[Treatment and prevention of portal hypertension in patients at elderly and senile patients].

The most significant complication of cirrhosis is portal hypertension syndrome. Varicose veins of the esophagus and stomach diagnosed in 50 - 80% of patients with liver cirrhosis and complicated by hemorrhage in 30 - 50%. Course, treatment and management of patients with portal hypertension in elderly people is poorly understood.

[Features of the HCV-infection in the elderly patients].

The problem of chronic HCV-infection in the elderly patients is poorly known. During the HCV-infection and progression of fibrosis in chronic liver diseases depends on age of the patient.

[Fundoplication as prophylaxis of reflux-esophagitis in patients with varicose esophageal veins].

AIM: To investigate the condition of esophageal mucosa (EM) before and after surgical and endoscopic treatment of varicose esophageal veins (VEV). MATERIAL AND METHODS: EM was examined in 100 patients (64 males and 36 females aged 33-74 years, mean age 528 +/- 5.7 years) with hepatic cirrhosis (HC). Of them, 80 patients have undergone endoscopic ligation of the esophageal veins, 20 patients--surgical disconnection of the azigoportal blood flow according to the original method with additional fundoplication. All the patients had intrahepatic portal hypertension caused by HC of different etiology. RESULTS: Before operation, 70% patients had inflammation-induced alterations of the EM of different severity. Endoscopic ligation of the esophageal veins did not change the rate of EM inflammation detection. In operated patients reflux-esophagitis was detected significantly less frequently. CONCLUSION: The above results show efficacy of fundoplication as a method of esophagitis prevention. Esophagitis is one of VEV hemorrhage risk factors. Fundoplication is not easy to make and is not indicated for all HC patients, especially in urgent situations. However, in case of decision to operate for prevention of VEV hemorrhage, it is advisable to conduct fundoplication.

[The state of the vascular bed of the small intestine in patients with portal hypertension].

AIM: To evaluate the condition of vascular channel of small bowel in patients with portal hypertension. MATERIALS AND METHODS: We examined 60 patients from 17 to 70 years, 30 with cirrhosis of different etiologies and 30 with other gastrointestinal diseases, amounted control group. Patients were divided into 2 groups: the main and control: group 1--primary--patients with cirrhosis and portal hypertension. Group 2--control--patients without liver disease and portal hypertension who underwent videocapsule endoscopy. RESULTS: On the results of research, we can conclude that all patients with liver cirrhosis and portal hypertension have various vascular changes of small bowel. We examined patients in the course of the work revealed the following: 1. Varicose vein expansion and increased vascular pattern in 70% of patients. 2. Arteriovenous malformation in 12% of patients. 3. Angiodisplaziya 11%. 4. Delafua defect in 4%. 5. Bleeding in 3%. The combination of vascular disease in patients with liver disease and portal hypertension syndrome accounted for 70%. In the control group of patients vascular channel pathology dated only in 2% of cases in the form of strengthening of vascular pattern of small bowel. CONCLUSION: Videocapsule endoscopy is a highly informative diagnostic method for assessing the condition of vascular channel of the intestine in patients with portal hypertension. Carrying out videocapsule endoscopy is highly effective and comfortable for patients, which greatly improves their quality of life. Timely detection of vascular disease in patients with portal hypertension using videocapsule endoscopy can prevent such severe complications as gastrointestinal bleeding especially from the deep divisions of bowel which are not available to other research methods.

[Capillary collusion of gastric mucosa in patients with Helicobacter pylori gastritis and portal hypertension].

INTRODUCTION: Prominent mucosal vasodilatation mediated by increased production of nitric oxide is thought to be manifestation of portal hypertensive gastropathy (PHG) in patients with chronic diffuse liver diseases. Recently was shown that Helicobacter pylori (Hp) infection could stimulate nitric oxide activity. AIM: To investigate if chronic Hp infection is involved in development of gastric mucosal capillary dilatation in patients with PHG. METHODS: The study was performed on 56 patients with PHG evaluated by upper endoscopy. The gastric biopsy was obtained from antrum and corpus. Hp status was assessed by rapid urease test and histology. Gastric mucosal capillary network (GMCN) assessed on histological sections immunostained for CD34, specific marker for endothelial cells. Nikon-CP995 camera and digital image analyzing system (DMI-1) was used for morphometry. RESULTS: Marked vasodilatation was observed in antrum mucosa of Hp- patients with PHG and Hp+ patients without PHG (p < 0.05), relative volume of vessels was also increased, but number of vessels was not changed significantly. The relative volume and number of vessels in corpus mucosa were significantly higher in Hp- with PHG and Hp+ without PHG (p < 0.01). The mean size of vessels in corpus mucosa was decreased in Hp- with PHG (p < 0.05), but was not changed in Hp+ patients. Morphometric parameters in Hp+ with PHG was not changed significantly as compared to Hp+ without PHG or Hp- patients. CONCLUSION: Hp provokes the same morphometric changes in GMCN as PHG. Hp may be one of factors important for regulation of GMCN function and structure. No additive effect between Hp infection and PHG on GMCN was observed in patients with PHG.

[Conservative treatment of patients with varicose esophagus veins cirrhosis].

UNLABELLED: The most significant complication of liver cirrhosis is the syndrome of portal hypertension. Varicose veins of the esophagus and stomach diagnosed in 50-80% of patients with liver cirrhosis and complicated by hemorrhage in 30-50%. The risk of bleeding is determined by the size of varicose veins, severity of liver cirrhosis, severity of inflammatory changes of esophageal mucosa. Conservative treatments don't always yield the desired result, which motivates the search for new pharmacological treatments of portal hypertension complications. OBJECTIVE: To evaluate the effectiveness of flavonoids diosmin with hesperidin using at liver cirrhosis with varying degrees of portal hypertension severity. MATERIALS AND METHODS: The study was based on the analysis of complex clinical, laboratory and instrumental examination of 125 patients with cirrhosis of different etiologies. The study didn't include patients with the presence of VEV III degree; hepatocellular insufficiency C class on the Child-Pugh classification; extrahepatic form of portal hypertension and patients with circulatory failure requiring continuous drug therapy. The ratio of male and female studied patients was 71 (56.8%) and 54 (43.2%), respectively, at the age of 33 to 74 years (mean age 52.8 +/- 5.7 years). According to etiology of the disease, all patients were divided into two groups. The first group included 82 (65.6%) patients, the cause of the LC was the abuse of alcohol, second group--43 (34.4%) persons with a viral etiology of LP (HBV or HCV). Endoscopic assessment of the VEV was perfomed by KJ Paquet classification (1983). All patients received therapy with flavonoids (diosmin with hesperidin) for 12 weeks. Efficacy of treatment was evaluated by endoscopic picture of the esophageal mucosa and the state of VEV at 4 and 12 weeks. RESULTS: Treatment with the flavonoids hesperidin with diasminom showed a positive result in the form of reducing the VEV and reduced the number of varicose veins with a statistically significant in patients with alcoholic liver cirrhosis (p < 0.05). CONCLUSION: The results indicated the effectiveness of therapy with flavonoids hesperidin with diasmin at portal hypertension in patients with alcoholic cirrhosis, which allows to include them in the complex treatment of medicamental prophylaxis of variceal bleeding.

[Cellular renewal of the gastric mucosa in patients with chronic gastritis and portal hypertension].

UNLABELLED: Portal gastropathy is common finding in patients with portal hypertension (PH) caused by liver cirrhosis, but influence of H. pylori on pathogenesis and natural history of this lesion is still not completely cleared up. The goal of the study was to evaluate histological changes in gastric mucosa at the patients with liver cirrhosis and portal hypertension and to establish role of H. pylori in development of portal gastropathy and related atrophy of gastric mucosa. The gastric biopsy was obtained from 54 patients (36 men and 18 women) in the age from 22 till 73 years. The diagnosis of liver cirrhosis was confirmed at 39, and chronic hepatitis at 15 patients. H. pylori was revealed in 37 patients. Four groups of the patients were discharged: I - 11 patients without attributes PH; II - 12 patients with PH, but without esophageal varicose phlebectasia; III - 17 patients with a varicose phlebectasia of esophagus - grade I, and IV - 14 patients with a varicose phlebectasia of esophagus - grade II. Proliferative activity in gastric mucosa was evaluated by immunostain for Ki-67. Patients from group III had more prominent inflammation, but only 35% of them were H. pylori (+). Gastric mucosa atrophy was frequently observed in this group. Severe atrophy of gastric mucosa was detected in patients in group IV but they had less activity of gastritis and only 29% of them were H. pylori (+). Nonmetaplastic type of atrophy was dominated in patients with portal hypertension. Proliferative activity in antral portion of gastric mucosa was decreased from 55% in group II to 23% in group-IV (P <0,01), but proliferation remained on the same level in corpus mucosa. Cellular proliferation had positive correlation with inflammation grade in groups II and III (P <0,05). The negative correlation of cellular proliferation with glandular atrophy was detected in patients with severe PH. Local discirculation, which depends on infringement of vascular permeability in gastric mucosa at patients with PH, may abolish trophic effect of gastrin and decrease cell proliferation activity. CONCLUSION: The downstroke of cellular proliferation in gastric mucosa at patients with severe PH cause nonmetaplastic type of atrophy. H. pylori promotes faster development of glandular atrophy in gastric mucosa at early stages of PH via exacerbation of inflammatory mechanisms.