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)

Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine involved in a wide range of important physiologic processes. This cytokine has a pathologic role in some diseases, and TNF-alpha antagonists are effective in treating inflammatory conditions. Given the putative role of TNF-alpha in host defense against tuberculosis and other infections, the risk of infection with TNF-alpha antagonists is a concern. Therefore, we searched the literature for reports of tuberculosis and other infections associated with TNF-alpha-antagonist therapy. Although tuberculosis was rarely reported in randomized clinical comparisons of these antagonists, case reports and submissions to the MedWatch program of the United States Food and Drug Administration have been numerous. Most instances were associated with infliximab, but etanercept and adalimumab may also be associated with an increased risk of tuberculosis. Histoplasmosis, listeriosis, aspergillosis, coccidioidomycosis, and candidiasis have been associated with TNF-alpha antagonists, but the causative relationship is not clear. Potential recipients of these drugs should be rigorously screened with skin testing, detailed questioning about recent travel and potential tuberculosis exposure, assessment for symptoms such as cough and weight loss, and chest radiography to minimize their risk of acquiring or reactivating tuberculosis. As with other immunosuppressant drugs, TNF-alpha antagonists should not be given to patients with active infection.
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PMID:Infections associated with tumor necrosis factor-alpha antagonists. 1616 93

Virus-associated hemophagocytic syndrome (VAHS) triggered by HHV-8 is extremely rare and has been reported only in 9 immunocompromised patients. We report the first case of HHV-8-associated VAHS in an HIV-negative, immunocompetent patient with plasmablastic variant (plasmablastic microlymphoma) of multicentric Castleman disease (MCD). This 61-year-old man presented with fever, cough, and bilateral inguinal lymphadenopathy. Biopsy of the right inguinal lymph node revealed plasmablastic MCD with nodular aggregates of plasmablasts expressing IgM, MUM1, HHV-8 latency-associated nuclear antigen, and viral interleukin-6. These plasmablasts were monotypic for Iglambda light chain expression but not Igkappa. All the B-cell clonality assays, including IgH-FR2, IgH-FR3, DH-JH, Igkappa, and Iglambda PCR, showed a polyclonal pattern. His serum human interleukin-6 level was markedly elevated and was negative for EBV acute infection/reactivation. The marrow aspirate showed florid hemophagocytosis. His disease progressed rapidly to multisystemic illness, and he died of acute respiratory failure in 1 month. Our case showed that HHV-8 might trigger VAHS in an immunocompetent patient with plasmablastic MCD. We speculated that our patient developed VAHS under the cytokine storm associated with the proliferating HHV-8-infected plasmablasts, similar to the EBV-triggered VAHS in patients with EBV-associated T-cell lymphoma.
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PMID:Fatal HHV-8-associated hemophagocytic syndrome in an HIV-negative immunocompetent patient with plasmablastic variant of multicentric Castleman disease (plasmablastic microlymphoma). 1633 Sep 52

Current data concerning epidemiology, clinical picture, pathogenesis, prevention and treatment of Avian influenza H5N1, data of pharmacodynamics and pharmacokinetics of antiviral drugs--neuraminidase inhibitors and M2 channels inhibitors, also the recommendation of WHO for prevention prevalence of infection were discussed in the review. Strategic measures of WHO aims to protect humans from contact with infected poultry, in case of contact, to prevent transmission of this infection from human to human and occurrence of pandemic. Infected birds were the major source of the H5N1 influenza virus among humans in Asia. Mainly humans became infected by eating infected birds, by poor hygiene procedures when cooking infected birds, or by close contact with infected poultry. At present transmission of the H5N1 influenza from human to human by aerosol way hasn't been registered, but ongoing monitoring for identification mutation and adaptation of H5N1 influenza virus to human is needed. Season influenza and avian H5N1 influenza differ by the ways of transmission, clinical picture, severity, pathogenesis, response to treatment. Diagnostic of infection is difficult due to non-specific initial symptoms, in most cases disease begins with disturbance of under respiratory ways and in rare cases--from upper respiratory ways. High viral titre is identified in pharynx but not in nose. Initial symptoms of the H5N1 influenza are: fever greater then 38 degrees Celsius, mild cold, cough and shortness of breath, practically all patient have viral pneumonia, later secondary bacterial infection occurs, mild to severe respiratory distress, diarrhea, vomiting and abdominal pain. Conjunctivitis is rarely diagnosed contrary to season influenza. Sometimes gastrointestinal disorder begins a week early then respiratory symptoms. Complication also includes renal and multi organ failure. The cytokine storm is commonly developed during H5N1 influenza. For treatment and for prevention (under certain conditions) of the H5N1 influenza neuraminidase inhibitors such as oseltamivir (Tamiflu) and zanamivir (Relenza) are recommended. Currently circulatory of the H5N1 strains are fully resistant to an older class of antiviral drugs--the M2 channels inhibitors (amantadine and rimantadine). The knowledge of epidemiology, pathogenesis, clinical picture, treatment of the H5N1 influenza in humans, in spite of progress isn't complete. Future coordination of scientific investigation of the H5N1 influenza in humans should be provided not only in the countries where infection was revealed, but all around the world.
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PMID:[Epidemiology, clinical picture, prevention and treatment of Avian influenza]. 1657 38

Airway pathologies have been comprehensively researched in adult asthma, but in children, the extent of airway inflammation associated with episodic wheeze, often diagnosed as asthma, has not been fully characterized. It is not clear whether persistent airway inflammation is present in the absence of wheezing symptoms, and there is controversy regarding the role of age and atopy. This study assessed cellular and cytokine markers of airway inflammation in asymptomatic children with a history of episodic wheeze. Children with a history of episodic wheeze and cough (study group) and nonasthmatic patients requiring elective surgery (control group) were recruited. All subjects in the study group had a history of significant episodic wheezing (>2 episodes per year), and used only as-needed beta-agonist treatment. Bronchoalveolar lavage (BAL) was obtained using bronchoscopic lavage (study group) and nonbronchoscopic lavage (control group). Differential cell counts of BAL and flow cytometry were performed to identify T-lymphocyte phenotypes, and intracellular cytokine profiles were measured after phorbol-12-myristate 13-acetate (PMA) stimulation of BAL fluid T-cells. Twenty-one children with a history of 2-12 episodes of wheeze per year and 21 nonasthmatic subjects without respiratory symptoms were recruited. Study and control subjects were matched for age (median age, 5 years) and demographic characteristics. Study subjects had higher IgE levels, but their measurements were still within normal range. No significant differences in BAL differential cell counts were noted, and in both groups, the majority of T-cells were CD3+ CD8+, with a median CD4:CD8 ratio of 0.6. There was no significant difference in T-cell expression of the activation markers HLA-DR and CD25 (IL-2 receptor), or in PMA-induced production of the intracellular cytokines IFN-gamma, IL-2, IL-4, IL-5, and IL-10. The results of this study suggest that significant T-cell-driven airway inflammation is absent in mild or nonatopic, asymptomatic children of this age group who have episodic wheeze. Our findings support asthma management guidelines that do not recommend long-term treatment of this group of patients with anti-inflammatory medications.
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PMID:Airway inflammation in asymptomatic children with episodic wheeze. 1661 54

Tumor necrosis factor (TNF) is a proinflammatory cytokine that has a key role in the pathogenesis of a variety of autoimmune diseases-including rheumatoid arthritis-and is an important constituent of the human immune response to infection. At present, three anti-TNF agents are approved (in the US and elsewhere) to treat selected autoimmune diseases: infliximab, etanercept, and adalimumab. These biologic agents have been associated with a variety of serious and 'routine' opportunistic infections; however, differences exist in the mechanisms of action of these agents that might confer variation in their associated risks of infection. From a public-health standpoint, the development of active tuberculosis in some patients who receive anti-TNF therapy is a matter of serious concern. Tuberculosis in such patients frequently presents as extrapulmonary or disseminated disease, and clinicians should be vigilant for tuberculosis in any patient taking anti-TNF therapy who develops fever, weight loss, or cough. To prevent the reactivation of latent tuberculosis infection during anti-TNF therapy, clinicians should screen all patients for tuberculosis, and begin treatment if latent infection is found, before anti-TNF therapy is initiated. Specific tuberculosis screening and treatment strategies vary between geographical regions and are reviewed in this document. The screening strategies employed in Europe and North America have reduced the occurrence of anti-TNF-associated tuberculosis and are clearly to be recommended, but the role of screening in the prevention of other opportunistic (e.g. fungal) infections is far less certain.
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PMID:Risk and prevention of tuberculosis and other serious opportunistic infections associated with the inhibition of tumor necrosis factor. 1707 99

To evaluate the clinical characteristics of Mycobacterium tuberculosis infection in rheumatoid arthritis (RA) patients, we examined the clinical manifestations and radiography/computed tomography (CT) findings in RA patients with tuberculosis (RA+/TB+). A total of 1121 tuberculosis patients were admitted to our hospital from 1995 to 2003, with the RA patients among them comprising 1.8% (20 cases; 9 men and 11 women). This is approximately three times as high as the prevalence of RA in the entire population in Japan. In addition, the RA+/TB+ patients were older and had a longer history of RA than the 140 outpatients in our RA clinic who did not have tuberculosis (RA+/TB-). Half of the RA+/TB+ patients had no symptoms (e.g., cough, sputum, pyrexia), and their tuberculosis was detected accidentally by radiography/CT. The positive rates of the bacilli in the smear and culture of the sputum from the RA+/TB+ patients were lower than those from 143 patients randomly selected from among 1091 tuberculosis patients without any collagen disease including RA (RA-/TB+). The RA+/TB+ patients had a higher incidence of extrapulmonary tuberculosis (30%), including four cases (20%) of miliary tuberculosis, an incidence seven times higher than among the general population of tuberculosis patients. Among 14 cases of pulmonary tuberculosis patients with RA, bilateral lesions and non-cavitary lesions were found in 71.4% and 64.3%, respectively, which tended to be a higher incidence than in the RA-/TB+ patients. The mortality rate and sputum conversion time of the RA+/TB+ patients were no different from those of the RA-/TB+ patients. The prevalence of tuberculosis in RA patients is expected to increase after introduction of anti-cytokine therapy in Japan, and careful observation should be done to avoid this complication in RA patients.
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PMID:Clinical characteristics of Mycobacterium tuberculosis infection among rheumatoid arthritis patients. 1714 64

Schisandra fructus has been used for treatment of cough and thirst in Korea. However, its therapeutic mechanisms remain largely unclear. To investigate the biological effect of Schisandra fructus water extract (SFWE), we examined the effect of SFWE on the phorbol 12-myristate 13-acetate (PMA) and calcium ionophore A23187-induced pro-inflammatory cytokine secretion in the human mast cell line HMC-1. HMC-1 cells were stimulated with PMA plus A23187 in the presence or absence of SFWE. Tumor necrosis factor (TNF)-alpha, interleukin 6 (IL-6), and granulocyte-macrophage colony-stimulating factor (GM-CSF) productions were measured by enzyme-linked immunosorbent assay and reverse transcription-polymerase chain reaction. Inhibitory IkappaB/nuclear factor-kappaB (NF-kappaB) expression was assessed by western blot. SFWE suppressed PMA plus A23187-induced TNF-alpha, IL-6, and GM-CSF production in dose-dependent manners. Furthermore, SFWE inhibited IkappaB degradation and NF-kappaB nuclear translocation. These results suggest that SFWE inhibits the secretion of pro-inflammatory cytokines in HMC-1 cells through blockade of IkappaB degradation and NF-kappaB activation. Taken together, these findings may help elucidate the mechanism of action of this medicine in the modulation of mast cell activation in inflammatory conditions.
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PMID:Effects of the Schisandra fructus water extract on cytokine release from a human mast cell line. 1720 33

Swine influenza viruses are an important pathogen in pig industry. In this study, we wanted to know whether swine H1N2 influenza viruses circulating in Korean pigs would cause clinical signs in pigs when experimentally infected. When pigs were infected with swine H1N2 viruses isolated from Korean pigs, pigs suffered from severe clinical signs of coughing, nasal discharge, labored breathing, facial edema, anorexia, and diarrhea. When the level of cytokine induction was measured using lung tissues, pro-inflammatory cytokines such as TNF-alpha, IL-1, and IL-8 were induced higher in lungs of infected pigs than in lungs of uninfected pigs. However, no increased induction of the anti-inflammatory cytokines such as IL-4 and IL-10 was observed in lungs of infected pigs. These results suggest that the pathogenesis induced in pigs by H1N2 influenza viruses may be induced by pro-inflammatory cytokines instead of anti-inflammatory cytokines.
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PMID:Pathogenesis and inflammatory responses of swine H1N2 influenza viruses in pigs. 1757 May 53

Radiation therapy (RT) is an important treatment modality for multiple thoracic malignancies. Incidental irradiation of the lungs, which are particularly susceptible to injury, is unavoidable and often dose-limiting. The most radiosensitive subunit of the lung is the alveolar/capillary complex, and RT-induced lung injury is often described as diffuse alveolar damage. Reactive oxygen species generated by RT are directly toxic to parenchymal cells and initiate a cascade of molecular events that alter the cytokine milieu of the microenvironment, creating a self-sustaining cycle of inflammation and chronic oxidative stress. Replacement of normal lung parenchyma by fibrosis is the culminating event. Depending on the dose and volume of lung irradiated, acute radiation pneumonitis may develop, characterized by dry cough and dyspnea. Fibrosis of the lung, which can also cause dyspnea, is the late complication. Imaging studies and pulmonary function tests can be used to quantify the extent of lung injury. While strict dose-volume constraints to minimize the risk of injury are difficult to impose, substantial data support some general guidelines. New modalities such as intensity-modulated radiation therapy and stereotactic body radiation therapy provide new treatment options but also pose new challenges in safely delivering thoracic RT.
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PMID:Radiation-induced lung injury. Assessment, management, and prevention. 1825 Dec 82

The currently circulating H3N2 and H1N1 subtypes of influenza A virus cause a transient, febrile upper respiratory illness in most adults and children ("seasonal influenza"), but infants, the elderly, immunodeficient and chronically ill persons may develop life-threatening primary viral pneumonia or complications such as bacterial pneumonia. By contrast, avian influenza viruses such as the H5N1 virus that recently emerged in Southeast Asia can cause severe disease when transferred from domestic poultry to previously healthy people ("avian influenza"). Most H5N1 patients present with fever, cough and shortness of breath that progress rapidly to adult respiratory distress syndrome. In seasonal influenza, viral replication remains confined to the respiratory tract, but limited studies indicate that H5N1 infections are characterized by systemic viral dissemination, high cytokine levels and multiorgan failure. Gastrointestinal infection and encephalitis also occur. The licensed anti-influenza drugs (the M2 ion channel blockers, amantadine and rimantadine, and the neuraminidase inhibitors, oseltamivir and zanamivir) are beneficial for uncomplicated seasonal influenza, but appropriate dosing regimens for severe seasonal or H5N1 viral infections have not been defined. Treatment options may be limited by the rapid emergence of drug-resistant viruses. Ribavirin has also been used to a limited extent to treat influenza. This article reviews licensed drugs and treatments under development, including high-dose oseltamivir; parenterally administered neuraminidase inhibitors, peramivir and zanamivir; dimeric forms of zanamivir; the RNA polymerase inhibitor T-705; a ribavirin prodrug, viramidine; polyvalent and monoclonal antibodies; and combination therapies.
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PMID:Current and future antiviral therapy of severe seasonal and avian influenza. 1832 78


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