Pediatric Acute Liver Failure Study Group
Please forward this pediatric Acute Liver Failure Study Group screen to sharedip-13214820582. Liver fibrosis is one of the processes that occurs when the liver is damaged. The current article summarizes what was presented about liver fibrosis therapy in that issue of the journal and adds commentaries to aid in interpreting the results. Liver fibrosis is a gradual process of increased secretion and decreased degradation of extracellular materials.
Most authors hold that the process is initiated by the damage of hepatic cells, which leads to activation and secretion of multiple cellular factors from Kupffer cells . BRIEF SUMMARY OF THE ORIGINAL RESEARCH ARTICLES Chinese research publications frequently display flaws in research design and reporting that make it difficult to interpret the results. Nie Guang commented: “It is worth pointing out that the level of recent studies is low, with many concrete tasks waiting to be done. Almost all published reports from China about traditional Chinese medicine therapies are positive ones.
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In traditional Chinese medical therapy, attempts are often made to address several aspects of a disease rather than only one of its manifestations. The Qinggan Capsule is an example of a broad formulation to treat hepatitis symptoms with a focus on the accompanying hepatic fibrosis in patients with chronic hepatitis B. Qinggan Capsule in improving pathological changes in the liver, particularly the antifibrosis effect, may be through mechanisms other than antiviral action. Liver fibrosis is the pathological process of fibrous connective tissue development secondary to inflammatory necrosis of liver cells. In this study, 86 out-patients with chronic hepatitis B were treated either with ginkgo tablets that each contained 2. It was found in this study that the serum level of PAF was elevated in patients with chronic hepatic cirrhosis, and in those after anti-fibrosis treatment , it could be lowered along with improving of the liver fibrosis in a positively correlated manner, suggesting that PAF participates in the genesis and development of liver fibrosis in chronic hepatitis.
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It was reported that good effect was obtained by using composite ginkgo leaf granule, containing ginkgo leaf and 9 other Chinese herbs to treat early stage liver fibrosis, with evident improvement in blood level of superoxide dismutase and malondialdehyde . These results indicate that ginkgo leaf has obvious effects of liver protection, anti-inflammation, and anti-fibrosis, and may even reverse liver fibrosis. Preparations of astragalus and salvia are frequently used to vitalize blood circulation and treat chronic diseases involving blood stasis. We consider that liver fibrosis is caused by evil damp-heat left behind by chronic hepatitis, and by the combination of liver stagnancy, spleen deficiency, and blood stasis resulting from the long-term course of the disease.
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In the early stage of liver disease, a TCM syndrome of pathogenic excess, such as qi stagnation and dampness accumulation, is manifested along with spleen qi deficiency. Fibronectin and laminin have an effect on the extra-cellular matrix, and they also regulate the cellular function. TCM holds that hepatic fibrosis is mainly caused by blood stasis, which manifests chiefly by symptoms such as hepatomegaly, splenomegaly, expanded venation on the abdominal wall, blood nevi , liver palm , and wiry, unsmooth pulse. Medicines which promote blood circulation to remove blood stasis are effective in treating these disorders and have been applied widely. Benefit Liver Granules is an effective drug for treatment of chronic hepatopathy prepared by professor Yao Xixian and his colleagues, consisting of high doses of Chinese herbal medicines for promoting blood circulation to remove stasis, such as salvia and tang-kuei.
It possesses the effects of improving symptoms of chronic hepatopathy, lowering transaminase, subsiding jaundice, softening the liver, and shrinking the spleen. One of the proposed mechanisms is to inhibit the hepatic stellate cells that proliferate and contribute substances to the hepatic extracellular matrix, forming the fibrotic mass. HSC apoptosis would be helpful in reverting liver fibrosis. The effect of IH764-3 in different concentrations on HSC proliferation was observed in this study. The results showed that IH764-3 is effective in obviously inhibiting HSC proliferation. The apoptotic rate of HSC as revealed with brown staining in the IH764-3 group was significantly higher than that in the blank control group.
The review article in the Journal of Integrated Traditional and Western Medicine relays information from articles published from 1992-2001. It concisely mentions test methods and results with some complex formulas, single herbs, and active components. 30 patients with chronic hepatitis B. 104 patients with chronic hepatitis B.
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The laboratory studies described here are especially relevant to acute processes of liver damage, but don’t readily address the problem of chronic liver disease. The clinical studies involved patients with advanced hepatitis B disease, the most common chronic hepatovirus infection that occurs in the Chinese population. There is no reason to believe that the effects would be any different with hepatitis C. Treatment times for clinical evaluations ranged from a minimum of three months up to a maximum of three years. Unless the underlying cause of liver fibrosis is removed, the treatment may need to be continued indefinitely, or, at the least, repeated from time to time.
Imperfections in the research methodology and reporting limit the interest that can be generated among researchers outside China to pursue the Chinese herb treatment of liver fibrosis in greater detail. However, Chinese researchers have already provided adequate data on the effects of salvia to justify further expenditure on research in this area. The main features of acute liver failure are rapid-onset jaundice, weakness, and eventually, changes in mental status that can begin as mild confusion but progress to coma. In ALF, hepatic encephalopathy leads to cerebral edema, coma, brain herniation, and eventually death. Detection of encephalopathy is central to the diagnosis of ALF.
Unfortunately, signs of elevated intracranial pressure, such as papilledema and loss of pupillary reflexes, are not reliable, and occur late in the disease process. Coagulopathy is another cardinal feature of ALF. The liver has the central role in the synthesis of almost all coagulation factors and some inhibitors of coagulation and fibrinolysis. ALF patients fulfil the criteria for systemic inflammatory syndrome irrespective of presence or absence of infection. This often contributes towards multi organ failure. Hyperdynamic circulation, with peripheral vasodilatation from low systemic vascular resistance, leads to hypotension. Severe lung injury and hypoxemia result in high mortality.
Most cases of severe lung injury are due to ARDS, with or without sepsis. In late pregnancy liver function decreases significantly, which can be easily monitored by blood tests. Early clinical manifestations of ALF in late pregnancy include hypodynamia, decrease in appetite, dark amber urine, deep jaundice, nausea, vomiting, and abdominal distention. Among patients whose deaths were attributed to ALF in late pregnancy, the majority had experienced vaginal deliveries.
All patients with clinical or laboratory evidence of moderate to severe acute hepatitis should have an immediate measurement of prothrombin time and careful evaluation of mental status. ALF should be strongly suspected, and hospital admission is mandatory. History taking should include a careful review of possible exposures to viral infection and drugs or other toxins. From history and clinical examination, the possibility of underlying chronic disease should be ruled out as it may require different management. A liver biopsy done via the transjugular route because of coagulopathy is not usually necessary, other than in occasional malignancies. ICU, or whether to transfer the patient to a transplant facility. The diagnosis of acute liver failure is based on physical exam, laboratory findings, patient history, and past medical history to establish mental status changes, coagulopathy, rapidity of onset, and absence of known prior liver disease respectively.
The exact definition of “rapid” is somewhat questionable, and different sub-divisions exist which are based on the time from onset of first hepatic symptoms to onset of encephalopathy. One scheme defines “acute hepatic failure” as the development of encephalopathy within 26 weeks of the onset of any hepatic symptoms. Because ALF often involves the rapid deterioration of mental status and the potential for multiorgan failure, patients should be managed in the intensive care unit. For patients not at a transplant center, the possibility of rapid progression of ALF makes early consultation with a transplant facility critical. II encephalopathy should be transferred to a liver transplant facility and listed for transplantation. Increased cardiac output and low systemic vascular resistance are characteristic of ALF.
Pulmonary artery catheterization should be considered. Pulmonary edema and pulmonary infections are commonly seen in patients with ALF. However, positive end-expiratory pressure can worsen cerebral edema. Impaired liver synthesis of clotting factors, low-grade fibrinolysis, and intravascular coagulation are typical of ALF. Thrombocytopenia is common and may also be dysfunctional. Replacement therapy is recommended only in the setting of bleeding or prior to an invasive procedure.
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Vitamin K can be given to treat an abnormal prothrombin time, regardless of whether there is poor nutritional status. In patients with grade I or II encephalopathy, enteral feeding should be initiated early. Parenteral nutrition should be used only if enteral feeding is contraindicated as it increases the risk of infection. Defective cellular and humoral immunity as well as presence of indwelling catheters, coma, broad-spectrum antibiotics, and medications that suppress immunity all predispose to infection.
In addition to transplantation, better critical care and the trend toward more benign causes, such as acetaminophen, all contribute to improved survival rates. Intravenous N-acetylcysteine has been found to be beneficial in both acetaminophen toxicity and non-acetaminophen-related acute liver failure. In recent years the advent of liver transplantation and multidisciplinary intensive care support have improved survival significantly. Several prognostic scoring systems have been devised to predict mortality and to identify who will require an early liver transplant.
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To date, no universally accepted nomenclature has been adopted. Trey and Davidson introduced the phrase fulminant hepatic failure in 1970, which they described as a ” potentially reversible condition, the consequence of severe liver injury, with an onset of encephalopathy within 8 weeks of the appearance of the first symptoms and in the absence of pre-existing liver disease”. Acute liver failure: redefining the syndromes”. Hepatic encephalopathy: An update of pathophysiologic mechanisms”. Brain edema in liver failure: basic physiologic principles and management”. Complications of intracranial pressure monitoring in fulminant hepatic failure”.
Fulminant and late onset hepatic failure”. The clinical importance of adrenal insufficiency in acute hepatic dysfunction”. Tissue hypoxia during fulminant hepatic failure”. Trewby PN, Warren R, Contini S, et al. Incidence and pathophysiology of pulmonary edema in fulminant hepatic failure”.
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Clinical characteristics of fulminant hepatitis in pregnancy”. Prognostic factors of fulminant hepatitis in pregnancy”. Pattern of necrosis in acute viral hepatitis. AASLD position paper: the management of acute liver failure”. Sleisenger, edited by Mark Feldman, Lawrence S. Early indicators of prognosis in fulminant hepatic failure”.
Acute liver failure: current management and future prospects”. Intracranial hypertension in acute liver failure: pathophysiological basis of rational management”. Moderate hypothermia prevents cerebral hyperemia and increase in intracranial pressure in patients undergoing liver transplantation for acute liver failure”. The effect of hypertonic sodium chloride on intracranial pressure in patients with acute liver failure”. Propofol to control intracranial pressure in fulminant hepatic failure”. Recombinant activated factor VII for coagulopathy in fulminant hepatic failure compared with conventional therapy”. Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society.
A survey of liver transplantation from living adult donors in the United States”. The New England Journal of Medicine. Liver transplantation for fulminant hepatic failure: experience with more than 200 patients over a 17-year period”. Lee WM, Hynan LS, Rossaro L, et al. Intravenous N-acetylcysteine improves transplant-free survival in early stage non-acetaminophen acute liver failure”. Fulminant hepatitis: Mayo Clinic experience with 34 cases”.
Ostapowicz G, Fontana RJ, Schiødt FV, et al. Results of a prospective study of acute liver failure at 17 tertiary care centers in the United States”. The management of fulminant hepatic failure”. Bernuau J, Goudeau A, Poynard T, et al. Multivariate analysis of prognostic factors in fulminant hepatitis B”. Late onset hepatic failure: clinical, serological and histological features”.
This page was last edited on 11 April 2018, at 01:43. What Are the Risk Factors for Pancreatitis? The pancreas is a large gland behind the stomach and next to the small intestine. It releases powerful digestive enzymes into the small intestine to aid the digestion of food. It releases the hormones insulin and glucagon into the bloodstream.
These hormones help the body control how it uses food for energy. Pancreatitis is a disease in which the pancreas becomes inflamed. Pancreatic damage happens when the digestive enzymes are activated before they are released into the small intestine and begin attacking the pancreas. There are two forms of pancreatitis: acute and chronic. Acute pancreatitis is a sudden inflammation that lasts for a short time. It may range from mild discomfort to a severe, life-threatening illness. Most people with acute pancreatitis recover completely after getting the right treatment.
Chronic pancreatitis is long-lasting inflammation of the pancreas. It most often happens after an episode of acute pancreatitis. Heavy alcohol drinking is another big cause. What Are the Symptoms of Pancreatitis? The symptoms of chronic pancreatitis are similar to those of acute pancreatitis.
Patients frequently feel constant pain in the upper abdomen that radiates to the back. In some patients, the pain may be disabling. In most cases, acute pancreatitis is caused by gallstones or heavy alcohol use. Pancreatitis can happen to anyone, but it is more common in people with certain risk factors. Acute pancreatitis may be the first sign of gallstones. Gallstones can block the pancreatic duct, which can cause acute pancreatitis. People with chronic pancreatitis are usually men between ages 30 and 40, but chronic pancreatitis also may occur in women.
In more advanced stages of the disease, doctors may use blood, urine, and stool tests to confirm the diagnosis. People with acute pancreatitis are typically treated with IV fluids and pain medications in the hospital. An acute attack of pancreatitis caused by gallstones may require removal of the gallbladder or surgery of the bile duct. Chronic pancreatitis can be difficult to treat. Doctors will try to relieve the patient’s pain and improve the nutrition problems. Patients are generally given pancreatic enzymes and may need insulin.
A low-fat diet may also help. Surgery may be done in some cases to help relieve abdominal pain, restore drainage of pancreatic enzymes or hormones, treat chronic pancreatitis caused by blockage of the pancreatic duct, or reduce the frequency of attacks. Patients must stop smoking and drinking alcoholic beverages, follow their doctor’s and dietitian’s dietary advice, and take the proper medications in order to have fewer and milder attacks of pancreatitis. Because most cases of pancreatitis are caused by alcohol abuse, prevention is directed at responsible drinking or no drinking at all. American Gastroenterological Association: ”Contrary to Popular Belief, Not All Cases of Chronic Pancreatitis are Alcohol- Induced. National Digestive Diseases Information Clearinghouse: ”Pancreatitis. Diverticulitis Diet Best and worst foods.
How to Live Gluten-Free Learn what foods to avoid. Dietary Fiber Will it help constipation? WebMD does not provide medical advice, diagnosis or treatment. Please confirm that you would like to log out of Medscape. If you log out, you will be required to enter your username and password the next time you visit. The ultrasonogram shows a hyperechoic mass representing hepatocellular carcinoma.