Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new, fatal complication of transtracheal aspiration is described in a cirrhotic patient. Death was related to gastrointestinal bleeding (rupture of oesophageal varices and Mallory-Weiss syndrome) due to unrestrainable coughing originating from transtracheal aspiration.
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PMID:A new fatal complication of transtracheal aspiration. 30 94

1. An infusion of 3 gamma/kg/min dopamine causes a significant increase in the renal plasma flow and the glomerulum filtration rate. This dosage does not cause a change of the mean systolic and arterial pressure. This effect may also be observed in patients with hepatic cirrhosis. 2. The wedged hepatic vein pressure, an indicator for the portal pressure, only shows a slight increase (9,46 +/- 9,41%) as compared to the initial pressure produced by the mentioned dose. Measurements of the spleen pulpa pressure, which likewise indicates the portal pressure, showed an increase of pressure up to 100% due to pressing or coughing. 3. If in the case of bleeding oesophageal varices acute renal failure might develop, the advantage of the effect of dopamine in stimulating the blood flow through the kidneys may be considered more important than the minute danger of a slight increase of the portal pressure, which might provoke haemorrhage.
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PMID:[Effect of dopamine on the portal pressure]. 122 May 17

With the use of two balloon catheters inserted in the right jugular vein, the following parameters were measured before and after injection of sotalol (1.5 mg/kg): cardiac output with the thermodilution method, hepatic output with the indocyanin green perfusion method, free sub-hepatic pressure, blocked sub-hepatic pressure recorded at rest and during coughing. After 30 minutes, the following modifications were recorded: the cardiac output goes from 6.8 +/- 2.1 to 5.9 +/- 1.9 L/min (NS), the hepatic output goes from 1.9 +/- 1.1 to 1.5 +/- 0.6 L/min (NS), the hepatic pressure gradient goes from 18.2 +/- 6.1 to 11.5 +/- 5.4 mmHg (p less than or equal to 0.0005); the blocked sus-hepatic pressure at rest goes from 25.0 +/- 7.8 to 19.8 +/- 8.0 mmHg (p less than or equal to 0.025); the blocked sus-hepatic pressure during coughing goes from 92 +/- 32 to 82 +/- 39 mmHg (NS). This study demonstrates: a) that the drop in the hepatic pressure gradient induced by a dose of sotalol is more important than that observed by Westaby et al. with propranolol: 37% vs 31% (NS); b) that sotalol cannot lower the blocked sub-hepatic pressure during coughing. This result suggests that the potential protective effect of sotalol toward esophageal varices rupture disappears during coughing.
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PMID:[Effects of sotalol on blocked suprahepatic pressure in cirrhotic patients]. 343 33

The portal venous-esophageal luminal pressure gradient may be more important than the absolute portal venous pressure in explaining hemorrhages caused by esophageal varices. A continuous recording of portal venous pressure and the esophageal luminal pressure enabled the authors to study the gradient between these pressures in 12 cirrhotic patients with varices of different size and under different circumstances, in particular inspiration, expiration, coughing and a Valsalva maneuver. A significant increase of portal venous pressure occurred during inspiration (+15%), coughing (+77%) and Valsalva maneuver (+157%). The value of portal venous-esophageal luminal pressure gradient increased during inspiration (+38%), coughing (+90%) and Valsalva maneuver (+69%) while it decreased during expiration (-14%).
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PMID:Portal venous-esophageal luminal pressure gradient in cirrhosis. 348 15

Pressure in oesophageal varices was measured endoscopically in 52 patients, in 16 of them central portal-vein pressure additionally by percutaneously introduced transhepatic portal-vein catheter. Only in the region of the cardia occlusion segment was the portal-vein pressure the same as that in the oesophageal varices. The larger the varices the higher the average variceal pressure. Depending on the time interval since a meal there were marked pressure variations during the day in portal-vein pressure. Intra-abdominal pressure rise (e.g. on coughing, choking or vomiting) induces a sudden and marked pressure rise in the portal vein as well as the oesophageal varices. The larger the varices the greater the danger of rupture when these pressure rises occur. Gastro-oesophageal reflux plays no role in the pathogenesis of bleeding from oesophageal varices.
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PMID:[Pathogenesis of bleeding esophageal varices]. 348 19

We compared arterial blood gas analysis and 99mTc-MAA lung perfusion scintigraphy before and after endoscopic injection sclerotherapy (EIS) in 17 cases of esophageal varices complicating liver cirrhosis. EIS was performed by the intra-variceal injection method with 5% ethanolamine oleate (EO) as the sclerosant agent. In blood gas analysis, the mean values of partial arterial oxygen tension (PaO2) and oxygen saturation (SaO2) were decreased, and the mean value of alveolar-arterial O2 difference (AaDO2) was increased, compared with before EIS while breathing room air. On lung perfusion scintigram, the pulmonary blood flow was markedly decreased, demonstrating hypoperfusion and/or perfusion defect, compared with before EIS in most the cases. It was suggested that pulmonary embolism and/or pulmonary circulatory disturbance occurred after EIS. It is important to note that pulmonary circulatory disturbances potentially may occur after EIS without any accompanying symptoms such as dyspnea, cough, or hemoptysis.
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PMID:[Pulmonary circulatory disturbance following endoscopic injection sclerotherapy]. 836 22

Here we report an autopsy case with anti-neutrophil antibodies (ANCA) associated vasculitis accompanied by autoimmune hepatitis and hepatocellular carcinoma. A 69-year-old woman was admitted to Tokyo Metropolitan Ohtsuka Hospital in October 1995 because of leg edema. She had presented cough in 1990 and diagnosed as interstitial pneumonia, esophageal varices and liver chirosis. On admission, laboratory data showed mild anemia, hypoproteinemia, and marked gammagloblinemia. IgM-HA antibody, HBs antigen, HBs antibody, HCV antibody and HDV antibody were negative. Anti-nuclear antibody, anticentromere antibody, anti-neutrophil cytoplasmic antibody against myeloperoxidase and cathepsin G (MPO-ANCA and cathepsin G), rheumatoid factor and direct coombs test were positive. Serum level of AFP and CEA were elevated. Ultrasonography and computed tomography of abdomen scowed liver chirosis and tumor in left lobe of liver. The diagnosis of liver chirosis based on autoimmune hepatitis and Interstitial pneumonia was made with clinical course, laboratory findings and radiographic findings although liver biopsy was not performed. She complained of bloody stool due to ulcer of the large intestine, and died of liver failure which progressed rapidly. The autopsy findings detected that pulmonary fibrosis, liver fibrosis with multiple hepatocellular carcinoma, necrotizing crescentic glomerulonephritis, and vasculitis of small artery inn colon. This was the first report of MPO-ANCA associated vasuculitis complicated with autoimmune hepatitis and hepatocellular carcinoma. Clinical significance of ANCA and immunogenetic background of these diseases were discussed.
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PMID:[An autopsy case of anti-neutrophil cytoplasmic antibodies associated vasculitis accompanied by autoimmune hepatitis and hepatocellular carcinoma]. 917 69

A 72-year-old woman who had had an endoscopic sclerotherapy for esophageal varices presented with high fever and severe cough. Chest X-ray and CT demonstrated a pneumopericardium and pericardial effusion. Esophagoscopy and esophagography revealed an esophageal perforation into the pericardial cavity and into the lung. Consequently, drainage and irrigation of the pericardial cavity and mediastinum were done for MRSA infection. However, these procedures failed to reduce the inflammation, and she expired because of liver failure soon after placing a covered stent in the esophagus. Postmortem examination revealed small cell carcinoma in the left lung invading into the esophagus and pericardium.
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PMID:[A case of lung cancer (small cell carcinoma) occurring esophago-pericardial fistula and purulent pericarditis]. 1051 69

Bleeding from gastric varices (GVs) is generally considered more severe than that from esophageal varices (EVs) but occurs less frequently. We review the risk factors for bleeding EVs and GVs. GVs were divided into 2 groups: cardiac varices (CVs, Lg-c) and fundal varices (FVs), i.e., varices involving the fundus alone (Lg-f) or varices involving both the cardia and fundus (Lg-cf). Elevated pressure in the portal vein is a risk factor for bleeding EVs. The portal pressure in patients with GVs and a gastrorenal shunt is lower than that in patients with EVs. The large size of varices is a risk factor for bleeding EVs. Red color signs are elevated red areas that are important for predicting the risk of variceal bleeding, and red wale markings, dilated venules oriented longitudinally on the mucosal surface, have been considered to be the sign with the highest risk. Red color signs are rare in FVs, possibly because of the pronounced thickness of the mucosal layer. Bleeding EVs are not associated with use of antiulcer drugs or nonsteroidal anti-inflammatory drugs (NSAIDs). Although, in patients with bleeding GVs, "occasional" use of an oral NSAID is an important step leading to variceal hemorrhage, especially from FVs, even if the mucosa is protected by antiulcer drugs. Constipation, vomiting, severe coughing, and excessive consumption of alcohol may precipitate rupture of EVs.
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PMID:Risk factors for bleeding esophagogastric varices. 2399 67