Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Portal hypertensive gastropathy (PHG) is characterized by changes in the endoscopic appearance of the gastric mucosa, specific for portal hypertension. The identification of the elementary lesions of PHG allowed the development of a reproducible classification, defining mild and severe pictures, and the execution of a natural history study. This study showed a 80% overall prevalence of PHG in patient with cirrhosis of the liver and a correlation between duration of the disease and development of PHG. PHG has often been shown to be a fluctuating condition, thus suggesting that its pathophysiology is not only related to portal hypertension, but also to other, yet unknown, factors. Bleeding from PHG did not occur in patients with a recent diagnosis of liver cirrhosis. Acute and chronic bleeding occurred in 2.5% and 12% of patients, respectively. The death rate from acute PHG bleeding was lower (12.5%) than the death rate of variceal bleeding (39.1%). Vasoactive drugs can be used in the treatment of acute PHG bleeding. For chronic bleeding, non selective 13-blockers and, if needed, iron, are the treatment of choice. TIPS or surgical portosystemic shunt may be considered for acute or chronic PHG bleeding, if medical treatment fails. Clinical controlled trials are needed to evaluate the efficacy of these or other treatments.
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PMID:[Portal hypertensive gastropathy in patients with cirrhosis of the liver]. 1182 93

Portal hypertensive gastropathy (PHG) and duodenopathy (PHD) are frequent in patients with cirrhosis, both are a dynamic condition that can progress from mild to severe and vice versa or even disappear completely. This study included 300 individuals classified into three groups. G I included 116 patients with mixed liver pathology (post-viral cirrhosis and post-Bilharzial fibrosis). G II included 84 patients with pure post hepatitic viral cirrhosis. Hundred healthy individual of comparable age and sex serving as control group. Upper endoscopic examination was done for all groups; gastric varices, gastric congestion and duodenal congestion were detected in 12%, 19.5% and 14.5%, respectively in Gs I & II with statistically significant difference when they were compared to controls (P- < 0.01). In conclusion, high prevalence of PHG and PHD in cirrhotic patients was either due to post-viral cirrhosis or mixed pathology.
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PMID:The prevalence of portal hypertensive gastropathy and duodenopathy in some Egyptian cirrhotic patients. 1558 17

The aim was to evaluate the predictability of portal diameter (PD) in the diagnosis of esophageal varices (EV) and of large size EV (F3EV) in a large series of patients with cirrhosis. Two-hundred sixty-six persons with cirrhosis (M:F = 153:113; mean age 65.4 +/- 10 y) were studied by abdominal sonography and upper endoscopy. Portal hypertensive gastropathy (PHG) was found in 16.1% and EV was found in 60.9% of patients. Only Child's class (B vs. A: OR 3.4, p < 0.0001; C vs. A: OR 10.3, p < 0.0001; C vs. B: OR 3.1, p = 0.01) and age (OR 1.04, p = 0.03) were independent predictors of EV, whereas PD was not (p = 0.4). Child's class and age were also the only independent predictors of F3EV. Mean PD showed a slight and not significant increase in PHG patients compared with patients with negative endoscopy, a reduction in F1EV patients and then a progressive increase in F2EV and F3EV patients. Patients with PD <12 mm showed a significantly higher prevalence of F1-F2EV (p < 0.05) and a near-significant lower prevalence of endoscopies negative for EV (p = 0.06) than patients with 12 < or = PD < or = 13 mm. PD was not able to predict EV or F3EV in a large series of patients with cirrhosis. The oscillatory trend of PD, proceeding from patients with negative endoscopy to F3EV patients, seems to indicate that EV may unload portal pressure in the initial phases of portal hypertension.
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PMID:Portal diameter in the diagnosis of esophageal varices in 266 cirrhotic patients: which role? 1733 12

Portal hypertensive gastropathy (PHG) is a pathological process in the gastric mucosa (GM) that develops due to portal hypertension (PH) and bears a high risk of hemorrhage. Eradication of esophageal varicose veins (EVV) is one of important factors influencing the course of PHG. The purpose of this study was to investigate the course of PHG after eradication of EVV in patients with hepatic cirrhosis (HC). Fifty-two HC patients (39 men, 13 women, mean age: 56.5 years), who underwent EVV ligation, were included in the study. The number of patients with PHG increased three months after EVV ligation; the severity of EVV also increased. The course of PHG differed depending on the time of its onset after surgery. Patients who had not had PHG before EVV ligation developed its signs in 75% of cases. In 31.3% of these patients PHG was resolved, while in 43.6% it did not change during the whole term of observation. In patients who had had PHG before EVV ligation, the latter resolved in 8.3% of cases, became more severe in 33.3% of cases, and remained at the same level in 58.3%. The authors distinguish four types of PHG course. Newly-developed PHG that occurred after EVV eradication, the signs of which remained during the whole period of observation (type I), took place in 13.5% of patients; transient PHG, the signs of which disappeared within three months of observation (type II), was seen in 15.4% of patients; persisting PHG, which was observed before EVV ligation and did not change during the whole study period (type III), was found in 40.3% of patients; progressing PHG, observed before or after EVV ligation and the severity of which grew during the observation period (type IV), was revealed in 23.1% of patients. In 4 (7.7%) of patients PHG signs were absent during the whole time of the study. PHG hemorrhage was observed in 11.5% of the patients. Thus, EVV ligation presents a risk factor of the onset and progression of pre-existing PHG in patients with HC.
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PMID:[The clinical course of portal hypertensive gastropathy after ligation of esophageal varicose veins]. 1766 5

Portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE) are two distinct gastric mucosal lesions that may cause acute and/or chronic upper gastrointestinal hemorrhage in patients with cirrhosis. Whereas PHG is associated with portal hypertension, GAVE may present in patients without portal hypertension or liver disease. Diagnosis is made upon visualization of the characteristic lesions with upper gastrointestinal endoscopy, although the differential may be difficult at times. PHG is characterized endoscopically by a mosaic pattern with or without red signs and a proximal distribution. PHG mainly causes chronic blood loss and anemia in patients with cirrhosis but also can cause acute hemorrhage. First-line therapy for chronic hemorrhage from PHG is a nonselective beta-blocker (propranolol or nadolol) and iron supplementation. If bleeding/anemia are not controlled with these measures and the patient is transfusion-dependent, shunt therapy (transjugular intrahepatic portosystemic shunt or shunt surgery) should be considered. Management of acute bleeding from PHG, an infrequent event, should be accomplished with a vasoactive drug, somatostatin (or its analogues) or terlipressin. If bleeding responds, the patient must be switched to a nonselective beta-blocker. Shunt therapy should be considered in patients who rebleed or continue to bleed despite adequate beta-blocker therapy. GAVE is less common than PHG. It is characterized by red spots without a background mosaic pattern, typically in the gastric antrum. When lesions have a linear distribution, the lesion is called "watermelon stomach." GAVE is a cause of chronic gastrointestinal bleeding and anemia in patients with cirrhosis. If lesions are localized, first-line therapy is argon plasma coagulation. In more diffuse lesions, therapy with argon plasma coagulation is more complicated. Preliminary data suggest that cryotherapy may be a reasonable option for diffuse GAVE lesions. Neither beta-blockers nor TIPS reduces the bleeding risk in patients with GAVE and thus should not be used in this setting.
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PMID:Treatment of gastropathy and gastric antral vascular ectasia in patients with portal hypertension. 1822 9

Portal hypertensive gastropathy (PHG) is often seen in patients with portal hypertension, and can lead to transfusion-dependent anemia as well as acute, life-threatening bleeding episodes. This Review focuses on the mechanisms that underlie the pathogenesis of PHG that provide reasonable grounds for the treatment of this condition, and ultimately enable translation of basic research into clinical practice. Increased portal pressure associated with cirrhosis and liver dysfunction is critical for the development of clinically significant PHG, and leads to impaired gastric mucosal defense mechanisms that render the stomach susceptible to mucosal injury. The use of pharmacological agents such as beta-blockers reduces the frequency of bleeding episodes in PHG. As a last resort, surgical decompression of the portal system, transjugular intrahepatic stent placement and liver transplantation can resolve this condition. Elimination of known risk factors for gastric injury such as alcohol, aspirin and traditional NSAIDs is critical. The role of Helicobacter pylori colonization of the gastric mucosa in PHG is not clear. Careful and critical interpretation of human and experimental data can be helpful to establish a rationale for the medical management of this important condition.
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PMID:Pathogenesis of portal hypertensive gastropathy: translating basic research into clinical practice. 1919 Jun

Portal hypertensive gastropathy and gastric antral vascular ectasia are gastric mucosal lesions that can cause chronic gastrointestinal haemorrhage and, consequently, chronic anaemia, in patients with cirrhosis. Although chronic anaemia is the most common clinical manifestation, these entities may also lead to acute gastrointestinal bleeding. Despite similar clinical manifestations, their pathophysiology and management are entirely different. Their diagnosis is endoscopic and although generally each of them has a characteristic endoscopic appearance and distribution, there are cases in which the differential is difficult and must rely on histology. This review focuses on the management of both entities. The mainstay of management of portal hypertensive gastropathy is based on portal-hypotensive pharmacological treatment whilst gastric antral vascular ectasia benefits from endoscopic therapy. More invasive options should be reserved for refractory cases.
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PMID:The management of portal hypertensive gastropathy and gastric antral vascular ectasia. 2109 66

A major cause of cirrhosis related morbidity and mortality is the development of variceal bleeding, a direct consequence of portal hypertension. Less common causes of gastrointestinal bleeding are peptic ulcers, malignancy, angiodysplasia, etc. Upper gastrointestinal bleeding has been classified according to the presence of a variceal or non-variceal bleeding. Although non-variceal gastrointestinal bleeding is not common in cirrhotic patients, gastroduodenal ulcers may develop as often as non-cirrhotic patients. Ulcers in cirrhotic patients may be more severe and less frequently associated with chronic intake of non-steroidal anti-inflammatory drugs, and may require more frequently endoscopic treatment. Portal hypertensive gastropathy (PHG) refers to changes in the mucosa of the stomach in patients with portal hypertension. Patients with portal hypertension may experience bleeding from the stomach, and pharmacologic or radiologic interventional procedure may be useful in preventing re-bleeding from PHG. Gastric antral vascular ectasia (GAVE) seems to be different disease entity from PHG, and endoscopic ablation can be the first-line treatment.
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PMID:Management of portal hypertensive gastropathy and other bleeding. 2475 52

Portal hypertensive gastropathy (GHP) is a complication of portal hypertension usually associated with liver cirrhosis. The pathogenesis is unclear but the presence of portal hypertension is an essential factor for its development. GHP may be asymptomatic or present as gastrointestinal bleeding or iron deficiency anemia. Endoscopic lesions vary from a mosaic pattern to diffuse red spots; the most common location is the fundus. Treatment is indicated when there is acute or chronic bleeding, as secondary prophylaxis. There is insufficient evidence to recommend primary prophylaxis in patients who have never bled. Drugs that decrease portal pressure, such as non-cardioselective beta-blockers, and/or endoscopic ablative treatments, such as argon-beam coagulation, may be used. The role of transarterial intrahepatic portosystemic shunt) or bypass surgery has been insufficiently analyzed. Antral vascular ectasia (EVA) is a rare entity in liver cirrhosis, whose pathophysiology is still unknown. Clinical presentation is similar to that of GHP and endoscopy usually shows red spots in the antrum. Biopsy is often required to differentiate EVA from GHP. There is no effective medical therapy, so endoscopic ablative therapy and, in severe cases, antrectomy are recommended.
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PMID:[Gastric vascular lesions in cirrhosis: gastropathy and antral vascular ectasia]. 2549 48

Portal hypertensive gastropathy (PHG) is a gastric mucosal lesion complicating portal hypertension, with higher prevalence in decompensated cirrhosis. PHG can sometimes complicate autosomal dominant polycystic kidney disease (ADPKD) due to the presence of multiple liver cysts. Besides, PHG is known to present as chest pain, with or without hematemesis. Other causes of chest pain in ADPKD include referred chest pain from progressively enlarging kidney cysts, and rare pericardial cysts. Chest pain, especially if pleuritic, in end-stage renal disease (ESRD) patients, is often ascribed to uremic pericarditis. We present recurrent pleuritic chest pain in a 24-year old ESRD patient with ADPKD that was initially misdiagnosed as uremic pericarditis. It was ultimately shown to represent symptomatic PHG with excellent therapeutic response to proton pump inhibitors.
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PMID:Pleuritic chest pain from portal hypertensive gastropathy in ESRD patient with autosomal dominant polycystic kidney disease misdiagnosed as pericarditis. 2706 69


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