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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 30-year old man of Myanmar origin was admitted to our hospital because of productive cough, anorexia, weight loss and fever. Sputum smear was strongly positive for M. tuberculosis (Gaffky 6) and sputum culture proved M. tuberculosis. Caseous necrosis with Langhans giant cells was observed in the biopsied specimens of the liver and bone marrow. He was diagnosed as miliary tuberculosis. Treatment with combined use of isoniazid, rifampicin, ethambutol and streptomycin was started. After one month, his cough resolved, fever subsided and chest X-ray findings improved. Two months later, non-productive cough and fever recurred. Chest radiograph and computed tomographic scan of the chest revealed diffuse ground-glass opacity. Specimens taken by transbronchial biopsy showed pneumocystis carinii in alveoli. Pulsed use of methyprednisolone with Trimethoprim-sulfamethoxazole was started. The symptoms and chest X-ray findings disappeared and he recovered uneventfully. Tests for HIV infection were negative. Anti-HTLV antibody was negative. There were no other suggestive evidences of immune suppression. CD4+T cell count was low, when Pneumocystis carinii pneumonia occurred. The relation between miliary tuberculosis, Pneumocystis carinii pneumonia and CD4-T lymphocytopenia has remained unelucidated.
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PMID:[A case of Pneumocystis carinii pneumonia during treatment for miliary tuberculosis]. 1260 38

The characteristics of cardiac tamponade in patients with human immunodeficiency virus (HIV) disease were examined by evaluating the cases, case series, and related articles, including autopsy series, identified through a comprehensive literature search. One-hundred eighty-five cases of cardiac tamponade have been reported in patients with HIV disease. Sex data were available in 176 patients, of whom 154 (87%) were males. The mean age was 34.7 +/- 10.4 years (range, 11 months to 61 years). Mean CD4 cell count was 98 +/- 95 cells/mm3 (range, 3 to 430 cells/mm3). The most common etiology of pericardial tamponade was mycobacterial infection (78 patients), including Mycobacterium tuberculosis, Mycobacterium avium-intracellulare, and Mycobacterium kansasii. A bacterial cause was found in 20 patients (11%). Staphylococcus aureus was the predominant bacteria, followed by streptococci, Pseudomonas aeruginosa, Listeria monocytogenes, Klebsiella pneumoniae, and Rhodococcus equi. Lymphoma was found in 15 (8%) patients and Kaposi sarcoma in 13 (7%) patients. Numerous unusual organisms, including Cryptococcus neoformans, Nocardia asteroides, Aspergillus species, cytomegalovirus, and herpes simplex were also associated with cardiac tamponade in HIV patients. Occasionally, HIV itself was involved in the pathogenesis. In 48 patients (26%), no cause was found or reported. The most common clinical presentation was dyspnea, followed by fever, cough, chest pain, and cardiac arrest. The predominant pericardial fluid color composition was serosanguineous. The majority of patients died during hospitalization or in the immediate follow-up period. Vigilance for cardiac tamponade in patients with HIV disease, especially in those with opportunistic infections and/or malignancies, and cardiac symptoms, may result in early and proper management of cardiac tamponade in these patients.
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PMID:Cardiac tamponade in patients with human immunodeficiency virus disease. 1293 67

Acute human immunodeficiency virus (HIV) seroconversion illness is a difficult diagnosis to make because of its nonspecific and protean manifestations. We present such a case in an adolescent. A 15-year-old boy presented with a 5-day history of fever, sore throat, vomiting, and diarrhea. The patient also reported a nonproductive cough, coryza, and fatigue. The patient's only risk factor for HIV infection was a history of unprotected intercourse with 5 girls. Physical examination was significant for fever, exudative tonsillopharyngitis, shotty cervical lymphadenopathy, and palpable purpura on both feet. Laboratory studies demonstrated lymphopenia and mild thrombocytopenia. Hemoglobin, serum creatinine, and urinalysis were normal. The following day, the patient remained febrile. Physical examination revealed oral ulcerations, conjunctivitis, and erythematous papules on the thorax; the purpura was unchanged. Serologies for hepatitis B, syphilis, HIV, and Epstein-Barr virus were negative. Bacterial cultures of blood and stool and viral cultures of throat and conjunctiva showed no pathogens. Coagulation profile and liver enzymes were normal. Within 1 week, all symptoms had resolved. The platelet count normalized. Repeat HIV serology was positive, as was HIV DNA polymerase chain reaction. Subsequent HIV viral load was 350 000, and the CD4 lymphocyte count was 351/mm3. HIV is the seventh leading cause of death among people aged 15 to 24 in the United States, and up to half of all new infections occur in adolescents. Our patient presented with many of the typical signs and symptoms of acute HIV infection: fever, fatigue, rash, pharyngitis, lymphadenopathy, oral ulcers, emesis, and diarrhea. Other symptoms commonly reported include headache, myalgias, arthralgias, aseptic meningitis, peripheral neuropathy, thrush, weight loss, night sweats, and genital ulcers. Common seroconversion laboratory findings include leukopenia, thrombocytopenia, and elevated transaminases. The suspicion of acute HIV illness should prompt virologic and serologic analysis. Initial serology is usually negative. Diagnosis therefore depends on direct detection of the virus, by assay of viral load (HIV RNA), DNA polymerase chain reaction, or p24 antigen. Both false-positive and false-negative results for these tests have been reported, further complicating early diagnosis. Pediatricians should play an active role in identifying HIV-infected patients. Our case, the first report of acute HIV illness in an adolescent, emphasizes that clinicians should consider acute HIV seroconversion in the appropriate setting. Recognition of acute HIV syndrome is especially important for improving prognosis and limiting transmission. It is imperative that we maintain a high index of suspicion as primary care physicians for adolescents who present with a viral syndrome and appropriate risk factors.
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PMID:Acute human immunodeficiency virus syndrome in an adolescent. 1452 19

A 51-year-old woman who had been treated for years for rheumatoid arthritis presented with a persistent dry cough and shortness of breath three weeks after administration of the ACE inhibitor temocapril hydrochloride against essential hypertension. Chest radiography and computed tomography showed diffuse reticular shadows and ground-grass opacities in both lung fields. Bronchoalveolar lavage fluid analysis showed an increase of lymphocytes and CD8+ T cells (93.3% of lymphocytes), and a decrease of the CD4/8 ratio of the T cell subset (0.04). Histopathological analysis of trans-bronchial lung biopsy specimens showed infiltration of lymphocytes into the alveolar septa and exudation of alveolar macrophages, signs characteristic of interstitial pneumonia. A drug lymphocyte stimulation test was positive for temocapril, but negative for other drugs. On the basis of these findings, we diagnosed temocapril hydrochloride-induced interstitial pneumonia.
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PMID:[A case of interstitial pneumonia induced by an ACE inhibitor (temocapril hydrochloride)]. 1453 3

Questionnaires were sent to 46 hospitals of all over Japan in order to obtain the clinical data on sarcoidosis patients who were treated with oral corticosteroids. The number of female patients was greater than that of male patients (1.5:1), and the average age was 44.9 +/- 16.5 with peaks at 20 and at 50 to 60. The markers of disease activity were high in serum or bronchoalveolar lavage fluids (BALF): specifically, the serum angiotensin-converting enzyme (sACE) was 27.9 +/- 31.9 IU/ml (n.v. < 21.4), and the CD4/CD8 lymphocyte ratio was 6.5 +/- 5.7. Eye involvement was the most common reason for systemic steroid therapy, followed in order by lung and heart involvement. The main reasons for steroid therapy were the exacerbation of ocular symptoms, visual disturbance, respiratory symptoms, such as cough or exertional dyspnea, progression of chest radiographic findings, heart failure and severe arrhythmia, such as AV block. The initial corticosteroid dose was usually 30 mg of predinisolone per day, but for some refractory cases, a 40-60 mg per day was used. Immunosuppressive drugs, such as methotrexate, were also used in the small number of patients who responded poorly to the steroid. Overall, a good clinical response to the drug was found in 70-80% of the steroid treated patients, but in those with cardiac disease, the response rate was only 48%.
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PMID:Clinical characteristics of 195 Japanese sarcoidosis patients treated with oral corticosteroids. 1462 Jan 65

This study describes the clinical, immunologic, genetic, and pathologic features of Irish Wolfhounds with rhinitis/bronchopneumonia syndrome. The dogs examined were from Belgium, The Netherlands, UK, Canada, Germany, and Switzerland. Signs included transient to persistent mucoid or mucopurulent rhinorrhea, cough, and respiratory dyspnea. Radiographic, rhinoscopic, and bronchoscopic findings were variable. Analysis of ciliary ultrastructure was performed in 5 affected dogs, but no characteristic primary ciliary defects (primary ciliary dyskinesia) were detected. Serum and bronchoalveolar lavage fluid (BALF) concentrations of IgA, IgG, and IgM were determined in some affected dogs and clinically normal Irish Wolfhounds. Serum IgA concentration was below the reference range in 5 of 8 affected dogs tested, whereas BALF IgA concentration was above the normal range in 2 affected adult dogs. The CD4 to CD8 lymphocyte subset ratio (CD4:CD8) in peripheral blood was tested in 3 affected dogs and was within the normal range. BALF CD4:CD8 was tested in 1 affected dog and was higher than the normal range. Decreased neutrophil phagocytosis was observed in 1 of the 4 dogs tested. Analysis of pedigrees of the Belgian, Canadian, German, and Swiss dogs revealed common ancestry, suggesting a heritable syndrome.
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PMID:Rhinitis/Bronchopneumonia syndrome in Irish Wolfhounds. 1465 22

Severe acute respiratory syndrome (SARS) is a highly infectious disease with a significant morbidity and case fatality. The major clinical features include persistent fever, chills/rigor, myalgia, malaise, dry cough, headache and dyspnoea. Less common symptoms include sputum production, sore throat, coryza, dizziness, nausea, vomiting and diarrhoea. Older subjects may present with decrease in general well-being, poor feeding, fall/fracture and delirium, without the typical febrile response. Common laboratory features include lymphopenia with depletion of CD4 and CD8 lymphocytes, thrombocytopenia, prolonged activated partial thromboplastin time, elevated D-Dimer, elevated alanine transminases, lactate dehydrogenase and creatinine kinase. The constellation of compatible clinical and laboratory findings, together with the rather characteristic radiological features especially on HRCT and the lack of clinical response to broad-spectrum antibiotics, should quickly arouse suspicion of SARS. The positivity rates of urine, nasophargyngeal aspirate and stool specimen have been reported to be 42%, 68% and 97%, respectively, on day 14 of illness, whereas serology for confirmation may take 28 days to reach a detection rate above 90%. Recently, quantitative measurement of blood SARS CoV RNA with real-time RT-PCR technique has been developed with a detection rate of 80% as early as day 1 of hospital admission but the detection rates drop to 75% and 42% on day 7 and day 14, respectively.
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PMID:SARS: clinical features and diagnosis. 1501 29

Rhodococcus equi is a facultative intracellular, obligate aerobe, partially acid fast, gram-positive pathogen that causes cavitary pneumonia in animals and immunocompromised humans. We describe 8 cases of R. equi pneumonia in patients with advanced HIV infection (CD4 counts less than 100/mm3), 7 males and 1 female (mean age 30.8 years), observed between 1991 and 1994. A history of exposure to farm animals was found in 4 patients. The most common presenting symptoms were fever, malaise, dyspnea, cough and hemoptysis, chest pain and weight loss. Chest x-rays showed tipical focal area of consolidation throughout the lung (3 upper, 3 lower and 2 middle fields) associated with cavitation in 4 cases. The definitive diagnosis in our hands was delayed only in the first case in which conflicting data resulted from blood culture (Bacillus sp. isolation) and sputum examen (acid-fast bacterium in the Ziehl-Neelsen stain). Final microbiological diagnosis depended on blood cultures (n=5), bronchoalveolar lavage (n=1), sputum (n=1), lung biopsy (n=1). All the patients were treated with prolonged courses of antibiotic therapy (259 days, range 120-340 in 6 dead patients; more than one year and two months respectively in two patients alive). According to microbial susceptibility TMP/SMX, vancomycin, imipenem, rifampin, aminoglycosides, macrolides and quinolons were more frequently used. Resistant R. equi mutants were selected during therapy with TMP/SMX (n=2), rifampin (n=1) and erythromycin (n=1). Five patient underwent pulmonary lobectomy after exclusion of metastatic bacterial lesions. Only 2 patients are alive, one after 365 days of antibiotic therapy and upper lung lobectomy, one after 60 days of antibiotic therapy. Optimal antimicrobial therapy and the role of surgery remain, in our experience, uncertain.
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PMID:[Not Available]. 1503 8

We describe a reconstitution syndrome of immune responses to Pneumocystis carinii pneumonia (PCP) in 2 HIV-infected individuals who received highly active antiretroviral therapy (HAART). Patient 1, who had been successfully treated for PCP 3 years before the initiation of HAART, developed cough and pulmonary shadows 6 weeks after the start of HAART. Patient 2 was introduced HAART immediately after completing the responsive treatment of PCP, and then showed dyspnea and diffuse pulmonary infiltrates 7 months later. Histologic findings of lung-tissue samples showed granulomatous tissue (patient 1) and organizing pneumonia with thickening of alveolar septa (patient 2), and immunohistochemical findings revealed both CD4 and CD8 cell subsets represented in the lesions. The tissue and bronchoalveolar lavage (BAL) specimens showed no organisms, but PCR methods with the BAL samples were positive for P. carinii DNA. It is hypothesized that these second respiratory episodes may have arisen as immune reconstitution syndrome in response to residual P. carinii antigen in the lung.
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PMID:Reconstitution of immune responses to Pneumocystis carinii pneumonia in patients with HIV infection who receive highly active antiretroviral therapy. 1508 Apr 97

A 77-year-old man was admitted to our hospital. He had first noticed a cough, sputum production, and low-grade fever during the summer of 1988. He was diagnosed as having summer-type hypersensitivity pneumonitis (HP) in 1989 on the basis of positive findings of anti-Trichosporon antibodies in the serum and bronchoalveolar lavage (BAL) fluid and and in environmental provocation tests. Thereafter, he presented with re-exacerbation of his disease in summer every year. In 1995, he retired from his work at a moldy hotel and moved to another house to avoid the causative antigen completely. There was no recurrence for the following 5 years. He suffered from cough, sputum production, and dyspnea 4 months after returning to his previous moldy house in October, 2000. A chest CT scan showed peribronchial and subpleural honeycombing, ground glass opacities, and traction bronchiectasis. BAL demonstrated that the lymphocyte count had changed from 78.9% to 42.9% and the CD4/CD8 ratio from 0.39 to 4.07 in 12 years. Antigen avoidance and steroid therapy have improved his condition. However, he stayed repeatedly in his moldy house, and finally died from acute exacerbation in March, 2002. Postmortem examination demonstrated diffuse alveolar damage (DAD) superimposed on honeycombing in the lungs.
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PMID:[Chronic summer-type hypersensitivity pneumonitis presenting with acute exacerbation]. 1511 53


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