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Arch Intern Med. Even though portal hypertension can result from prehepatic alterations portal vein or splenic vein hypertension, posthepatic alterations Budd-Chiari Syndrome, or non-cirrhotic intrahepatic causes schistosomiasis, sinusoidal obstruction syndrome, hepatic cirrhosis is the most common cause of portal hypertension and thus is the most widely studied.
A hepatic venous pressure gradient HVPG of 10 mmHg or higher has been documented to identify a group of patients with a more aggressive clinical course, such as the development of gastric and esophageal varices, clinical decompensation the development of ascites, variceal hemorrhage, and encephalopathy, complications after hepatic resection decompensation or death thereafter, and the development of hepatocellular carcinoma.
Variceal bleeding in the cirrhotic patient is the most direct complication of portal hypertension and results in a high morbidity and mortality rate. However, recent data suggest an improvement in these indicators through the advances in prophylaxis and treatment, when compared with previously reported studies.
There are no data corresponding to the Mexican health system, but similar or worse figures could be expected, given the lack of available guidelines in Spanish. The information in this area has been managed largely through consensus conferences among experts in which the events and outcomes have been defined and the existing evidence has been carefully reviewed, resulting in practical recommendations.
The first of these conferences took place in 1986 in Groningen, Holland, and since then these reunions have alternated between Europe the Baveno conference and the United States the American Association for the Study of Liver Diseases.
This situation illustrates the growing need for a Mexican Consensus with guidelines based on the best current evidence for the management of patients presenting with portal hypertension.
This consensus in Spanish aims to improve the clinical practice regarding portal hypertension in Mexico. Methodology In the first stage, a working committee was formed that proposed the consensus methodology and elaborated a basic questionnaire.
This preliminary document was then transformed into the final version of the "Portal Hypertension Treatment Guidelines". This committee included Mexican specialists in gastroenterology, endoscopy, and hepatology.
The basic questionnaire formulated by the working committee was made up of statements that examined the following 3 modules of knowledge: preprimary and primary prophylaxis, acute hemorrhage, and secondary prophylaxis.
These statements were reviewed, discussed, and finally approved during the work meetings, and in this manner the basis for writing the future treatment guidelines was laid out. The answers with a score of 6 or higher were regarded as being "in agreement" with the statement.
At this meeting, the coordinators presented the statements to be evaluated for the final consensus.
Those in which there was no consensus were defined as "no agreement" and put on hold until the availability of further scientific evidence.
First module. Preprimary and primary prophylaxis in portal hypertension Introduction Portal hypertension, pressure above 5 mmHg, causes the development of esophageal varices EV.
These are regarded as one of the most important complications; they form portosystemic collaterals that are responsible for variceal bleeding.
Even with current treatments, the morbidity and mortality associated with this condition is high, emphasizing the need for more effective preventive treatment.
The increase in resistance is as much structural distortion of the hepatic vascular architecture from fibrosis and regenerative nodules as it is dynamic with myofibroblast contraction, stellate cell activation causing an increase in vascular tone due to endothelial dysfunction and a decrease in the bioavailability of nitric oxide, and an elevated activity in endogenous vasoconstrictors such as endothelin, alpha-adrenergic stimulus, and angiotensin, among others.
In addition, there appears to be an elevated expression of angiogenic factors in the splanchnic vasculature, as the expression of VEGF.
Risk for bleeding is closely correlated with the degree of portal pressure. Clinical course and outcome Variceal bleeding is the last step in a series of events that begin with an increase in portal pressure, followed by the development and progressive dilatation of varices until they finally burst and bleed.
This system demonstrated high specificity for predicting variceal bleeding, but it was not sensitive and had a low positive predictive value.
The Child-Pugh score has been shown to systematically have an influence on the progression of EV, but the advance of hepatic disease and consequently that of portal hypertension appear to be the most important factors.
One study found a significantly higher HVPG in those patients that developed variceal bleeding 20.