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Long-term control of portal hypertension strategy
Portal hypertension is caused by a variety of reasons obstruction of portal vein blood flow and (or) blood flow, resulting in portal vein and its tributaries blood pressure increased, the formation of collateral circulation with a group of clinical syndromes, including ascites, esophageal variceal bleeding (EVB), hepatic encephalopathy, hepatorenal syndrome, hepatopulmonary syndrome, such as portal hypertensive gastropathy.
Cirrhosis and portal hypertension in China the most common cause. Present study suggests that liver function and hepatic venous pressure gradient Reserve (HVPG) is to determine the complications of portal hypertension an important factor; 50% of patients with decompensated cirrhosis esophageal varices does not occur within 10 years, and the other low incidence of complications ; and gastric varices was 20% to 25%. Electronic endoscopy esophageal varices is the most reliable screening method. Decompensated cirrhosis patients with an average survival time of 12 years, mostly cause of death or liver decompensation occurs independent; decompensated cirrhosis patients with an average survival of 2 years. In general, from compensation to decompensation of development, the annual incidence rate of 5% to 7%.
Of decompensated cirrhosis and portal hypertension indicators (such as varicose veins, platelets, spleen size, Î³ globulin) is an important indicator of mortality prediction; and decompensated cirrhosis, circulatory dysfunction, the occurrence of liver cancer is predicted important indicator of death. Child-Pugh Evaluation of liver reserve function is still relatively good indicator.
First, clinical therapy of
Treatment of portal hypertension the main purpose is to combat EVB. With drugs, endoscopic therapy of portal hypertension and the progress of basic research, the case fatality rate 6 weeks EVB dropped to 20%.
Surgical procedures (including the transjugular intrahepatic portosystemic shunt) to a certain extent can reduce portal pressure, prevention of complications related to portal hypertension. However, hepatic encephalopathy, rebleeding and mortality was no significant difference in terms of the patient's long-term prognosis has not changed. Endoscopic therapy [including endoscopic band ligation (EVL) and endoscopic variceal sclerotherapy (EIS)] is an effective treatment for EVB. The shorter the interval between EVL, varicose veins disappear faster, and repeated treatment in patients with poor compliance. Clinical studies have shown that, EVL, EIS and tissue adhesive effect of controlling acute EVB similarity with somatostatin and its analogues; EVL as high efficacy, re-bleeding rate and adverse reactions that better than EIS, but mortality and long-term prognosis no significant difference. Propranolol or EVL alone a non-selective Î²-blocker (EVL) is an effective method of prevention of variceal bleeding, liver disease in 2008 Societ
Second, hepatic stellate cells and portal hypertension
The past 20 years studies have shown: the activation of hepatic stellate cells (HSC) in the regulation of sinusoidal blood flow in intrahepatic resistance and play an important role. HSC activation of smooth muscle cell-like characteristics with by the regulation of a variety of vasoactive substances. Therefore, activation of HSC as a target for drug long-term adjustment to provide a basis of portal vein pressure.
1. HSC and vascular dilatation of gaseous molecules
Present the view that the resistance increase was mainly due to liver vasoactive substances in the liver and metabolic imbalance generated. Sinusoidal NO deficiency and increased contraction of vasoactive substances, HSC relaxing factor on the reactivity of vascular damage, sensitivity decreased, both resistance increased in the portal vein plays a very important role. In animal models of liver cirrhosis decreased NO levels, NO was mainly due to the absence of endothelial nitric oxide synthase (eNOS) activity decreased. NO impact on how H2S? Some studies showed that a single vasodilator with effects caused by H2S is very weak, and in the presence of NO vasodilatory effect of an increase of 13 times. The one hand, NO can increase vascular smooth muscle cystathionine-Î³-lyase (CSE) activity; the other hand, NO can also directly increase the level of smooth muscle transcription of CSE, which increased the expression of CSE. These results suggest that NO may promote HSC synthesis and secretion of H2S.
The results show that, CO and H2S vascular smooth muscle cells by regulating vasomotor, proliferation and apoptosis, the process involved in the pathogenesis of hypertension. Hypoxic pulmonary hypertension in rat pulmonary artery smooth muscle cells of H2S can be increased synthesis and secretion in the level of CO, CO given after the substrate was significantly inhibited vascular smooth muscle cells in the H2S levels, CSE mRNA transcription was significantly reduced, suggesting that CO on artery pressure in hypoxic vascular smooth muscle cells play an inhibitory H2S/CSE system. Cirrhotic portal hypertension in the pathogenesis of whether a similar regulatory role, remains unclear.
Portal hypertension in liver cirrhosis, the liver H2S sources, CSE activity and its expression is still worth studying. In short, in-depth study H2S, NO and CO and mechanism of the relationship between portal hypertension may be the prevention and treatment to bring the new strategy.
2. HSC express a variety of vasoactive receptor
The regulatory mechanism of hepatic microcirculation is very complicated, HSC on the regulation of hepatic sinusoidal microcirculation plays an important role. HSC activation has the characteristics of vascular smooth muscle cells by a variety of vasoactive substances (such as endothelin, NO, etc.) of the regulation and expression of its receptor, such as the endothelin receptor. Also seen under the microscope sinusoidal contraction caused by endothelin and prove sinusoidal HSC contraction and fluorescence area is part of the same. Our results show that activated HSC also express somatostatin receptors (SSTR1-5), somatostatin can inhibit the contraction of endothelin on the role of HSC for clinical application of somatostatin in the treatment of portal hypertension provided a theoretical basis. Valerian angiotensin receptor antagonist 2 yarn resistance and Tanzania to reduce intrahepatic portal vein pressure, also shown exciting results.
Third, long-term control of HSC as the target portal vein pressure
Although portal hypertension in clinical and basic research has made great progress, prevention and treatment has greatly improved, but so far still no liver cirrhosis and portal hypertension ideal control methods. For advice and treatment of mild varicose veins are varicose veins in patients with cirrhosis with drugs to prevent the occurrence, the current lack of reliable clinical control study. Available data show that propranolol does not prevent the occurrence of varicose veins to develop. However, in theory, continue to reduce portal pressure, which can effectively prevent, treat cirrhosis and portal hypertension related complications. Therefore, the long-acting somatostatin analogues or other antihypertensive drugs (propranolol, valerian yarn Tanzania, etc.) may be combined with long-term effective control of portal hypertension hope. However, portal vein thrombosis or fibrosis of liver failure is the effect of lowering portal pressure drugs an important factor, is another challenge facing clinicians. The activation of HSC self-secrete a variety of vasoactive substances, and are subject to the regulation of these substances affect the intrahepatic resistance and portal pressure, therefore, it may be long-term control of portal pressure targets.
Fourth, monitoring and evaluation of portal pressure
The current lack of clinically effective, non-invasive means of monitoring of portal pressure, therefore, the evaluation of various therapeutic agents difficult. Although HVPG to predict whether portal hypertension-related complications occurred and the evaluation of portal pressure reduction ideal indicators of drug efficacy, but there are some traumatic, patient compliance is poor. Interestingly, in 2006 the annual meeting of the European liver disease, some experts reported, the use of non-invasive method of liver stiffness measurement can reflect the HVPG. FibroScan can be non-invasive, rapid and repeated measurements of liver stiffness, evaluation of portal hypertension may be a good way.
- Source: Health News 2004.09.23 Version 7
The eyes of the majority of patients, portal hypertension is indeed a rather abstract concept, which the body in front of the portal vein is a vein? High portal pressure is how it formed? When should treatment? Should be treated?
Increased portal pressure is the body to maintain an important compensatory mechanism of liver function
Portal vein is the blood of the gastrointestinal tract into the liver, a vital channel for exchange, the liver is an essential nutrient structure, blood flow within the various nutrients contained in the negative to maintain normal liver function is an important condition. Cirrhosis, the liver vascular channels increased resistance, portal venous blood returning through the liver when blocked, this time, the body will be reflected through a series of mechanisms to significantly increased portal pressure, portal vein blood to ensure the "smooth" and nutrition into the liver. We can easily imagine, liver cirrhosis, if there is no corresponding increase in portal pressure, then the portal vein into the liver is significantly reduced, which is not conducive to the maintenance of liver function. Can be seen, when cirrhosis increased portal pressure is the body to maintain perfusion of liver sclerosis important compensatory mechanism for the maintenance of liver function is necessary.
Increased portal pressure is the "double-edged sword"
Cirrhosis, portal pressure increased as the body to maintain the stability of its essential function, but also harmful, it is a "double-edged sword."
In general, patients with chronic liver disease can be broadly divided into three stages: stage of chronic hepatitis, cirrhosis and portal hypertension phase. Three phases with each other, overlap, there is no clear boundary between.
In chronic liver disease stage, the disease is mainly sustained damage to liver cells and liver fibrosis caused by structural damage. At this point, the liver venous access has not changed obviously, no significant increase in portal pressure. In general, develop into liver cirrhosis from viral hepatitis requires a longer period of time, 10 to 30 years. From the clinical point of view, the rate of hepatitis C cirrhosis compared with hepatitis B faster.
Continued development of liver inflammation, fibrosis and further increase on to the liver cirrhosis stage, this time, a significant hardening of the liver occurs, the liver's portal vein to become distorted and narrow, blood flow increased significantly by the resistance, portal venous pressure began to increase, and gradually increased. This stage in time the most difficult to define, depending on the length of time each of the stability of liver function differ.
When cirrhosis develops to a certain extent, then enter the portal hypertension phase. Portal pressure continues to rise, the inevitable happened esophagus - gastric varices, splenomegaly and hypersplenism. When the further development of the disease, primary peritonitis occurs, recurrent ascites or refractory ascites, many patients will emerge even recurrent esophageal - gastric variceal bleeding. With the gradual decline in liver function, patients with liver failure often occurs, or hepatic encephalopathy, or even liver cancer.
We can see that for a long time in patients with cirrhosis has been able to maintain liver function, portal pressure and a compensatory increase are inseparable. However, the continued increase in portal pressure, cirrhosis of the liver has become more complicated and critical condition late the direct cause.
Surgical treatment of portal hypertension mainly for the serious complications of cirrhosis rather than its own in the early and mid-term, even if there is portal hypertension, due to rarely cause bleeding esophageal varices, splenomegaly with hypersplenism, ascites, and other serious complications, medical treatment should be based, including the protection of liver cells, anti-virus, prevention and treatment of liver fibrosis. With the development of liver cirrhosis, portal hypertension persists, a serious complication of the above would have appeared. At this point, medical treatment alone is not enough to improve the condition and need surgical treatment or endoscopic therapy and other means.
The main objective of surgical treatment of portal hypertension is the prevention of serious complications, not the treatment itself. Surgical treatment of the most basic and most common surgical resection is the spleen breaking of pericardial blood vessel surgery. Splenectomy for hypersplenism effectively improve the situation, so that the peripheral blood platelet and white blood cell count rose to normal levels; breaking of pericardial blood can maximize prevention of esophageal surgery - variceal bleeding, so that patients rebleeding to minimize the possibility.
Of course, surgery on the stability or recovery of liver function also has a certain role, such as through the removal of the spleen, hypersplenism improved conditions, can effectively prevent the occurrence of primary peritonitis, which is the stability of liver function is good for prevent the development of cirrhosis of the liver is also a role. Through the prevention of upper gastrointestinal bleeding, also the maximum to avoid the bleeding and even liver damage caused by the body.
Visible, portal hypertension surgery to treat complications although the role is the emergence of a stable liver function but it also has a crucial role. Because, if not timely surgical treatment, patients often because of complications of portal hypertension in liver function and lose, or even catch a life.
"Higher on the Treatment of" tragedy brewing
Clinically, patients with portal hypertension due to lack of the correct understanding of the pathophysiology, treatment of the tragedy are not uncommon. Many patients in the portal vein pressure is not too high, accept the shunt surgery, the portal vein pressure was significantly reduced, the portal vein on liver perfusion sharp decline, resulting in liver function rapidly deteriorated; there are some patients, although the portal vein pressure is high blood pressure does need some measures, but because of excessive portal pressure reduced, overkill, treatment counterproductive. Had a patient, male, 37 years old, because of cirrhosis and portal hypertension at a local hospital line splenorenal shunt, after 1 month that there is a clear hepatic coma, can lead to half a day to eat eggs, half consciousness, And the trend of more severe symptoms. March 2004 to hepatobiliary surgery treatment in our hospital, our patient's condition based on combined years of clinical experience in treatment of similar patients, that the rapid deterioration of liver function in patients with mainly related to inadequate shunt decisively to implement the operation for patients . Intraoperative findings in patients with portal pressure has been reduced to near normal levels, portal vein blood by a thick split-channel "steal" away the blood of the portal vein into the liver, almost zero, the liver because of the lack of adequate blood supply going to get small and hard. The diversion channel will be closed, the portal vein pressure increased to half the normal level, portal vein perfusion of the liver restored. Postoperative recovery was smooth, hepatic coma symptoms, liver function also improved significantly.
It is worth mentioning, like the above example not only for individual patients, but rather more common. These patients have such a common law because of cirrhosis and portal hypertension occurred in upper gastrointestinal bleeding and other complications, received shunt for treatment of different forms of liver function after 3 to 5 years showed a rapid deterioration of the trend, until a ascites, hepatic coma and other symptoms of liver dysfunction. The triage patients over 3 years after receiving a timely manner to correct, liver function decline under control, it is lucky.
Beijing Railway General Hospital, Chief Physician Sun Wenbing article entry: cross-flow sea Editor: lyw
First, the knowledge portal system
1. Portal overview
2. Extrahepatic portal venous system
3. Intrahepatic portal venous system
4. And the portal vein system related to important organs
Second, liver cirrhosis causes of portal hypertension
1. Viral Hepatitis
3. Autoimmune hepatitis
4. Long-term or repeated cholestatic biliary tract infection
5. Chronic alcoholic liver injury
6. Genetic and metabolic liver disease
7. Drug induced liver injury
8. Congestive liver disease
9. Other rare causes
Third, portal hypertension the natural history
1. Liver disease "trilogy"
2. Sick why hardened liver
3. Cirrhosis of the early signals
4. Why can form liver cirrhosis and portal hypertension
5. How to diagnose portal hypertension
Fourth, tests and checklists on portal hypertension
3. Stool routine
4. Liver function
5. Renal function
6. Electrolyte Check
7. Prothrombin time and activity
8. Oral glucose tolerance test
9. Indole indocyanine clearance test
10. Protein electrophoresis test
11. Liver fibrosis
12. Serum virus markers check
14. Upper gastrointestinal barium meal
18. Computed tomography
20. Radionuclide scan
21. Digital subtraction angiography
22. Liver biopsy
Five portal hypertension which affect the body 0 to
1. Esophageal varices a
2. Splenic enlargement and hypersplenism
3. Intestinal flora and gastrointestinal disorders
4. Chronic pancreatitis
5. Lung dys
6. Hepatorenal syndrome
7. Central nervous system damage
8. Refractory ascites
9. Acute peritonitis
10. Lead to the production of liver cancer
Six are likely to cause esophageal and gastric variceal bleeding a factor
1. Liver function is good or bad the impact of
2. The harm caused by improper diet
3. To avoid the risk of various infections caused by circumstances
4. To establish the importance of good daily habits
5. Attention to emotional changes
6. Learn to judge the results of gastroscopy
Seven, the psychological characteristics of patients with liver disease
1. EDITORIAL words
2. The source of psychological stress
3. In response to psychological stress
4. Common psychological type of liver disease
Non-surgical treatment articles
Preparation before surgery articles
After surgery articles
Appendix commonly used indicators of the normal value and significance of inspection