Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 66-year-old male presented to our hospital in January 1990 with chief complaints of hemoptysis and cough. These symptoms had developed 10 months previously and had gradually increased. Fine crepitations were audible over the right lower lung field. There were no results suggesting an inflammatory process such as leucocytosis, elevation of ESR or positive CRP reaction. Chest X-ray film on the first visit showed fine nodular shadows in the right lower lung field, and chest CT revealed fine nodular shadows and mild dilatation of the right lower lobe bronchus. Transbronchial lung biopsy specimens showed granulomas with multinucleated giant cells, alveolitis and Masson bodies. The open lung biopsy specimens showed numerous macrophages and foreign body giant cells, and extensive organizing exudates in the bronchioles and alveolar spaces. Proliferation of smooth muscle and fibrosis around the dilated bronchioles were also seen. Thus, this patient demonstrated BOOP pattern, with granulomas and foreign body giant cells. His hemoptysis appeared to have resulted from inflammation of dilated bronchioles. His symptoms and abnormal shadows on chest X-ray improved without any therapy after admission. After treatment with corticosteroid, the diffuse fine nodular shadows disappeared. There has been no recurrence of symptoms to date, although this patient has continued living in the same environment as prior to admission. BAL findings during his prolonged follow-up revealed decrease in lymphocytes and elevation of CD4/CD8 ratio. Although the presence of granulomas suggests the possibility of an allergic reaction, no antigenic material could be identified in this case.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of interstitial pneumonitis with hemoptysis, BOOP (bronchiolitis obliterans organizing pneumonia) pattern, granulomas and foreign body giant cells in lung biopsy]. 150 90

We report a case of azathioprine-induced haemorrhagic alveolitis, in a 14-year-old boy, after renal transplantation. On day 25 the patient developed haemoptysis, fever and hypoxaemia. Chest X-ray showed diffuse reticulo-nodular shadows in both lung fields. Bronchoalveolar lavage samples were haemorrhagic and demonstrated a relative neutrophilia and a mild lymphocytosis, with a normal CD4/CD8 ratio. Azathioprine was discontinued on day 26. The patient required mechanical ventilation for 4 days. A positive leucocyte migration inhibition test and the recurrence of the symptoms after a second short course of azathioprine therapy suggested a cell-mediated mechanism. This patient is, to our knowledge, the first child to suffer from azathioprine-induced pulmonary haemorrhage.
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PMID:Azathioprine-induced pulmonary haemorrhage in a child after renal transplantation. 757 11

From 1983 to 1991 only isolated cases of aspergillosis in AIDS patients were reported; since 1991, an increasing number of cases have been reported suggesting a recent emergence of this fungal infection. Aspergillosis occurs about 10 to 25 months after AIDS diagnosis in patients with CD4 below 50/mm3. Neutropenia and/or steroid therapy, which are known as predisposing factors in aspergillosis, are noticed in about one half of the patients. Previous pulmonary infection, especially pneumocystosis, are very common. Clinical signs are typical of an invasive pulmonary aspergillosis: constant fever, cough, dyspnea, frequent thoracic pains and haemoptysis. Radiologic signs frequently indicate an interstitial infiltration. Nodular and cavitating lesions, pleural effusions, thoracic lymph node enlargement are often present. Diagnosis procedures are realised on bronchoalveolar lavage by direct examination, culture and antigen detection. Aspergillus fumigatus is the most usually species detected. Post-mortem diagnosis is frequent. Invasive bronchial aspergillosis, localised infections (aspergilloma, otitis, sinusitis) or disseminated infections (nervous system, heart, kidney, lymph nodes, thyroid) are also described. Prognosis is poor even with treatment (amphotericin B or itraconazole). An earlier diagnosis and treatment of the bronchial colonization could probably improve this prognosis.
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PMID:[Aspergillosis in acquired immunodeficiency syndrome]. 787 56

We identified 31 patients with human immunodeficiency virus (HIV) infection and lung abscess. All patients had advanced HIV disease, and the mean CD4 cell count was 17/mm3 (range, 2-50/mm3). Twenty-two patients (71%) had previous opportunistic infections, and 24 (77%) had previous pulmonary infections. Symptoms at the time of presentation included fever (90% of patients), cough (87%), dyspnea (35%), pleuritic chest pain (26%), and hemoptysis (10%). The microbiological etiology was established for 28 patients, and the pathogens recovered were bacteria (65%), Pneumocystis carinii (6%), fungi (3%), and mixed microorganisms (16%). The pathogens included Pseudomonas aeruginosa (11), Streptococcus pneumoniae (6), P. carinii (5), Klebsiella pneumoniae (5), Staphylococcus aureus (4), Aspergillus species (3), viridans streptococcus (2), Haemophilus influenzae (1), Streptococcus milleri (1), Proteus mirabilis (1), and Cryptococcus neoformans (1). Mycobacterium tuberculosis was not isolated; two patients for whom a microbiological etiology was not established responded to antituberculous therapy. Patients were treated for 2-12 weeks; 25% of the patients received > 4 weeks of therapy. The outcome was poor: 36% of the patients had recurrences, and 19% died. In patients with AIDS, lung abscess is associated with advanced HIV infection, is due to a broad spectrum of pathogens, responds poorly to antibiotics, and has a poor prognosis.
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PMID:Lung abscess in patients with AIDS. 882 70

An 84-year-old man was admitted to Yonezawa City Hospital with fever, cough, hemoptysis and progressive dyspnea. He had complained of wheezing asthmatoid and exertional dyspnea for the previous 10 years, regardless of the season. On admission, chest radiographs revealed a diffuse ground-glass shadow, fibrotic change, and volume reduction. Arterial blood gas analysis showed extreme hypoxemia. A computed tomographic (CT) scan of the chest showed not only faint ground-glass opacities and dense patches in the whole lung field, but also central bronchiectasis. Laboratory tests revealed that both total serum levels of IgE and specific IgE for Candida albicans were elevated. In the bronchoalveolar lavage fluid, lymphocyte, neutrophil and eosinophil percentages were high, and the CD4/CD8 ratio was low. We diagnosed the fibrotic stage of allergic bronchopulmonary candidiasis. During treatment with hydrocortisone and fluconazole, eosinophilia in the peripheral blood was observed, and serum candida antigen was positive. In addition, high serum levels of soluble interleukin 2 receptors were observed in this patient.
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PMID:[A patient with allergic bronchopulmonary candidiasis showing a high serum level of soluble interleukin 2 receptors]. 949 58

Although hematologic dysplasia is common in HIV disease, evolution to AML is unusual. We report a case of AML in a patient with stage-C3 AIDS who had been previously treated with granulocyte colony-stimulating factor (G-CSF). This 41-year-old black man presented with pancytopenia (Hg 8.6 g/dl, Hct 24.3%, platelets 16,000/mm3, WBC 0.6 x 10(3)/mm3) and hemoptysis. His peripheral smear manifested 19% blasts. His bone marrow biopsy was hypocellular (20%) with greater than 90% blasts, which were positive for myeloperoxidase and Sudan black B. The blasts were negative for nonspecific esterase. Immunophenotypic analysis by flow cytometry showed the majority of cells to be of myeloid lineage, expressing CD13, and CD45 at low intensity. In addition, there was aberrant expression of CD2 and no expression of CD14 or CD4. The diagnosis of AML-FAB-M1 was made. The patient refused chemotherapy. Of the rare cases of AML in HIV patients previously reported in the literature, the majority were of the monocytic or myelomonocytic subtype. This case is of special interest because of prior G-CSF therapy. In this setting, the relationship between HIV, G-CSF, and subsequent AML is controversial.
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PMID:Acute myelogenous leukemia (FAB AML-M1) in the setting of HIV infection and G-CSF therapy: a case report and review of the literature. 976 Jan 57

The objectives of this study were to describe the clinical and radiological features at presentation, and the natural history of HIV-related bronchopulmonary Kaposi's sarcoma. A retrospective review of medical records and chest radiographs was performed in 106 HIV-infected homosexual men with bronchopulmonary Kaposi's sarcoma diagnosed at bronchoscopy between September 1988 and November 1994. The majority of patients had evidence of advanced HIV disease at diagnosis (median CD4 cell count was 15 x 10(6)/l, range 0-288), and 93% had had a diagnosis of cutaneous Kaposi's sarcoma for a median duration of 11 months prior to diagnosis of their bronchopulmonary disease. The most frequent symptoms at presentation were cough (92%), dyspnoea (69%), pleuritic pain (20%), haemoptysis (13%) and wheezing (10%). The most common radiological finding in 73% of our series was of poorly defined and confluent opacities, with predominant middle and lower zone involvement. Median survival was 4 months (range 0-37 months) from diagnosis and 9 months (range 1-25) from the onset of symptoms. Treatment with either chemotherapy or radiotherapy was associated with a significantly reduced risk of death (hazards ratio (HR)=0.48, 95% CI=0.26-0.87). Factors associated with a poor survival, after adjustment for treatment effect were older age (HR=1.79, 95% CI=1.22-2.84) for each 10-year increase in age; a history of pleuritic pain (HR=2.97, 95% CI=1.39-6.32); presence of pleural effusion on X-ray (HR=2.01, 95% CI=1.13-3.59) and a prior diagnosis of cutaneous Kaposi's sarcoma (HR=1.8, 95% CI=1.00, 3.24). Bronchopulmonary Kaposi's sarcoma occurs mainly in patients with advanced HIV disease and a prior history of cutaneous disease. Survival is poor, and adverse prognostic factors include older age at diagnosis and the presence of pleural disease.
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PMID:Bronchopulmonary Kaposi's sarcoma in 106 HIV-1 infected patients. 976 35

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

PRESENTING FEATURES: A 53-year-old man who had human immunodeficiency virus (HIV) presented to the Johns Hopkins Hospital with a 3-month history of increasing dysphagia, cough, dyspnea, chest pain, and an episode of syncope. His past medical history was notable for oral and presumptive esophageal candidiasis that was treated with fluconazole 6 months prior to presentation. Three months prior to presentation, he discontinued his medications, and his symptoms of dysphagia recurred. During that time he developed intermittent fevers and chills, progressively worsening dyspnea on exertion, and a cough productive of white sputum. He also reported a 40-lb weight loss over the past 3 months. On the day prior to presentation, he had chest pain and shortness of breath followed by weakness, dizziness, and a brief syncopal episode. He denied orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, jaundice, hemoptysis, hematemesis, melena, hematochezia, or diarrhea. There was no history of alcohol use, and he stopped smoking tobacco approximately 1 month previously. He smoked cocaine but denied injection drug use. The patient had never been on antiretroviral therapy and had never had his CD4 count or viral load measured. On physical examination, the patient was a thin, cachectic man who appeared older than his stated age. His vital signs were notable for blood pressure of 102/69 mm Hg, resting tachycardia of 102 beats per minute, resting oxygen saturation of 92% on room air, normal resting respiratory rate, and a temperature of 38.1 degrees C. His oropharynx was clear, with no signs of thrush or mucosal ulcers. His pulmonary examination was notable for diminished breath sounds in the lower lung fields bilaterally. Cardiac, abdominal, and neurologic examinations were normal. His skin was intact, with no visible petechiae, rashes, nodules, or ulcers. Laboratory studies showed a total white blood cell count of 3.2 x 10(3)/microL, with a total lymphocyte count of 330/microL, hematocrit of 30.2%, a serum sodium level of 129 mEq/L, and a serum lactate dehydrogenase level of 219 IU/L. The patient had an absolute CD4 count of 8 cells/mm3 and a HIV viral load of 86,457 copies/mL. His arterial blood gas on room air had a pH of 7.51, a PCO2 of 33 mm Hg, and a PO2 of 55 mm Hg. Electrocardiogram and serial serum cardiac enzymes were normal. A chest radiograph showed bilateral upper lobe patchy infiltrates with left upper lobe consolidation. Computed tomographic (CT) scan of the chest with contrast showed bilateral ground glass infiltrates with focal consolidation (Figure 1) and no evidence of pulmonary embolism. Induced sputum was negative for Pneumocystis carinii, fungi, or acid-fast bacilli. A bronchoalveolar lavage was performed. What is the diagnosis?
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PMID:Cases from the Osler Medical Service at Johns Hopkins University. Diagnosis: P. carinii pneumonia and primary pulmonary sporotrichosis. 1533 85

Tuberculosis (TB) is often mistaken for community-acquired pneumonia (CAP). To avoid missing the diagnosis, we recommend that any CAP patient with upper lobe infiltrate, cavitation, miliary pattern, hemoptysis or >1 month of any of cough, fever, malaise,weakness, night sweats, or significant weight loss, should have sputa submitted for Mycobacterium tuberculosis smear and culture. Any CAP patient failing or relapsing after empiric therapy should be investigated for TB. In the presence of HIV with low CD4 count (< or = 200 cells/mL), the presentation may be atypical, and therefore sputa should be submitted for M tuberculosis. Any HIV patient, regardless of CD4 count, with a known history of positive tuberculin skin test, previous TB, or recent exposure to TB, who presents with CAP, should be investigated for TB.
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PMID:Tuberculosis: still overlooked as a cause of community-acquired pneumonia--how not to miss it. 1576 19


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