there are two types of hyponatremia. hyponatremia is due to important losses of extracellular fluid, most commonly from the kidneys (because of overdiuresis due to treatment with excessive doses of diuretics) or from the gastrointestinal tract( hypovolemic hyponatremia) hyponatremia develops in the setting of expanded extracellular fluid volume and plasma volume with ascites and edema.This condition is known as hypervolemic or dilutional hyponatremia.A marked impairment of renal solute-free water excretion, resulting in disproportionate renal retention of water with respect to sodium retention.In SALT trail showed that tolvaptan showed improvement in Na+ concentration from baseline at 4 ,30 day. It acts on by increasing free water generation by blocking ADH receptors in distal convoluted tubule. A study by Patel et al in 2017 showed that midodrine also increasing the Na+ by increasing the free water delivery to distal convoluted tubules(in cirrhosis usually there is less water delivery to distal convoluted tubules in view of less GFR).Till now there is no study has been done as combination of midodrine and tolvaptan whether superior to tolvaptan alone or not .So our aim is to study combination of midodrine and tolvaptan verses tolvaptan alone in patients with hyponatremia.
In critically ill patients with liver disease like cirrhosis or ACLF, fluid therapy needs to be instituted after identification of patients who will be fluid responsive and initiate appropriate inotropes early to prevent the mortality associated with fluid overload. The parameters and methodology used for assessing fluid responsiveness have been studied earlier, but the optimum method is not established. Existing recommendations based on data regarding fluid responsiveness and choice of fluid for resuscitation from intensive care units in general cannot be applied to those with liver disease as the hemodynamic alterations that occur with liver disease, presence of hypoalbuminemia at baseline and presence of cardiac dysfunction interfere with the conventional methods of fluid status assessment, fluid responsiveness as well as the response to different types of resuscitation fluids. Therefore the investigators attempt to compare various methods to estimate current intravascular volume status of patient which could be helpful in guiding fluid therapy.
The cumulative risk of refractory ascites is in the order of 20% within five years of the development of ascites. An elevated sinusoidal pressure is essential for the development of ascites, as fluid accumulation does not develop at portal pressure gradient below 8 mm Hg, and rising corrected sinusoidal pressure correlates with decreased 24-hour urinary excretion of sodium.More recently, it has been hypothesised that bacterial translocation associated with portal hypertension in cirrhosis and related pathogen-associated, molecular pattern activated innate immune responses lead to systemic inflammation.This is associated with vasodilatation as well as release of proinflammatory cytokines, reactive oxygen and nitrogen species, contributing to organ dysfunction.This activates sympathetic nervous system stimulating reabsorption of sodium in proximal,distal tubules, loop of Henle and collecting duct as well as the renin-angiotensin-aldosterone system, leading to sodium absorption from distal tubule and collecting duct.[5]Renal sodium retention and eventual free water clearance due to non-osmoticrelease of arginine-vasopressin and its action on V2 receptor in the collectingduct underlie the fluid retention associated with oedema and ascites in cirrhosis.The lowering of portal pressure using non selective beta blocker has also been shown to reduce the development of ascites, refractory ascites and hepatorenal syndrome.Furthermore, the effect of non slective beta blocker on intestinal permeability, bacterial translocation and inflammatory response has been proposed to mitigate the risk of developing spontaneous bacterial peritonitis.