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 57-year-old man presented with cough, chest pain and dyspnea. Peripheral lung opacities detected radiologically on admission were surgically resected and histologically confirmed as pulmonary infarcts. Subsequent radiological examinations revealed a stricture of the right pulmonary artery with evidence of pulmonary hypertension. The patient was commenced on anticoagulant therapy, which resulted in some clinical improvement. A hilar mass detected later was resected together with the right lung. Pathological examination of the hilar mass revealed a tumour within the lumen of the pulmonary artery causing almost total occlusion of the artery. Histology showed angiosarcomatous and osteosarcomatous areas. The patient is well and disease-free 9 months following resection.
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PMID:Right pulmonary artery sarcoma. 1135 63

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
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PMID:[Mountaineering and altitude sickness]. 1144 1

The Bezold-Jarisch reflex is an eponym for a triad of responses (apnea, bradycardia, and hypotension) following intravenous injection of veratrum alkaloids in experimental animals. The observation was first reported in 1867 by von Bezold and Hirt, and confirmed in 1938-1940 by Jarisch. The triad depends on intact vagi and is mediated through cranial nervous medullary centers controlling respiration, heart rate, and vasomotor tone. The respiratory effects are mediated through pulmonary vagal afferents and the bradycardia and vasodepression through cardiac vagal afferents. The veratrum alkaloids activate all known receptors in the carotid-aortic and cardiopulmonary areas. The cardiopulmonary receptors (baroreceptors, cough receptors, and parenchymal stretch receptors) also respond to other chemical substances: nicotine, capsaicin, venom, antihistaminics, halogenated anesthetics, diguanides, and serotonin (5-hydroxytryptamine). Derivatives of last-mentioned amine activate Type 1, 2, or 3 receptors and have potential therapeutic use. Since several types of cardiopulmonary receptors participate in the Bezold-Jarisch reflex, it has been difficult to develop a blockade to one type of receptor for therapeutic use (cough, bronchospasm, pulmonary hypertension, or coronary vasospasm). Axon reflexes influence pulmonary blood vessels, bronchial blood vessels, and bronchial smooth muscles. These intrapulmonary reflexes need further study as to how they relate to the Bezold-Jarisch reflex in health and disease. The cardiopulmonary and carotid-aortic reflexes can serve as defense mechanisms against chemical hazards that are likely to be inhaled in the workplace and in the environment.
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PMID:The Bezold-Jarisch reflex. A historical perspective of cardiopulmonary reflexes. 1145 3

High-altitude heart disease, a form of chronic mountain sickness, has been well established in both Tibet and Qinghai provinces of China, although little is known regarding this syndrome in other countries, particularly in the West. This review presents a general overview of high-altitude heart disease in China and briefly summarizes the existing data with regard to the prevalence, clinical features, and pathophysiology of the illness. The definition of high-altitude heart disease is right ventricular enlargement that develops primarily (by high-altitude exposure) to pulmonary hypertension without excessive polycythemia. The prevalence is higher in children than adults and in men than women, but is lower in both sexes of Tibetan high-altitude residents compared with acclimatized newcomers, such as Han Chinese. Clinical symptoms consist of headache, dyspnea, cough, irritability, and sleeplessness. Physical findings include a marked cyanosis, rapid heart and respiratory rates, edema of the face, liver enlargement, and rales. Most patients have complete recovery on descent to a lower altitude, but symptoms recur with a return to high altitude. Right ventricular enlargement, pulmonary hypertension, and remodeling of pulmonary arterioles are hallmarks of high-altitude heart disease. It is hoped that this information will assist in understanding this type of chronic mountain sickness, facilitate international exchange of data, and stimulate further research into this poorly understood condition.
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PMID:Current concept of chronic mountain sickness: pulmonary hypertension-related high-altitude heart disease. 1156 18

We report a case of subacute pulmonary hypertension caused by microscopic pulmonary tumor embolism due to the dissemination of gastric cancer cells. The patient, a 61-year-old man with no history of malignant diseases, was admitted to our hospital on October 14 in 1998 because of cough and dyspnea on effort, that had developed since the previous month. On admission, chest radiography including CT scans showed slight cardiomegaly and disseminated reticulonodular shadows predominating in the lower lung fields of both lungs, and arterial blood gas analysis disclosed severe hypoxemia. Lung perfusion scintigraphy revealed multiple irregular defects in both lungs. Echocardiography indicated right ventricular overload, and the pulmonary artery systolic pressure was estimated to be higher than 80 mmHg. Disseminated intravascular coagulation (DIC) developed on the 6th day of hospitalization. Multiple pulmonary embolism with DIC of unknown cause was diagnosed, and the patient was given anticoagulant therapy with heparin. However, he died of respiratory failure on the 7th day of hospitalization. At autopsy, an invasive cancer was found in the stomach, resembling type IIc early gastric cancer. The lumens of the pulmonary arterioles were significantly narrowed by fibrocellular proliferation and thrombi accompanying tumor cell clusters, and some of the microvessels were completely occluded. Disseminated microscopic pulmonary metastasis of malignant tumors should be included in the differential diagnosis of subacute pulmonary hypertension due to multiple pulmonary embolism of unknown cause.
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PMID:[Subacute cor pulmonale due to microscopic pulmonary tumor embolism]. 1157 31

In this prospective study 37 children (ranging 2 months-15 years) with acute pneumonia were evaluated by Doppler echocardiography for the presence of pulmonary hypertension (PH). The goal of this study was to determine the frequency of PH in children with acute pneumonia because the diagnosis of PH influenced the treatment of pneumonia in these patients. The patients who had more than 35 mmHg of systolic pulmonary arterial pressure were considered to have PH. In our study PH was found in 15 (40.5%) of 37 patients. We did not find any significant difference for the parameters including the age, weight, height, clinical symptoms and signs (fever, cough, dyspnea, tachycardia and tachypnea etc.), and laboratory findings such as hemoglobin, PCO2, HCO3 and PO2 between the patients with and without PH (p>0.05). However, there was a significant difference in cyanosis, cardiac failure, blood pH level and O2 saturation measured by pulse oximetry between the patients with and without PH (p<0.05).
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PMID:Doppler echocardiographic evaluation of pulmonary artery pressure in children with acute pneumonia. 1189 Feb 20

Hemoptysis, the expectoration of blood or bloody mucus from the respiratory tract at or below the larynx, was retrospectively evaluated in 36 dogs. Cough, tachypnea, and dyspnea were common historical and physical examination signs. Anemia was documented in 11 dogs, but was severe in only one dog. Other clinicopathological findings reflected the underlying diseases. All thoracic radiographs obtained were abnormal; alveolar and interstitial patterns were most common. Diseases predisposing to hemoptysis included bacterial bronchopneumonia (n=7), neoplasia (n=5), trauma (n=5), immune-mediated thrombocytopenia (n=4), heartworm disease (n=4), rodenticide poisoning (n=3), lung-lobe torsion (n=1), left-sided congestive heart failure (n=1), pulmonary hypertension (n=1), and foreign-body pneumonia (n=1). Four additional dogs had more than one underlying disease process. Nine dogs were either euthanized or died in the hospital during the initial visit. While at least half of the 27 dogs discharged went on to completely recover, five dogs discharged were known to have either died or been euthanized as a result of their disease in <6 months.
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PMID:Clinical signs, clinicopathological findings, etiology, and outcome associated with hemoptysis in dogs: 36 cases (1990-1999). 1190 30

Pulmonary vein (PV) stenosis has emerged recently as an important issue in patients who received radiofrequency (RF) ablation of atrial fibrillation (AF). Serial pathophysiological responses, including thrombosis, metaplasia, proliferation and neovascularization, may lead to PV stenosis after RF energy application around or inside the PV ostia. The clinical manifestations of PV stenosis consist of chest pain, dyspnea, cough, hemoptysis, recurrent lung infection and pulmonary hypertension. Although PV stenosis can be asymptomatic, its severity may be related to the numbers of stenotic PVs, the degree and chronicity of PV stenosis. The incidence of PV stenosis (defined as luminal diameter reduction >50%) detected by spiral computer tomography scan or three dimensional magnetic resonance angiography was from 0 to 7% per PV after isolation of PVs from left atria. Furthermore, some patients may show late progression of PV stenosis during follow-up. The first choice of treatment for symptomatic PV stenosis is PV angioplasty with stenting; however, restenosis were reported occasionally. Several studies have analyzed the predictors of PV stenosis, and the results are controversial. However, the consensus for prevention of PV stenosis should include less energy application and the ablation site more close to the atrial site.
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PMID:Evaluation of pulmonary vein stenosis after catheter ablation of atrial fibrillation. 1243 19

Pulmonary complications of hematopoietic stem cell transplantation (HSCT), including peripheral blood stem cell transplantation (PBSCT) and bone marrow transplantation, are frequent and often life-threatening. Differentiating acute infectious from noninfectious pulmonary complications is difficult but critical for proper treatment. The authors describe an 11-year-old boy who developed a sudden fever and cough associated with a normal chest radiograph 2 months after successful haploidentical PBSCT for severe aplastic anemia. High-resolution chest computed tomography revealed numerous tiny peripheral pulmonary nodules. Lung biopsy demonstrated an unusual occlusive thrombotic vascular lesion associated with hemorrhagic infarction without evidence of infection. The thrombi were composed of intensely basophilic granular material recently described as "cytolytic" thrombi. Symptoms and chest computed tomography improved rapidly following intravenous corticosteroids and cyclosporin. However, the patient subsequently died of rapidly progressive pulmonary hypertension. Our patient illustrates the importance of considering this noninfectious complication in the acute pulmonary disorders associated with HSCT as this condition may represent a pulmonary manifestation of acute graft-versus-host disease.
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PMID:Pulmonary cytolytic thrombi: unusual complication of hematopoietic stem cell transplantation. 1254 82

Extensive reviews of pulmonary infections in AIDS have reported few herpetic infections. Generally these infections are due to Herpes simplex type 1. Pneumonia due to herpes type 2 is extremely rare. We describe a 40 year-old HIV positive woman who complained of fever, cough and dyspnea for seven years. She had signs of heart failure and the appearance of her genital vesicles was highly suggestive of genital herpes. Echocardiography showed marked pulmonary hypertension, right ventricular hypertrophy and tricuspid insufficiency. After a few days of hospitalization she was treated with Aciclovir and later with Ganciclovir. An open pulmonary biopsy revealed an interstitial inflammation, localized in the alveolar walls. Some pulmonary arteries had widened walls and focal hyaline degeneration. Immunohistochemistry indicated that the nuclei had herpes simplex virus type 2 in many endothelial cells (including vessels with widened walls), macrophages in the alveolar septa and pneumocytes. There was clinical improvement after treatment for herpes. We concluded that as a consequence of herpes infection, endothelial involvement and interstitial inflammation supervene, with thickening of vascular walls and partial obliteration of the vessel lumen. A direct consequence of these changes in pulmonary vasculature was pulmonary hypertension followed by heart failure.
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PMID:Herpes simplex type 2 pneumonia. 1258 74


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