Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 37-year-old man with progressive exertional dyspnea had pulmonary hypertension associated with pulmonary arterial and venous obstruction. An autopsy revealed that the cause of death was idiopathic pulmonary hilar fibrosis, a variant of mediastinal fibrosis. Pulmonary hilar fibrosis can mimic thromboembolic pulmonary hypertension, pulmonary veno-occlusive disease, and pulmonary venous hypertension.
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PMID:Idiopathic pulmonary hilar fibrosis: an unusual cause of pulmonary hypertension. 833 79

A 77-year-old woman with hypertension was admitted to our hospital because of exertional dyspnea end peripheral edema. Chest X-ray showed cardiomegaly, pulmonary congestion and right pleural effusion. Hypertensive heart failure was diagnosed and treated, and right pleural effusion disappeared in 2 weeks. Abnormalities on laboratory data, i.e. anemia and increased ESR et al. continued after the improvement of heart failure. Serum IgG was elevated (2570 mg/dl), while IgA and IgM were decreased. Immunoelectrophoresis indicated the presence of monoclonal IgG-lambda in the serum. Bone marrow puncture revealed an increase in atypical plasma cells (38.4%). Multiple myeloma was diagnosed from these findings and treated with melphalan and prednisolone. But increases in atypical plasma cells (43.2%) and serum IgG (2573 mg/dl) continued. During treatment, right pleural effusion increased again. Thoracocentesis showed bloody effusion with numerous atypical plasma cells, and the presence of monoclonal IgG-lambda was indicated by immunoelectrophoresis. The patient died of renal and heart failure 2 months after the onset of malignant pleural effusion. Cytological examination and immunoelectrophoresis are necessary for pleural effusion in multiple myeloma.
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PMID:[A case of multiple myeloma associated with abnormal plasma cells and M-protein in pleural effusion]. 864 97

Congestive heart failure (CHF) is a progressive disease with multiple possible causes. Systolic heart failure, defined as contractile failure of the myocardium leading to a reduced ejection fraction, is the most common type. Systolic heart failure may result from coronary artery disease, hypertension, a metabolic disorder, infection, or an infiltrative or other disease, or it may be idiopathic. Recognition of CHF can be difficult, especially in elderly patients with several medical conditions. An early clinical sign may be dyspnea on exertion. The extent of workup needed is often indicated by findings on history taking and physical examination. In all patients suspected of having new-onset CHF, a chest film, an electrocardiogram, and left ventricular ejection fraction should be obtained and a search for complicating and causative factors undertaken. Early treatment may halt the otherwise inevitable decline in cardiac function and improve prognosis.
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PMID:Causes of congestive heart failure. Prompt diagnosis may affect prognosis. 900 88

A 91-year-old man was admitted with colliquative diarrhea, anorexia and weight loss. He had a history of healed tuberculosis, hypertension and atherosclerotic abdominal aortic aneurysms. On admission, shortness of breath without cough, exertional dyspnea, and ascites were also noticed. His chest X-ray and CT showed almost normal findings in the lung fields except for calcified old pleurisy. Since laboratory tests revealed thrombocytopenia, low fibrinogen, and increased CA19-9. DIC induced by an unknown cancer was diagnosed. He died on the eighth day due to progressive respiratory failure which did not respond to oxygen therapy. Autopsy revealed that he had a poorly differentiated adenocarcinoma in the cecum complicated with pulmonary lymphangitis carcinomatosa. Lymphangitis should be considered in the case of unexplained progressive respiratory failure developing in patient with cancer, even in the absence of X-ray findings.
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PMID:[A very elderly autopsy case of cecal cancer with pulmonary lymphangitis carcinomatosa]. 1103 30

We describe an unusual case of periductal carctation of the aorta in a 40-year-old patient presenting to the echocardiography laboratory for evaluation of a heart murmur. Subsequent clinical history revealed easy fatigability, dyspnea on exertion, and hypertension. Despite a lack of left ventricular hypertrophy, aortic coarctation was suggested by echocardiography. It was later confirmed to be severe by multiple additional imaging modalities, despite an absence of overt collateral arterial channels. The importance of echocardiography in the diagnosis of coarctation of the aorta and the management of this complicated patient is discussed.
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PMID:Severe Aortic Coarctation in an Adult Without Left Ventricular Hypertrophy Nor Overt Collateral Channels. 1117 72

We report a case of multicentric, biatrial cardiac myxoma in a 29-year-old female who complained of exertional dyspnea, abdominal distension and peripheral edema. Any other associated skin lesions, breast mass or endocrine disorder presenting complex form were' not seen on her. Also, there was no contributory medical history, hypertension and diabetes mellitus. By using transthoracic echocardiography, we identified a biatrial myxoma attached to the interatrial septum. During surgical excision, we found a large right atrial myxoma with extension through the fossa ovalis into the left atrium and small myxoma attached to the right atrial free wall. After successful resection of interatrial septum and free wall, atrial septal defect was created during the resection and safely repaired by bovine pericardial patch.
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PMID:Multicentric biatrial myxoma in a young female patient: case report. 1124 13

Portopulmonary hypertension is now recognized as one of the pulmonary complications of chronic liver disease. However, previous studies reported that the incidence ranged from 0.25% to 2%, excluding fortuitous coincidence. In this study, we aimed to determine the variant hemodynamic and clinical features of portopulmonary hypertension in an area with a high prevalence of viral cirrhosis. After reviewing the hemodynamic data of 322 patients with portal hypertension admitted to the Taipei Veterans General Hospital between 1987 and 1999, we found 10 with portopulmonary hypertension. The overall incidence was, therefore, 3.1% in all patients with portal hypertension. Most of the patients with portopulmonary hypertension experienced exertional dyspnea. The survival times ranged from 2 to 86 months. In our series, most of the patients who died, died of complications related to cirrhosis and portal hypertension, but not of complications related to pulmonary hypertension. This study suggested that portopulmonary hypertension was not a frequent complication in cirrhotic patients and was not associated with an adverse outcome.
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PMID:Portopulmonary hypertension: distinctive hemodynamic and clinical manifestations. 1129 81

In the conventionally treated group of patients with chronic myelogenous leukemia (CML) the prognosis has been significantly improved by interferon-alpha (IFN-alpha). Several side effects in association with IFN-alpha treatment have been reported. Here we present the first case of a CML patient with reversible pulmonary artery hypertension (PAH) during IFN-alpha therapy. The patient received IFN-alpha-2b (up to 10 million U/day) for 6 months until he started to complain of dyspnea on exertion and an afebrile non-productive cough. An echocardiography and right heart catheterization showed signs of right heart failure with PAH (80 mmHg). A reduced carbon monoxide diffusion capacity and partial respiratory insufficiency were noted. Inflammatory markers were not elevated and pulmonary infiltrates could not be detected. Respiratory infections, thromboembolic causes or autoimmune diseases were carefully ruled out. IFN-alpha was suspected as causative agent, because experimental investigations in sheep showed that IFN-alpha can stimulate the thromboxane cascade which resulted in transient PAH. A reduced pulmonary diffusion capacity had been observed secondary to PAH. After discontinuation of IFN-alpha, our patient's clinical status improved rapidly. After 6 months the pulmonary artery pressure had returned to near normal values (35 mmHg) and the pulmonary diffusion capacity was normal. It took one year until the electrocardiogram reverted to the pre-IFN-alpha pattern. PAH should be included in the differential diagnosis of patients treated with IFN-alpha who complain of exertional dyspnea in the absence of inflammatory signs.
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PMID:Pulmonary artery hypertension during interferon-alpha therapy for chronic myelogenous leukemia. 1144 36

Although the benefit of angiotensin converting enzyme (ACE) inhibitors in diabetic nephropathy is well documented in double-blind randomized, controlled clinical trials, it is uncertain whether the benefit extends to unselected patients with diabetes mellitus and arterial hypertension in general practice. In 2504 unselected patients with type 2 diabetes mellitus (mean age 63+/-10 years) blood pressure, cardiovascular, renal, and metabolic parameters were assessed at baseline and during a treatment period of 1 year with the ACE inhibitor cilazapril by primary care physicians. The average dose of cilazapril was 2.5 mg/day. Outcome measures were blood pressure, serum creatinine, proteinuria (dip stick), HbA1c levels, evaluation of edema, and exertional dyspnea. In the study cohort, systolic blood pressure decreased by 24+/-17 mm Hg and diastolic blood pressure by 12+/-11 mm Hg. An increase in serum creatinine (> 0.2 mg/dL) occurred more frequently in patients with than in those without renal involvement (19% v 7%; P < .05). Serum creatinine decreased more frequently in patients with renal involvement than in those without (26%+/-4% v 12%+/-3.8%; P < .05). Overall renal function in patients with diabetic nephropathy (n = 318) improved (2.1+/-1.6 mg/dL v 1.7+/-1.4 mg/dL; P < .05). The frequency of proteinuria was lower after 1 year than at baseline (62%+/-9% v 82%+/-8%; P < .05). Metabolic control of diabetes mellitus improved in parallel (median HbA1c 8.0% v 7.0%; P < .01). Scores for edema formation and exertional dyspnea improved as well (P < .01). In this outcome survey of unselected patients with type 2 diabetes mellitus and arterial hypertension, the ACE inhibitor cilazapril effectively lowered blood pressure, which was associated with an improvement in glucose metabolism, cardiac function, and renal function.
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PMID:Outcome survey in unselected hypertensive patients with type 2 diabetes mellitus: effects of ACE inhibition. 1146 52

Each year about 550,000 new patients are diagnosed as having congestive heart failure, which for acutely symptomatic patients is also referred to as acutely decompensated heart failure. The incidence of congestive heart failure is approximately 10 per 1000 for Americans over the age of 65 years. Men and women are affected in equal numbers, and 5-year mortality has been reported to be as high as 50%. Increased longevity increases the likelihood that heart failure will develop as a consequence of pathophysiologic processes that gradually weaken the myocardium and the vascular system. Patients who present to the emergency department with complaints of shortness of breath, dyspnea on exertion, increasing lower extremity edema, and/or worsening fatigue should have heart failure included in the differential diagnosis. Heart failure patients experiencing symptoms consistent with cardiac ischemia, hypoxia, potentially lethal arrhythmias, marked hypertension, or hypotension should be immediately triaged to a critical care area. The approval of nesiritide by the U.S. Food and Drug Administration in 2001 has stimulated the development of revisions in strategies for the emergency department treatment of acute decompensated heart failure patients. The early use of nesiritide, along with topical nitroglycerin and a loop diuretic, may lead to more rapid resolution of these patients' acute symptoms and hemodynamic dysfunction.
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PMID:Acutely decompensated heart failure: opportunities to improve care and outcomes in the emergency department. 1243 25


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