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)

Pneumonia is one manifestation of acute Q fever following infection with Coxiella burnetii. Fever, headache, and myalgia dominate the clinical picture of Q fever pneumonia. Cough is nonproductive and may be absent despite the presence of pneumonia. While in most instances pneumonia results in an illness of mild-to-moderate severity, on occasion it is rapidly progressive and results in respiratory failure. Infection occurs as a result of inhalation of contaminated aerosols. Infected cattle, sheep, and goats are the usual reservoirs for this zoonosis. In some areas, infected parturient cats serve as the reservoir, and in such instances, rounded opacities are seen on the chest radiograph. The diagnosis of C. burnetii pneumonia is usually confirmed by demonstration of a fourfold or greater rise in antibody titer. Treatment is usually with a tetracycline or rifampin for 7 to 10 days.
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PMID:Coxiella burnetii (Q fever) pneumonia. 874 74

Acute pulmonary reactions to nitrofurantoin are an uncommon side effect of therapy and can cause minor or life-threatening pulmonary dysfunction. Symptoms include fever, chills, cough, pleuritic chest pain, dyspnea. Rarely, pleural effusion and/or pulmonary hemorrhage may occur. Diagnosis is made by clinical suspicion and exclusion of other causes of respiratory compromise. Bronchoalveolar lavage (BAL) may be used to rule out infectious etiologies, and an increase in BAL fluid eosinophils is suggestive of drug-induced toxicity. The acute reaction to nitrofurantoin is believed to be mediated by an immune mechanism. Treatment is mainly discontinuation of the drug, however, corticosteroid therapy is recommended for severe reactions. A chronic reaction associated with long-term treatment with nitrofurantoin has also been reported and causes irreversible pulmonary fibrosis. Nitrofurantoin is commonly used to treat urinary tract infections during pregnancy. Despite the known pulmonary side effects of nitrofurantoin, there is no report of this toxicity occurring in pregnant patients. We present a case of respiratory failure occurring in a woman at 16 weeks' gestation who was being treated with nitrofurantoin for a urinary tract infection.
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PMID:Nitrofurantoin-induced pulmonary toxicity during pregnancy: a report of a case and review of the literature. 877 75

Atelectasis occurs frequently in patients with spinal cord injury (SCI). Impaired cough leads to ineffective clearance of secretions. If the secretions cannot be cleared and become thick and purulent, atelectasis may occur. Recombinant human DNase (rhDNase) has been shown to decrease purulent sputum viscosity in vitro. We report two SCI patients with respiratory failure due to recurrent atelectasis from purulent secretions in whom conventional treatment methods had failed. Administration of rhDNase resulted in successful resolution of atelectasis. These results suggest the need for a controlled clinical trial.
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PMID:Resolution of recurrent atelectasis in spinal cord injury patients with administration of recombinant human DNase. 881 75

We described a 4-month-old boy with cerebral infarction due to streptococcal meningitis. He complained of cough and high fever for 2 days. On the next day he admitted to our hospital because of bad humor, drowsiness, and vomiting associated with high fever, respiratory failure and loss of consciousness. On admission, he had opisthotonic posturing, anisocoria and elevated deep tendon reflexes with left side dominance. The cerebrospinal fluid showed increased cells (564/mm3), protein (295 mg/dl), and decreased sugar (1 mg/dl). Streptococcus pneumoniae was detected in the cerebrospinal fluid. Despite intensive treatment by antibiotics, glycerol, and dexamethasone, general condition was worsened, MRI showed a high intense area along the territory of bilateral anterior cerebral arteries and left middle cerebral artery 3-D time-of-flight MRA revealed a decreased signal of these arteries, confirming cerebral infarction. Recanalization of the arteries were observed 17 days after the first MRA examination. Since complication of cerebral infarction influences the prognosis of meningitis, repetitive MRA is very beneficial in patients with bacterial meningitis in order to evaluate the vascular lesion.
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PMID:[Usefulness of MRA in an infant with cerebral infarction due to streptococcal meningitis]. 894 Aug 80

A 61-year-old woman was admitted to our hospital with a two week history of knee-joint pain, dry coughing and dyspnea on exertion. A chest roentgenogram revealed bilateral patchy and infiltrative shadows. Laboratory examination revealed high CK and aldolase levels. Although myositic symptoms were absent, the respiratory symptoms rapidly worsened and respiratory failure developed. An open-lung biopsy and a muscle biopsy were done. The open-lung biopsy specimen showed bronchiolitis obliterans organizing pneumonia (BOOP), but the muscle biopsy specimen revealed non-specific findings. After 4 weeks of intravenous intermittent high-dose corticosteroid therapy, 50mg of cyclophosphamide was given daily, along with 20mg of prednisolone on alternate days. There were marked clinical, physiological and roentgenographic improvements. A test for anti-Jo-1 antibody was positive, which suggested that this patients had pulmonary manifestations of polymyositis/dermatomyositis. Although BOOP can have an indolent course and a good prognosis, it may rapidly worsen and respiratory failure may develop, in which case it should be treated aggressively with a combination of intravenous high-dose corticosteroids and immunosuppressants.
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PMID:[Rapidly progressing BOOP in a patient with positive anti-Jo-1 antibody: response to corticosteroid pulse and immunosuppressant therapy]. 895 14

Cyclophosphamide-induced lung toxicity may be difficult to recognize because of the presence of confounding variables such as concomitant use of other cytotoxic drugs, opportunistic infections, diffuse pulmonary malignancy, radiation pneumonitis, and oxygen toxicity. The purpose of this retrospective analysis was to identify the clinical spectrum of pulmonary toxicity of cyclophosphamide. In our review of case records, we sought to identify patients in whom cyclophosphamide was the only identifiable etiologic factor for lung toxicity. In a 20-yr period six patients were identified with cyclophosphamide-induced lung disease, including five men and one woman ranging in age from 42 to 78 yr. Clinical features of toxicity include dyspnea, fever, cough, new parenchymal infiltrates, gas exchange abnormalities on pulmonary function tests, and pleural thickening on chest roentgenogram. Two patterns of cyclophosphamide-induced lung toxicity were identified. A single patient presented with early-onset pneumonitis and responded to discontinuation of the drug. Five patients with late-onset pneumonitis developed progressive pulmonary fibrosis associated with bilateral pleural thickening. Patients with late-onset pneumonitis showed no response to cessation of cyclophosphamide and institution of corticosteroid therapy. Three of these patients died of respiratory failure. Careful review of the individual cases reported in the literature as cyclophosphamide lung toxicity revealed only 12 cases in whom none of the additional confounding factors could be identified. These could easily be divided in the same two categories. Early-onset pneumonitis is reversible and may respond to corticosteroid therapy. Late-onset pneumonitis, frequently associated with pleural thickening, is clinically distinct from idiopathic pulmonary fibrosis but has a chronically progressive course. It appears unresponsive to corticosteroid therapy.
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PMID:Lung toxicity associated with cyclophosphamide use. Two distinct patterns. 897 Mar 80

A 69-year-old male was admitted to our hospital because of dry cough. Chest X-P and CT scans showed a mass shadow in the right lung, thickening of pulmonary vessels and pleural effusion. Cytological examination of transbronchial brushing specimen revealed lung adenocarcinoma. Cancer cells were also detected in pleural effusion. High levels of CA 19.9 were noticed: 48,400 U/ml in serum and 395,000 U/ml in pleural effusion, respectively. Two courses of combined chemotherapy (CDDP + VDS) were done. Concurrent chest radiation therapy (40 Gy) to primary tumor was also performed. After treatment the primary tumor decreased in size on CT scan analysis, but the patient suffered from respiratory failure due to the increase of sputa and pleural effusion and died 104 days after admission.
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PMID:[A case of lung adenocarcinoma associated with remarkably high levels of CA 19-9 and lymphangitis carcinomatosa]. 902 Sep 51

The records of patients in whom Pneumocystis carinii pneumonia (PCP) was diagnosed between January 1989 and December 1991 were reviewed. Thirty-two patients--all immunocompromised--were included in the study: 41% were HIV-positive and 59% HIV-negative. In 23 patients (72%) concomitant pathogens were isolated, most frequently Cytomegalovirus. Presenting symptoms included fever (97%), cough (75%) and dyspnea (63%). All HIV-infected patients had a T4-lymphocyte count below 200/mm3 (or 20%). The majority of patients (80%) treated with trimethoprim-sulfamethoxazole experienced adverse events which were usually well tolerated so that a therapy change was necessary in only 12% of patients. PCP was fatal in 34% of the patients. Respiratory failure requiring mechanical ventilation carries a poor prognosis. The ratio of non-AIDS/AIDS patients infected with PC is increasing. This increase is due to the growing contribution of patients treated with immunosuppressive agents and patients with disease-associated immunodeficiencies other than AIDS. Our study suggests that treatment of PCP is more successful with early diagnosis. In addition, as mortality rate is high in non-AIDS patients, our data suggest that the more frequent use of PCP prophylaxis in patients given immunosuppressive drugs, might reduce the incidence of PCP and PCP related mortality.
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PMID:Pneumocystis carinii pneumonia. Review of 32 cases in immunocompromised hosts. 908 15

We report an 8-year-old boy who developed cough and respiratory failure 7 months after bone marrow transplantation (BMT) coinciding with the onset of chronic graft-versus-host disease (GVHD). Lung function data, imaging studies, lung biopsy and bronchoalveolar lavage were consistent with the diagnosis of bronchiolitis obliterans organizing pneumonia. While this has been reported in association with chronic graft-versus-host disease in one adult case previously, we report the simultaneous occurrence of BOOP and chronic GVHD in a child after bone marrow transplantation for the first time.
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PMID:Bronchiolitis obliterans organizing pneumonia and chronic graft-versus-host disease in a child after allogeneic bone marrow transplantation. 913 79

We studied clinicopathological characteristics of interstitial pneumonia associated with amyopathic dermatomyositis. The subjects comprised two men and three women, and their mean age was 58.2 years. All subjects had cruptions specific for dermatomyositis, but had no signs of myositis. They all presented with acutely or subacutely developed coughing and dyspnea. Results of tests for anti-Jo-1 antibody were negative in all cases. Chest X-ray films showed infiltrations or streaky shadows, or both in the middle and lower lung fields. Analysis of bronchoalveolar lavage fluid revealed abnormally high percentages of lymphocytes and neutrophils. In one patients a specimen obtained by open lung biopsy showed homogeneous cell infiltrations in alveolar septa and regional alveolar damage. That patient was successfully treated with cyclosporin and corticosteroids in early phase of the disease. The other four patients received immunosuppressive agents after respiratory failure developed. All four died despite having received high-dose corticosteroid and immunosuppressive therapy. Examination of autopsy specimens showed diffuse alveolar damage.
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PMID:[Clinicopathological features of interstitial pneumonia associated with amyopathic dermatomyositis]. 916 43


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