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

Under conditions of a maximum security laboratory, four cross-bred sheep were inoculated intradermally only or intradermally and intratracheally with a West African isolate of sheep pox virus. All sheep had increased temperature and depression by the fourth or fifth day after infection. Nasal and lacrimal discharge and coughing occurred in all sheep but were more severe in sheep receiving the virus via the tracheal route. From the fifth day after infection, numerous papular erythematous skin lesions developed at the inoculation sites. These were 3-7 mm in diameter and gradually became nodular. Some of these lesions healed and others coalesced to form tumorlike masses. In one sheep, euthanized 14 days after intradermal and intratracheal inoculation, nodular lesions were found in the skin around the eyes, nostrils, oral and perianal regions, the mucosa of the rumen and throughout the lungs. Histologically, skin nodules were characterized by ischemic necrosis, vasculitis, microvesicualtion, eosinophilic cytoplasmic inclusions in the dermal epithelial cells and vacuolar nuclear degeneration. The pulmonary lesion was that of proliferative alveolitis with occasional cytoplasmic inclusions in the alveolar cells and macrophages. Ultrastructurally, large cuboidal virus particles were found both in the skin lesion and inoculated tissue cultures. The sheep pox virus structure was easily distinguished from contagious ecthyma virus, a parapoxvirus which causes sporadic disease in Canada. Serum neutralizing antibodies developed in all the sheep by 14 days postinfection.The clinical and pathological characteristics of experimental sheep pox produced with this West African isolate were similar to those caused by Neethling virus of lumpy skin disease in cattle.
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PMID:Sheep pox: experimental studies with a west african isolate. 1742 83

A 72-year-old man with cough and sputum showed esophageal wall thickening and pneumonia in chest computed tomography (CT) scan. Following endoscopy, we diagnosed reflux esophagitis and subscribed proton pump inhibitor. The esophageal lesion, however, was intractable. We diagnosed microscopic polyangiitis (MPA) because of vasculitis symptoms, cytoplasmic antineutrophil cytoplasmic antibodies (cANCA) in blood and no granulomatous change in the esophagus. We adopted pulse therapy of cyclophosphamide and oral prednisolone; the symptoms and esophageal lesion were markedly improved. We concluded that the esophageal lesion was an aspect of MPA. To our knowledge, this is the first report of esophageal involvement in MPA.
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PMID:Esophageal involvement in microscopic polyangiitis: a case report and review of literature. 1752 40

This study presents the case of rapidly progressing pulmonary aspergillosis in a 47-year-old woman who had healed cavitations of pulmonary tuberculosis in the right upper lobe. She had been treated for pulmonary tuberculosis seven years prior to admission. The initial manifestations of the disease on admission included cough, dyspnea, hemoptysis, pulmonary infiltrate, and renal failure. As anti-myeloperoxidase anti-neutrophil cytoplasmic antibodies (MPO-ANCA) were positive, she was diagnosed with ANCA-associated vasculitis and treated with corticosteroids. This treatment resulted in remission of the vasculitis. However, she developed new pulmonary symptoms and an enlarged cavitary lesion associated with the rapid formation of a fungal, ball-shaped shadow that was serially observed by radiological analysis. Pulmonary resection was finally performed because of acute progressive respiratory failure due to massive recurrent hemoptysis. A subsequent pathological analysis revealed a mass of hyphae with acute-angle branching, features consistent with Aspergillus, within the cavitary lesion, and she was diagnosed with pulmonary aspergillosis. The rapid development of pulmonary aspergillosis associated with the formation of an Aspergillus mycetoma should be attributed to the loss of normal immune mechanisms due to immunosuppressive treatment.
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PMID:Rapid formation of Aspergillus mycetoma in a patient receiving corticosteroid treatment. Serial radiographic observation over two months. 1754 Dec 25

Pulmonary hemosiderosis is rarely associated with urticarial vaculitis especially if normocomplementemic. An eigth year old girl presented with relapsing and remitting chronic and persistent urticarial lesions, conjunctival injection, recurrent cough and hemoptysis. Respiratory findings started at seven years of age. Physical examination revealed diffuse skin lesions mainly settled on the extremities, non-purulent conjunctival injection, rare ronchi and fine crackles in bilateral lower zones of the lungs. Biopsy of the urticaria like skin lesions demonstrated leukocytoclastic vasculitis. Rheumatological markers were negative. Levels of complement fractions 3 and 4 were normal. Chest x-ray demonstrated diffuse alveolar infiltrative images. High Resolution Computed Tomography of the chest revealed diffuse ground-glass appearance, increased interstitial density. Diagnostic flexible fiberoptic bronchoscopy was performed and bronchoalveolar lavage fluid revealed hemosiderin laden alveolar macrophages. She was started on systemic corticosteroid treatment. During follow up, pulmonary symptoms disappeared, however skin lesions and conjunctival symptoms persisted and exacerbated four times in two years. CT of lungs after two years of treatment revealed rare patchy areas of ground glass appearance in bilateral lower lobes and right upper lobe as well as a few of millimetric pleural nodules. This patient is still followed up under low dose steroids and pulmonary findings regressed but low grade inflammation due to vasculitis is thought to continue as supported by the persistence of tomographic findings in the lungs despite the absence of any symptoms. This case demonstrates association of urticarial vasculitis and pulmonary hemosiderosis in the setting of normocomplementemia.
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PMID:Pulmonary hemosiderosis with normocomplementemic urticarial vasculitis in a child. 1756 86

Microscopic polyangiitis is a necrotizing angiitis involving capillaries, venules, and arterioles. The vascular beds of various organs may be involved, causing varying presentations. To our knowledge, this is the first case of anti-myeloperoxidase (anti-MPO) antibody small-vessel vasculitis causing prostatic vasculitis. A 79 year-old nonsmoker American man presented with symptoms of fevers, malaise, weight loss, and cough. Urine analysis revealed hematuria. Blood tests were remarkable for an elevated prostate-specific antigen (PSA) and a serum creatinine of 3.1 mg/dl (baseline, 1.2 mg/dl). Computed tomography (CT) scan of the thorax revealed a 4.7-cm mass in the left lower lobe of the lung. Metastatic prostate cancer was suspected. Therefore, prostatic biopsy was performed. The biopsy revealed fibrinoid degeneration with vasculitic changes involving the arterioles. When evaluated by nephrology, his serum creatinine was 9.9 mg/dl. A renal biopsy was performed, which revealed focal segmental necrotizing glomerulopathy with microscopic vasculitis. All the serologies were normal, with the exception of low C4, and positive perinuclear antineutrophil cytoplasmic antibodies (ANCA) associated with anti-MPO. The patient was started on intermittent hemodialysis, steroids, and oral cytoxan. Despite treatment, with improvement of the respiratory and constitutional symptoms, the patient remained dialysis-dependent. He later decided to discontinue dialysis and subsequently expired. Vasculitic involvement of the prostate is an uncommon manifestation of microscopic polyangiitis. This bedazzling entity is challenging to diagnose and thus makes it difficult to treat in a timely manner.
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PMID:Anti-MPO small-vessel vasculitis causing prostatis and nephritis. 1759 20

We report on the case of a 60-year-old woman with complaints of fatigue, coughing, anorexia, atypical chest pain, recurrent fever, and also ear pain and hearing loss. A test for anti-neutrophil cytoplasmic antibody (ANCA) was myeloperoxidase positive with p-ANCA specificity. Laboratory acute phase parameters were increased. A 2-deoxy-2-[(18)F]fluoro-D: -glucose positron emission tomography/computed tomography investigation showed pathological uptake in the aorta ascendens, with no other involvement of the large vessels. After therapy with methylprednisolon intravenously and later prednisolon orally with methothrexate, her general condition and hearing loss improved both subjectively and objectively. "Atypical" Cogan's syndrome was diagnosed on the basis of sensorineural deafness with improvement on steroids and large-vessel vasculitis of the aortic arch.
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PMID:The role of PET/CT in Cogan's syndrome. 1763 64

Wegener's granulomatosis was diagnosed in 2 boys, aged 17 and 16 years. The first presented with pain in the right flank, without coughing or dyspnoea. He did have peaks of fever, night sweats, weight loss, headache, and epistaxis. The second presented with progressive dyspnoea, haemoptysis, malaise, and headache. Because an infection was suspected, both were given antibiotics, but without effect. Chest X-rays revealed infiltrative abnormalities. A lung biopsy in the first patient and a nasal biopsy in the second revealed a granulomatous inflammation, and both patients had an elevated titre of antineutrophilic cytoplasmic antibodies (ANCA), with a cytoplasmic pattern, and an elevated result of the ELISA test for antiproteinase-3 (PR3). Both patients recovered after aggressive immunosuppressive treatment. Wegener's granulomatosis is a systemic necrotising vasculitis, mostly localised in airways and kidneys. The disease is very rare in children, but may be life-threatening. Therefore, in children with pulmonary problems resistant to antibiotics, it is important to consider a diagnosis of Wegener's granulomatosis and test for ANCA and PR3.
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PMID:[Wegener's granulomatosis in 2 adolescents]. 1776 12

The prognosis for patients with Wegener's granulomatosis has improved considerably over the last decades. The aim of the study was to assess the early death risk based on the prediction model in a population-based cohort of 60 patients with Wegener's granulomatosis. Clinical analysis has been conducted using the disease extent index (DEI) and Birmingham Vasculitis Activity Score for Wegener's Granulomatosis (BVAS/WG) questionnaires for disease activity. Logistic regression analysis and a Wilcoxon test were included into the statistics. Survival time and death risk were assessed using the Kaplan-Meier estimator and the Cox proportional hazard model. An Receiver Operating Characteristic curve or ROC curve was employed to estimate the value of logistic regression. The early death risk was 16 times higher (P<0.02) in the dialyzed patients and 15 times higher (P<0.05) in the patients with cough as compared with the patients without those predicaments. Predictors of early death are: disease duration, hemoglobin concentration, necessity of dialysis and occurrence of cough. Simultaneous renal and respiratory tract involvement is associated with the highest early death risk.
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PMID:Analysis of early death based on the prediction model in Wegener's granulomatosis with pulmonary and renal involvement. 1820 97

Alpha-1-antitrypsin deficiency (AATD) is a genetic disorder that manifests as pulmonary emphysema, liver cirrhosis and, rarely, as the skin disease panniculitis, and is characterized by low serum levels of AAT, the main protease inhibitor (PI) in human serum. The prevalence in Western Europe and in the USA is estimated at approximately 1 in 2,500 and 1 : 5,000 newborns, and is highly dependent on the Scandinavian descent within the population. The most common deficiency alleles in North Europe are PI Z and PI S, and the majority of individuals with severe AATD are PI type ZZ. The clinical manifestations may widely vary between patients, ranging from asymptomatic in some to fatal liver or lung disease in others. Type ZZ and SZ AATD are risk factors for the development of respiratory symptoms (dyspnoea, coughing), early onset emphysema, and airflow obstruction early in adult life. Environmental factors such as cigarette smoking, and dust exposure are additional risk factors and have been linked to an accelerated progression of this condition. Type ZZ AATD may also lead to the development of acute or chronic liver disease in childhood or adulthood: prolonged jaundice after birth with conjugated hyperbilirubinemia and abnormal liver enzymes are characteristic clinical signs. Cirrhotic liver failure may occur around age 50. In very rare cases, necrotizing panniculitis and secondary vasculitis may occur. AATD is caused by mutations in the SERPINA1 gene encoding AAT, and is inherited as an autosomal recessive trait. The diagnosis can be established by detection of low serum levels of AAT and isoelectric focusing. Differential diagnoses should exclude bleeding disorders or jaundice, viral infection, hemochromatosis, Wilson's disease and autoimmune hepatitis. For treatment of lung disease, intravenous alpha-1-antitrypsin augmentation therapy, annual flu vaccination and a pneumococcal vaccine every 5 years are recommended. Relief of breathlessness may be obtained with long-acting bronchodilators and inhaled corticosteroids. The end-stage liver and lung disease can be treated by organ transplantation. In AATD patients with cirrhosis, prognosis is generally grave.
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PMID:Hereditary alpha-1-antitrypsin deficiency and its clinical consequences. 1856 11

Invasive fungal sinusitis should be suspected in immunocompromised or diabetic patients who present with acute sinusitis, inflammation of nasal septal mucosa, unexplained fever or cough, or the orbital apex syndrome. Histopathological studies are required to differentiate among these syndromes. Acute (fulminant) invasive fungal sinusitis has been called mucormycosis, zygomycosis and fulminant invasive sinusitis. Fever, cough, crusting of nasal mucosa, epistaxis, and headache are the most common presenting symptoms. Histopathological studies show hyphal invasion of blood vessels, vasculitis with thrombosis, and tissue infarction. Reports of granulomatous invasive fungal sinusitis come primarily from Sudan, but also from India, Pakistan, and the United States. Patients usually present with proptosis, appear to be immunocompetent and are infected almost exclusively with A. flavus. Chronic invasive fungal sinusitis can be distinguished from the two other forms of invasive fungal sinusitis by its chronic course, dense accumulation of hyphae resembling a mycetoma, and association with the orbital apex syndrome, diabetes mellitus, and corticosteroid treatment. Biopsy and orbital exploration show vascular invasion by fungal elements and only a sparse chronic inflammatory infiltrate.
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PMID:Syndromes of invasive fungal sinusitis. 1865 20


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