Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0206061 (interstitial pneumonia)
6,105 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypersensitivity pneumonitis (HP) represents a group of lung disorders caused by the inhalation of a wide variety of organic particles by susceptible individuals. HP occurs mainly in nonsmokers, but smoking may promote an insidious and chronic disease. The prevalence of HP is difficult to estimate accurately since several antigens can produce the disease, but the range spans infancy to old age. Regardless of the causative antigen or its environmental setting, the clinical manifestations are essentially the same. Three different clinical presentations have been recognized: acute, subacute, and chronic. In the acute form, patients show flu-like symptomatology, followed by dyspnea and dry cough. Symptoms subside a few hours or days later. The subacute and chronic forms result from recurrent low-level antigen exposure and are characterized by progressive dyspnea and dry cough. Other constitutional symptoms such as fatigue, anorexia, and weight loss can be apparent. Fever may occur in the subacute form. Importantly, chronic HP may evolve insidiously or may result from repeated acute/subacute episodes. Recurrent acute, subacute, and chronic HP may progress to irreversible lung fibrosis or provoke emphysematous changes.HP can be difficult to identify, and precise diagnosis requires a history of exposure and a constellation of clinical, imaging, laboratory, bronchoalveolar lavage and pathologic findings. General laboratory tests show an increase of acute phase reactants. Specific precipitating antibodies, when present, are evidence of antigen exposure, and are a hallmark for diagnosis. Chest radiograph usually reveals widespread ground-glass attenuation, and nodular or reticulonodular shadowing. High-resolution CT features include diffuse or patchy ground-glass opacities with small poorly defined nodules and air trapping. Pulmonary function tests are characterized by a predominantly restrictive ventilatory defect with loss of lung volume and hypoxemia at rest that worsens with exercise. Bronchoalveolar lavage reveals a significant increase in lymphocytes, mostly over 40%. In the acute form there is also an increase in neutrophils. Antigen-induced lymphocyte proliferation, and environmental or laboratory-controlled inhalation challenge, may be used for diagnostic purposes and can help to establish a diagnosis of insidious forms of HP. In subacute or chronic cases, lung biopsy may be necessary. Typical findings include bronchiolitis, lymphocytic alveolitis, and loosely formed granulomas, although occasionally other morphologic patterns such as nonspecific interstitial pneumonia may exist. Treatment focuses on avoiding further exposure to the offending antigen(s). Corticosteroids are recommended in subacute and chronic forms. The usual regimen consists of initial high doses of systemic corticosteroid (e.g. prednisone 0.5-1.0 mg/kg/day), followed by gradual tapering.
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PMID:Hypersensitivity pneumonitis : a broader perspective. 1669 87

Acute Q fever is a zoonotic disease caused by the obligate intracellular bacterium Coxiella burnetii and can manifest as a flu-like illness, pneumonia, or hepatitis. A need exists in Q fever research for animal models mimicking both the typical route of infection (inhalation) and the clinical illness seen in human cases of Q fever. A guinea pig aerosol challenge model was developed using C. burnetii Nine Mile phase I (RSA 493), administered using a specialized chamber designed to deliver droplet nuclei directly to the alveolar spaces. Guinea pigs were given 10(1) to 10(6) organisms and evaluated for 28 days postinfection. Clinical signs included fever, weight loss, respiratory difficulty, and death, with the degree and duration of response corresponding to the dose of organism delivered. Histopathologic evaluation of the lungs of animals infected with a high dose showed coalescing panleukocytic bronchointerstitial pneumonia at 7 days postinfection that resolved to multifocal lymphohistiocytic interstitial pneumonia by 28 days. Guinea pigs receiving a killed whole-cell vaccine prior to challenge with the highest dose of C. burnetii were protected against lethal infection and did not develop fever. Clinical signs and pathological changes noted for these guinea pigs were comparable to those seen in human acute Q fever, making this an accurate and valuable animal model of human disease.
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PMID:Clinical and pathologic changes in a guinea pig aerosol challenge model of acute Q fever. 1705 87

The combination therapy with pegylated interferon alpha and ribavirin has increasingly prescribed for chronic hepatitis C. Although many side effects of interferon such as flu-like symptoms, gastrointestinal and neuropsychiatric symptoms are well known, only several cases of interferon-induced pulmonary toxicity have been reported. Interferon-induced pulmonary toxicity usually develops from 2 weeks to 12 weeks after treatment for HCV infection. Diagnosis is commonly based on clinical findings such as a dry cough, dyspnea, hypoxemia, and a restrictive pattern in pulmonary function testing, bilateral diffuse parenchymal infiltrations, histopathological findings of interstitial pneumonitis, and exclusion of any other causative agents. Prompt withdrawal of the drug is the cornerstone of treatment. We report a case of PEG-IFN alpha-2a induced pulmonary toxicity in a 50-year-old male patient with hepatitis C. To our knowledge, this is the first case of pegylated interferon alpha-2a induced pulmonary toxicity in Korea.
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PMID:[Pulmonary toxicity by pegylated interferon alpha-2a in a patient with chronic hepatitis C]. 1738 81

Paraffin tissue blocks from 27 cases with sporadic myocarditis were collected during a 12-year period at a single medical examiner's office. Blocks were studied by using histopathology; immunohistochemistry for viruses (adenovirus, enterovirus, influenza A and B, and human herpes types 4 and 5), bacteria (Neisseria meningitidis, Ehrlichia sp, spotted fever group Rickettsia) and parasites (Toxoplasma gondii and Trypanosoma cruzi); and polymerase chain reaction (PCR)/RT-PCR for adenovirus and enterovirus. We identified enterovirus in 5 (18.5%) cases and Sarcocystis in a 36-year-old woman who had focal inflammation and myocyte necrosis. Immunohistochemical evidence of enteroviruses was found in the myocytes of 2 patients less than 6 months old who had diffuse mononuclear myocardial inflammation, interstitial pneumonitis; one also had encephalitis. In these 2 patients, the presence of enterovirus was confirmed by RT-PCR targeting the 5' nontranslated region and was serotyped as coxsackievirus B2 by sequencing the VP1 capsid region. In another 3 cases (ages 12, 47, and 54), enterovirus was detected by the 5' nontranslated region region; VP1 sequencing identified these as echoviruses 6, 13, and 7, respectively. Accurately identifying an infectious agent is the foundation for clinical and public health interventions. Despite using multiple diagnostic methods, an organism could only be detected in a small proportion of sporadic myocarditis cases.
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PMID:Histopathologic, immunohistochemical, and polymerase chain reaction assays in the study of cases with fatal sporadic myocarditis. 1760 24

Organizing pneumonia (OP) is a specific type of interstitial pneumonia that has been noted as one of the pulmonary manifestations during the course of rheumatoid arthritis (RA). In this study, we report a case with a simultaneous development of OP and RA. The patient presented with concurrent flu-like symptoms and arthralgia of multiple joints, and antibiotic therapy was not effective. The rheumatoid factor (RF) and anti-cyclic citrullinated antibodies were both high. Multiple air-space opacities on chest radiographs and bilateral peripheral consolidations on high-resolution computed tomography films were evident. The histology of transbronchial lung biopsy samples was characterized by intra-alveolar buds of granulation tissue consisting of intermixed myofibroblasts and connective tissues. Treatment with prednisolone induced a complete recovery from OP without relapses. Our review of previous reports about RA-associated OP (RA-OP) suggested that the high titer of RF and increased disease activity of RA indicate a great risk of developing OP. This condition may represent a lung's reaction in the RA-associated inflammatory and/or immune process. We should be aware of RA-OP cases in which pulmonary manifestations precede articular symptoms. In these cases, respiratory manifestations are the main evidence of RA activity. In most cases of steroid-resistant RA-OP, the use of immunosuppressants was effective. Since OP may progress to fibrotic lung disease during the course of RA, we may consider performing a second lung biopsy for steroid-resistant patients, even if they have once been diagnosed as OP.
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PMID:A simultaneous onset of organizing pneumonia and rheumatoid arthritis, along with a review of the literature. 1815 67

(1) Interstitial pneumonia usually develops gradually. The signs and symptoms are non-specific, and generally include dyspnea, cough, fatigue, and weight loss. In other cases onset is acute, sometimes beginning with a flu-like syndrome. Interstitial pneumonia can lead to acute respiratory failure, sometimes gradual deterioration of respiratory function, and pulmonary fibrosis progressing to respiratory failure. The fibrosis does not regress when the causal factor is withdrawn. (2) There are numerous causes of interstitial pneumonia, including medicinal drugs. (3) Amiodarone generally induces slow and insidious lung disease. (4) Methotrexate induces lung disease. Most cytotoxic drugs cause chronic dose-dependent lung disease and fibrosis, in some cases long after treatment cessation. (5) The many other implicated drugs include nitrofurantoin, Nonsteroidal antiandrogens, drugs that induce connective tissue diseases, laxatives based on mineral oil, and many other drugs, some of which are known to cause hypersensitivity reactions. (6) In practice, a drug-related cause should be kept in mind in cases of interstitial pneumonia, as symptoms generally improve after drug withdrawal, unless fibrosis has already started to develop.
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PMID:Drug-induced interstitial pneumonia. 1851 14

Foscarnet, licenced by Astra pharmaceutical products, is a pyrophosphate analogue that selectively inhibits replication of viruses in infected cells. It inhibits in vitro the replication of all herpes viruses, including human cytomegalovirus (HCMV) at concentrations of 100 to 300 mumol/l and has a dose-related inhibitory effect on HIV-1 virus, influenza virus and hepatitis B virus. It does not require intra-cellular phosphorylation for antiviral activity. Oral bioavailability of foscarnet is low (12-22%), and foscarnet must be administered intravenously. It is mainly eliminated unchanged by the kidneys. Mean half-life in plasma ranges from 3.4 to 5 h. For acute therapy, the currently recommended regimen is 60 mg/kg t.i.d. or 90-100 mg/kg b.i.d. In AIDS patients, foscarnet is an effective treatment of HCMV retinitis. Healing or stabilisation of lesions is obtained in 85-95% of patients after 2 weeks or 3 weeks therapy. For HCMV gastrointestinal disease, complete or partial response rates of 57-95% have been reported with foscarnet. The optimal maintenance dosage of foscarnet necessary in CMV infections in AIDS patients remains to be clearly established. Data from small samples size studies have shown that foscarnet decreased significantly circulating levels of HIV antigen in AIDS patients with HCMV disease. Foscarnet is an effective treatment for acyclovir-resistant herpes simplex virus and for acyclovir-resistant varicella-zoster virus (40 mg/kg every 8 h). In patients with immunosuppression not HIV-related HCMV infections, particularly interstitial pneumonia in transplant recipients, experience with foscarnet is limited. The major adverse effect of foscarnet is reversible renal dysfunction, due to acute tubular toxicity. In may be partially prevented by hyperhydratation during the treatment. Fluctuations in serum calcium and phosphore levels, with both increase and decrease are also frequent adverse reactions. Most clinical symptoms are related to decrease in ionized calcium levels. Hyperphosphatemia, a clinically benign phenomenom, reflects the incorporation of foscarnet in bone. Penile ulcerations have been described and may result from mococutaneous direct toxicity of foscarnet eliminated in urine. Although relapses frequently occur after a few months of maintenance therapy, foscarnet that shows a marked activity against HCMV in vitro, has allowed important progress in therapy of HCMV infections in AIDS patients.
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PMID:Pharmacology and clinical use of foscarnet. 1861 71

Infections of the respiratory system are responsible for the majority of hospitalizations and deaths in pediatric patients in developing countries. We selected 177 necropsies of pediatric patients who died as a result of serious respiratory infections. The histopathological findings and epidemiological data were reviewed, and lung tissue samples were separated for immunohistochemistry testing. Conventional immunohistochemistry techniques were used to detect viral antigens in formalin-fixed, paraffin-embedded (FF-PE) lung tissue samples using a pool of monoclonal antibodies against respiratory viruses (respiratory syncytial virus, influenza A and B, adenovirus, and parainfluenza 1, 2, and 3 viruses) as primary antibodies. The histopathological findings were classified into bronchopneumonia (BCP) and interstitial pneumonitis (IP) patterns. The immunohistochemistry results were compared with histopathological patterns and epidemiological data. Positive results for viruses were found in 34% and 62.5% of the BCP and IP cases, respectively. Males and infants below 1 year of age were more frequent in the group that had positive results for viruses. Acute enteritis was the main cause of hospitalization and sepsis the most frequent cause of death in this group. A clear seasonal distribution was observed, with the majority of cases occurring in the 2nd and 3rd trimesters (autumn and winter) of each year in the period studied. Immunohistochemistry is an affordable and easy-to-perform method for viral-antigen detection in FF-PE tissue samples. Although BCP is a classic histopathological pattern found in bacterial infections, it is possible that children with serious respiratory infections had concomitant viral and bacterial infections, regardless of their previous immunologic state.
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PMID:Respiratory viruses in pediatric necropsies: an immunohistochemical study. 1901 65

Chinese rhesus macaques infected with influenza virus A/Tiger/Harbin/01/2002 (H5N1) developed acute interstitial pneumonia with diffuse alveolar damage. The results of virus isolation, reverse transcriptase polymerase chain reaction, immunohistochemistry, and in situ hybridization showed that the lung was the major target organ of the H5N1 virus infection. No virus was detected in the extrapulmonary organs. The results of immunohistochemistry and in situ hybridization also showed that pneumocytes and macrophages of the lower airway, not the ciliary epithelium of the trachea and bronchi, were the chief target cells in the lung tissue of the infected Chinese rhesus macaque. Our data indicate that the Chinese rhesus macaque is suitable as a new primate model for H5N1 virus research, especially for the study of H5N1 virus transmission. The predilection of the H5N1 virus to infect the lower airway suggests that the failure of the virus to attach to the ciliary epithelium of the trachea and bronchi may be a limiting factor in human-to-human transmissibility of the H5N1 virus.
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PMID:Pathological lesions and viral localization of influenza A (H5N1) virus in experimentally infected Chinese rhesus macaques: implications for pathogenesis and viral transmission. 1913 Jan 69

The H1N1, H3N2 and, more recently, H1N2 subtypes of influenza A virus are presently co-circulating in swine herds in several countries. The objectives of this study were to investigate the pathogenesis of Sw/Italy/1521/98 (H1N2) influenza virus, isolated from respiratory tissues of pigs from herds in Northern Italy, and to evaluate its potential cross-protection against the Sw/Fin/2899/82 (H1N1) strain. In the pathogenesis test, eight pigs were intranasally infected with H1N2 virus; at pre-determined intervals, these animals were killed and necropsied, along with eight uninfected animals. In the cross-protection test, sixteen pigs were infected by intranasal (i.n.) and intratracheal (i.t.) routes with either H1N2 or H1N1 virus. Twenty days later, all pigs were challenged (by the same route), with either the homologous H1N2 or heterologous H1N1 virus strains. Control group was inoculated with culture medium alone. On post-challenge days (PCD) 1 and 3, two pigs from each infected group, along with one control pig, were killed. Clinical, virological, serological and histopathological investigations were performed in both the pathogenicity and cross-protection tests. In the pathogenicity test, mild clinical signs were observed in two pigs during 3 and 4 days, respectively. Virus was isolated from two pigs over 6 days and from lung samples of pigs killed on post-infection days 2 and 4. Seroconversion was detected in the two infected animals killed 15 days after infection. In the cross-protection study, mild clinical respiratory signs were detected in all pigs infected with either the H1N2 or H1N1 virus. The virus was isolated from nasal swabs of almost all pigs till 6 days. After the challenge infection, the pigs remained clinically healthy and virus isolation from the nasal secretions or lung samples was sporadic. Antibody titres in H1N1 or H1N2 infected groups were similar, whereas the H1N2 sub-type induced less protection against re-infection by homologous and heterologous virus than H1N1 sub-type. The controls had no signs of the disease. In the H1N2 infected pigs, a reduced number of goblet cells in nasal and tracheal mucosa and small foci of lymphomononuclear cell infiltrates in the submucosa were detected. Furthermore, the goblet cell reduction was related to the time of infection. Diffuse mild interstitial pneumonia was also recorded in pigs infected with the H1N2 virus and challenged with either H1N1or H1N2 pigs. These studies showed the moderate virulence of the H1N2 virus and a partial cross-protection against heterologous infection.
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PMID:Pathogenesis and subsequent cross-protection of influenza virus infection in pigs sustained by an H1N2 strain. 1953 54


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