Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085593 (chills)
 4,268 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chest radiographs of 39 patients with ankylosing spondylitis were studied. Three showed apical pulmonary fibrosis, two with cavitary lesions. Other known causes of lung disease were excluded. Symptoms and roentgenographic evidence of spondylitis were present for many years prior to the onset of pulmonary symptoms, which variably included shortness of breath, cough, hemoptysis, pleuritic chest pain, fever, and chills. Apical pulmonary lesions of unknown cause were absent in 53 age, sex, and racematched osteoarthritis control patients. The findings suggest that apical pulmonary fibrosis may be an extra-skeletal manifestation of ankylosing spondylitis, the frequency of which approaches that of spondylitic heart disease.
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PMID:Pulmonary manifestations of ankylosing spondylitis. 120 76

We evaluated nine patients with humoral immunodeficiency (6 immunodeficiency with hyper-IgM, 2 X-linked agammaglobulinemia, 1 common variable immunodeficiency) who were being treated with intravenous immunoglobulins (IVIG). After the use of the IVIG regimen in a dose of 250-300 mg/kg/4 weeks for one year, the severity and frequency of infections, even in patients with chronic lung disease, decreased significantly. An improvement in pulmonary function tests was observed in four patients who had airway obstruction prior to IVIG therapy. Side effects such as chills and fever were observed in 21 of 91 infusions, particularly in the early months of therapy. Preinfusion administration of aspirin and diphenhydramine prevented these side effects. The inversion of the CD4+/CD8+ ratio was detected in most patients during both intramuscular gammaglobulins (IMIG) and IVIG therapy.
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PMID:Effects of intravenous immunoglobulin on clinical and immunological findings of patients with humoral immunodeficiency diseases. 130 39

The use of serial chest radiographs to assess disease activity in patients with sarcoidosis is controversial. However, reliance on the symptomatic clinical course to assess disease activity may be misleading. As many patients being treated with corticosteroids have an abrupt clinical deterioration when doses of those medications are decreased, we questioned whether the chest radiograph could depict alterations in disease activity as measured by spirometry in this subset of patients. We retrospectively reviewed the clinical course of all patients with pulmonary sarcoidosis in whom the corticosteroid dose was reduced during a 6-month period. The 15 patients without fever, chills, or purulent sputum during that time were then examined to determine the presence (n = 10) or absence (n = 5) of a symptomatic relapse. All patients who had a symptomatic relapse also had a fall in forced vital capacity of at least 10%, suggesting an increase in disease activity. Serial chest radiographs were evaluated during and after corticosteroid dose reductions and after clinical recovery on higher steroid doses in the patients who had had a relapse. In eight patients, the disease was in radiographic stage 2 (hilar adenopathy and parenchymal lung disease); in seven patients it was in radiographic stage 3 (parenchymal lung disease alone). The disease did not change stage in any patient during the study. Chest radiographs worsened more frequently in patients who had a clinical relapse (seven of 10) than in those who did not have a relapse (zero of five, p less than .05). An alveolar chest radiographic pattern (n = 4) or reticulonodular pattern (n = 3) was noted in the seven patients who had a relapse, with worsening on radiographs often occurring before detection of relapse by symptomatology (four of seven) or spirometry (three of seven). Spirometry and radiographs improved or stabilized after an increase in corticosteroid dose in all 10 patients who had a relapse. We conclude that serial chest radiographs can reflect clinical relapse in patients with sarcoidosis during corticosteroid dose reduction. Furthermore, worsening seen on chest radiographs may be the first evidence of relapse.
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PMID:Do chest radiographic findings reflect the clinical course of patients with sarcoidosis during corticosteroid withdrawal? 210 8

The case is reported of a 40-year-old woman who developed an eosinophilic lung infiltration during malaria prophylaxis with pyrimethamine-sulfadoxine (Fansidar). The patient had a severe condition with cough, fever, chills, dyspnea, weight loss and an unusual but characteristic radiologic picture. Corticosteroid medication was followed by a dramatic improvement in symptoms and complete resolution of the radiographic opacities within a few days. There was no recurrence after cessation of steroids. The authors believe that the cause of this lung disease was an allergic reaction to pyrimethamine-sulfadoxine (Fansidar). Some aspects of drug-induced eosinophilic pulmonary infiltrations are discussed.
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PMID:[Eosinophilic lung infiltration during malaria prophylaxis with pyrimethamine-sulfadoxine (Fansidar)]. 404 13

A case of a 69-year-old man admitted with procarbazine pneumonitis and a review of the literature are presented. The patient completed a second course of MOPP chemotherapy for Hodgkin's disease three days before admission. He presented with a recent onset of fever, chills, anorexia, and malaise. Chest radiography indicated diffuse bilateral interstitial pneumonitis, and pulmonary function studies revealed restrictive lung disease. Attempts to identify an infectious etiology, including open lung biopsy, were negative, and empirical antibiotic therapy was ineffective. The diagnosis was drug-induced hypersensitivity reaction, most likely due to procarbazine. Corticosteroid therapy was instituted with gradual improvement. Six other cases of pneumonitis associated with procarbazine therapy are briefly reviewed, and the use of pulmonary function tests to identify the type and degree of injury and monitor therapy is discussed.
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PMID:Acute pneumonitis associated with MOPP chemotherapy of Hodgkin's disease. 610 Dec 51

A case of hypersensitivity pneumonitis due to pigeon-dropping antigens is reported in a 9 year old girl, and compared with other seven previous reports in children. The insidious nature of this disease, as well as the importance of detailed environmental information in children with unexplained respiratory disease are emphasized. In this case, lung function tests showed a classic restrictive ventilatory defect, and a serious obstructive ventilatory defect evidenced in the narrowing of the smaller airways, and a reduction in the forced expiratory flow at small lung volumes. Hypersensitivity pneumonitis is a lung disease that results from sensitization by inhalation of a variety of organic dusts. Patients usually have circulating antibodies against the etiologic agents. Most patients with this disease also have sensitized T-cells to these agents. Long-term exposure can lead to irreversible lung disease. The histopathologic features are chronic interstitial and alveolar inflammation frequently accompanied by a granulomatous response. The most common symptomatic features are fever, chills and dyspnea 4 to 8 hours after exposure. Antibody activity to antigens is detected in the serum of both symptomatic and asymptomatic breeder's lung. Cellular hypersensitivity to antigens is demonstrated "in vitro" with peripheral lymphocyte populations in almost all symptomatic patients.
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PMID:[Bird breeder's lung in children]. 697 Oct 47

In any febrile patient with an unexplained chest radiographic abnormality who is on medication, the possibility that the observed abnormality is drug-induced must be kept in mind. This is a significant problem in the immunocompromised host receiving chemotherapeutic agents because these agents are almost always associated with a fever, although the fever may not be daily and is usually not associated with sweats or shaking chills. The infiltrate initially can be quite focal and then unilateral, exhibiting diffuse lung disease before becoming bilateral. Thus, in its early stages, it mimics an infectious process. Unfortunately there is no diagnostic test to rule in drug-induced lung disease because it really is a condition of exclusion. Lung biopsy may be required to exclude other causes. It is also important to remember that drugs may be a factor in the immunocompetent patient who is taking medication and has a fever. It is important for the clinician to be aware of which drugs can do this.
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PMID:Drug-induced pulmonary disease. 756 3

Hypersensitivity pneumonitis or extrinsic allergic alveolitis is an immunologically mediated lung disease caused by repeated inhalations of organic antigens. The basic histological lesion consists of a diffuse mononuclear cell infiltration of alveolar wall, alveoli, terminal bronchioles, and neighboring interstitium. The inflammation is often followed by granulomas, which then may progress to fibrosis. Unlike other infectious and noninfectious granulomatous disorders, hypersensitivity pneumonitis is limited to the lung. The disease occurs more frequently in men than in women and children. The acute form of hypersensitivity pneumonitis, characterized by fever, chills, myalgias, cough, and dyspnea, may be confused with acute pneumonitis. Although there is no single radiological, physiological, or immunologic test specific for hypersensitivity pneumonitis, the diagnosis can often be suspected on the basis of a compatible temporal relationship between pulmonary symptoms and a history of environmental or occupational exposure. Once the diagnosis is suspected, the presence of serum precipitating antibodies (immunoglobulin [lg] G), suppressor cytotoxic lymphocytosis in bronchoalveolar lavage (BAL) fluid, and granulomatous alveolitis in lung biopsy specimens is extremely helpful in confirming the diagnosis. For patients in whom the diagnosis is confirmed, avoidance of the causative antigen is the best therapy, although corticosteroids are used to suppress inflammation. Once the fibrosis has developed, the patient may gradually develop respiratory failure or cor pulmonale, possibly resulting in death.
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PMID:Hypersensitivity pneumonitis: a noninfectious granulomatosis. 756 4

Pulmonary mycotoxicosis (PM), also termed organic dust toxic syndrome or silo unloader's syndrome, is an acute illness resulting from massive inhalation of microbial toxins in organic dusts. It has not been well described histologically. Three cases of PM are presented in this report. Open lung biopsies were examined in each case. All of the patients were farmers with no prior lung disease. One had burning in his eyes, throat, and chest after exposure to moldy silage; chills, fever, dry cough, malaise, and weakness developed within 24 hours. Two patients presented with fever, progressive dyspnea, cough, and fatigue within 24 hours of emptying a corncrib, cleaning a chicken coop, and baling hay. Bilateral alveolar and interstitial infiltrates on chest roentgenograms and leukocytosis with neutrophilia were observed in all of the three patients. Two patients became hypoxemic and required mechanical ventilation. Histologic examination showed acute and organizing diffuse alveolar damage in two biopsy specimens and an acute bronchopneumonia in the third. One specimen had 1- to 10-microm ovoid organisms demonstrable with methenamine silver stains; cultures grew Fusarium and Penicillium species. The other two biopsy specimens had negative tissue cultures and special stains for organisms, although Penicillium species were grown from a preoperative bronchoalveolar lavage in one case. The two patients on mechanical ventilation recovered completely with high-dose steroids. The third patient recovered without steroids. No patient had residual functional deficits or chest radiographic abnormalities. PM can be distinguished from allergic and infectious diseases common in individuals exposed to large amounts of organic dust by its clinicopathologic features.
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PMID:Pulmonary mycotoxicosis: a clinicopathologic study of three cases. 961 95

1. Environmental contact with cold air is a common cause of respiratory distress in obstructive lung disease, and direct and reflex changes in bronchial calibre are well documented with this stimulus when it is inhaled or contacts the exposed skin respectively. It is now known that skin chilling does not amplify the effects of breathing cold air, but it is not established if this lack of interaction is unique, or applies to other forms of airway constrictors. 2. To provide data on this issue, 10 subjects with atopic asthma underwent methacholine bronchoprovocations with and without chilling of the integument of their heads and thoraces for 30 min. Chilling was accomplished with a specially designed thermal garment. Spirometry as well as core and skin temperatures were serially monitored during all experiments. 3. In the control phase (no cooling), integumental temperatures rose slightly, the forced expiratory volume in 1.0 s (FEV1.0) did not change, and the mean provocative concentration of methacholine required to reduce the FEV1.0 by 20% (PC20 meth) was 0.47 +/- 0.17 mg/ml (2.4 +/- 0.87 mmol/l). In the cold trial, the temperature of the back fell 5.1 +/- 1.7 degrees C to 28.7 +/- 1.8 degrees C (P < 0.01), core temperatures did not change, and airway obstruction developed (delta FEV1.0 = -6.7 +/- 2.1%; P < 0.05). The PC20 meth, however, was unaltered [PC20 meth = 0.45 +/- 0.13 mg/ml (2.3 +/- 0.66 mmol/l); P = 0.85]. 4. These results demonstrate that although skin cooling produces mild airway obstruction in subjects with asthma, it does not change the response to non-specific bronchoconstrictors such as methacholine.
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PMID:Effects of skin cooling on airway reactivity in asthma. 968 76


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