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)

To determine whether a better understanding of primary pulmonary hypertension has affected its clinical presentation, natural history, and prognosis, we retrospectively compared patients with primary pulmonary hypertension presenting to our institution during two different periods: 1962 to 1978 (group 1, n = 38) and 1979 to 1989 (group 2, n = 33). Demographic characteristics were similar in both groups. Dyspnea on exertion was the most frequent presenting symptom in both groups. Fatigue, cough, dizziness, right heart failure, and cyanosis were more frequent in group 1. The electrocardiographic, radiographic, and echocardiographic findings did not differ between groups. Hemodynamic measurements revealed severe pulmonary hypertension and a normal pulmonary capillary wedge pressure and cardiac index; these measurements were similar in both groups. Complications related to cardiac catheterization were more frequent in group 1 (32%) than in group 2 (3%). Causes of death were comparable in both groups, the most frequent being progressive right heart failure, sudden death, and death of unknown cause. Patients from both groups received standard treatment with digitalis, diuretics, and vasodilators; however, group 2 had a higher probability of survival than group 1. We conclude that patients with pulmonary hypertension seen in more recent years tend to present at earlier stages of disease, have fewer complications during cardiac catheterization, and probably survive longer than those seen several decades ago. A clear cause for the longer survival could not be identified, although it may be partly related to earlier presentation in the course of disease.
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PMID:Primary pulmonary hypertension, then and now: 28 years of experience. 152 74

Familial primary pulmonary hypertension was found in two siblings (sister and brother). The woman noted exertional dyspnea at the age of 28 yr. The younger brother noticed exertional dyspnea, cough with bloody sputum and pretibial edema at the age of 38 yr. We diagnosed them as primary pulmonary hypertension as based on hemodynamic and histopathological findings. Regardless of the treatment, both patients died of right-sided heart failure with a short time course. We examined their family members, but there were no other members with primary pulmonary hypertension.
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PMID:Familial primary pulmonary hypertension--report of two siblings. 183 76

Described is an outbreak of nosocomial RSV infection, following the admission of a 20-day-old and 11-day-old newborn with lower respiratory infections, diagnosed as being caused by RSV through detection of viral antigens by direct FAT (fluorescent antibody test) of nasopharyngeal samples. Later on, 5 of the other 20 newborn in patients in the same care unit also showed positive results in direct FAT, for RSV. The clinical manifestations of these patients were mild even in those cases with underlying PHT and cardiac disease and consisted of: cough (5/5), nasal discharge (3/5), poor feeding (1/5), sneezing (1/5), distress (1/5) and irritability (1/5). The rapid diagnosis of RSV though the direct FAT enables us to establish hygienic restrictions and patients isolation to keep the virus from spreading.
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PMID:[Outbreak of respiratory syncytial virus in a neonatal unit]. 267 77

A Haitian woman with the human immunodeficiency virus (HIV) presented with dyspnea, cough, fatigue and lower abdominal pain of recent onset. Clinical, radiologic and hemodynamic investigations demonstrated pulmonary hypertension. The patient died a few days later. The pathological findings were compatible with primary pulmonary hypertension. This case is similar to others that have been reported and indicates a possible link between HIV infection and rapidly progressive primary pulmonary hypertension.
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PMID:Primary pulmonary hypertension associated with HIV infection. 842 54

We report the clinical features, electrocardiographic and chest X-ray findings, and Doppler-measured pulmonary artery pressures in 22 children admitted to Goroka Base Hospital with primary pulmonary hypertension and compare them with findings in 10 controls. Symptoms frequently reported by patients were recurrent cough (95%) and shortness of breath (77%). 82% of the patients had increased intensity of the pulmonary component of the second heart sound. 45% of the patients had clinical evidence of right heart failure. Chest X-rays were readable in 14 patients: the mean cardio-thoracic ratio was 65% and in the controls 58%; the mean diameter of the descending branch of the right pulmonary artery was 9 mm and in the controls 6.4 mm. 13 patients and 8 controls had electrocardiograms: 11 patients had right axis deviation, 2 a normal axis, and all showed evidence of right ventricular hypertrophy; 7 controls had a normal axis, 1 had right axis deviation, and 3 controls had right ventricular hypertrophy. Pulmonary artery pressures in the patients ranged from 41 to 137 mmHg with a mean of 79 mmHg. The control group had a mean pulmonary artery pressure of 28 mmHg, but 5 of the 10 controls had pulmonary artery pressures greater than the accepted norm (peak systolic pressure less than 30 mmHg). Altitude and chest infection may be playing a role in the pathogenesis of pulmonary hypertension in patients in the highlands but further studies need to be done to define the causes and the pathological changes in the pulmonary vasculature, as well as to determine local norms and the natural history of pulmonary hypertension in highland children.
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PMID:Unexplained pulmonary hypertension in children in the highlands of Papua New Guinea. 857 77

Various drugs are associated with adverse respiratory disorders (ARDs) ranging in severity from mild, moderate to severe and even fatal. Cardioselective and nonselective beta-blockers, calcium antagonists and dipyridamole can induce asthma. ACE inhibitors are mainly associated with cough. Amiodarone is related to a form of interstitial pneumonitis (IP) which can be fatal, tocainidine and flecainidine to a form of IP, and hydrochlorothiazide to a form of IP and pulmonary oedema. Antiasthmatic drugs can be associated with a paradoxical bronchospasm, while leukotriene antagonists are linked to the development of Churg-Strauss syndrome. Nonsteroidal anti-inflammatory drugs including aspirin (acetylsalicylic acid) may induce asthma. Gold is mainly related to IP, penicillamine to IP, systemic lupus erythematosus, bronchiolitis obliterans, and Goodpasture's syndrome. Acute respiratory reactions to nitrofurantoin include dyspnoea, cough, IP, and pleural effusion while IP and fibrosis are common in chronic reactions. Other antibacterials mainly evoke pneumonitis, pulmonary infiltrates and eosinophilia, and bronchiolitis obliterans. ARDs are similar for most categories of cytotoxic agents, with chronic pneumonitis and fibrosis being the most common. Noncardiogenic pulmonary oedema occurs as the most common respiratory complication in opioid agonist addiction. Psychotropic drugs such as phenothiazides, butyrophenones and tricyclic antidepressants can also induce pulmonary oedema. Oral contraceptives may produce asthma exacerbation, while long term use and/or high doses of postmenopausal hormone replacement therapy increase the risk of asthma. Bromocriptine is mainly associated with pleural effusion, while methysergide is usually associated with pleural effusion and fibrosis. Some anorectic agents have been linked to the development of primary pulmonary hypertension. The possibility of the occurrence of ARDs should be taken into account in each individual patient. Although in most cases the adverse effects are unpredictable, they can be reduced to a minimum or prevented if some drugs are avoided or stopped in time.
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PMID:Drug-induced respiratory disorders: incidence, prevention and management. 1094 76

Iloprost is a stable prostacyclin analogue with a pharmacokinetic profile allowing nebulised administration in patients with primary pulmonary hypertension (PPH). Inhaled iloprost is a potent acute pulmonary vasodilator with a duration of action of about 60 minutes. It may exert additional long-term benefit through antiproliferative and antithrombotic effects. Inhaled iloprost 2.5 or 5 microg six or nine times daily for 12 weeks (n = 101) significantly (p < 0.01) improved a combined clinical endpoint of a > or =10% increase in distance walked in 6 minutes and an improvement of > or =1 class in New York Heart Association functional class without clinical deterioration or death (16.8 versus 4.9% of placebo recipients, n = 102) in patients with severe PPH or selected forms of nonprimary pulmonary hypertension. Statistical analysis of the response for the PPH subgroup (20.8 versus 5.5% with placebo; n = 51 and 51) was not reported. Improvements from baseline in exercise capacity and haemodynamic/gas exchange variables have been reported in patients with PPH with continued use of inhaled iloprost. In addition, improvement in preinhalation vascular resistance occurred after 12 weeks of inhaled iloprost (p < 0.01 versus placebo) in a large randomised trial. Increased cough, headache, flushing and an influenza-like syndrome were the most common adverse events in the largest trial of patients receiving inhaled iloprost. Headache, flushing and jaw pain occurred significantly more frequently with inhaled iloprost than with placebo.
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PMID:Inhaled iloprost: in primary pulmonary hypertension. 1502 51

We describe a patient wih subacute cor pulmonale caused by tumor emboli in the lungs. A 64-year-old female suffering from a subacute progressive cough and shortness of breathing died of severe pulmonary hypertension seven days after admission. Neither chest CT scans nor lung perfusion scintigraphy showed any abnormal findings. Microscopic examination after an autopsy revealed diffuse intravascular tumor emboli occluding not only the small pulmonary arteries and arterioles, but also the lymphatic vessels, which were suggested to be metastases of a breast carcinoma resected five years previously. Thus, pulmonary tumor embolism should be considered in the differential diagnosis of primary pulmonary hypertension, particularly in patients with a past history of cancers.
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PMID:Subacute cor pulmonale due to tumor embolism. 1520 57

The inhaled route has a number of attractive features for treatment of pulmonary hypertension, including delivery of drug directly to the target organ, thus enhancing pulmonary specificity and reducing systemic adverse effects. It can also improve ventilation/perfusion matching by dilating vessels supplying ventilated regions, thus improving gas exchange. Furthermore, it can achieve higher local drug concentrations at a lower overall dose, potentially reducing drug cost. Accordingly, a number of inhaled agents have been developed to treat pulmonary hypertension. Most in current use are prostacyclins, including epoprostenol, which has been cleared for intravenous applications but is used off-label in acute care settings as a continuously nebulized medication. Aerosolized iloprost and treprostinil are both prostacyclins that have been cleared by the FDA to treat pulmonary arterial hypertension (PAH). Both require frequent administration (6 and 4 times daily, respectively), and both have a tendency to cause airway symptoms, including cough and wheeze, which can lead to intolerance. These agents cannot be used to substitute for the infused routes of prostacyclin because they do not permit delivery of medication at high doses. Inhaled nitric oxide (INO) is cleared for the treatment of primary pulmonary hypertension in newborns. It is also used off-label to test acute vasoreactivity in PAH during right-heart catheterization and to treat acute right-heart failure in hospitalized patients. In addition, some studies on long-term application of INO either have been recently completed with results pending or are under consideration. In the future, because of its inherent advantages in targeting the lung, the inhaled route is likely to be tested using a variety of small molecules that show promise as PAH therapies.
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PMID:Inhaled Therapies for Pulmonary Hypertension. 2607 May 75

Pulmonary capillary hemangiomatosis (PCH) is a rare cause of primary pulmonary hypertension (PPH) diagnosed in children and young adults with a nonspecific clinical presentation of dyspnea, cough, chest pain, and fatigue. It is characterized by extensive proliferation of pulmonary capillaries within alveolar septa. The imaging features include diffuse centrilobular ground-glass opacities with features of pulmonary hypertension. We present a case of PCH in an 11-year-old boy who was diagnosed with PPH in echocardiography and referred for diagnostic imaging.
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PMID:Pulmonary capillary hemangiomatosis: An unusual cause of primary pulmonary hypertension in a child with characteristic computed tomography imaging features. 3082 52


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