Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0729233 (Thoracic)
 6,478 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence of nontuberculous mycobacteria (NTM) pulmonary diseases in HIV-negative patients was studied prospectively from January 1, 2001 to December 31, 2003 by 32 sentinel sites distributed throughout France. In total, 262 patients who yielded NTM isolates from respiratory clinical specimens, met the bacteriological, radiological and clinical criteria established by the American Thoracic Society for NTM respiratory disease. Among the 262 NTM isolates, 234 were slow-growing mycobacteria (125 Mycobacterium avium-intracellulare complex (MAC), 66 M. xenopi, 34 M. kansasii) and 28 were rapidly growing mycobacteria (25 M. abscessus complex). In the Paris area, M. xenopi was the most frequently isolated species, followed by MAC. Most patients (>50%), except those with M. kansasii, had underlying predisposing factors such as pre-existing pulmonary disease or immune deficiency. Asthenia, weight loss, chronic cough and dyspnoea were the most common clinical symptoms. The classical radiological appearance of NTM infections was indistinguishable from that observed in patients with pulmonary tuberculosis. In summary, the incidence of nontuberculous mycobacteria pulmonary infections in HIV-negative patients was estimated at 0.74, 0.73 and 0.72 cases per 100,000 inhabitants in 2001, 2002 and 2003, respectively.
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PMID:Respiratory infections associated with nontuberculous mycobacteria in non-HIV patients. 1766 65

Described by Reich and Johnson in 1992 [2], the Lady Windermere syndrome occurs exclusively in non-smoking women over the age of 60 years, without significant pre-existing pulmonary disease. It comprises bronchial dilatation, typically in the middle lobe and lingula, together with secondary infection by atypical mycobacteria (Mycobacterium avium in the first cases). Among the 17 cases of atypical mycobacterial infection that we have seen in the past 14 years, there were seven cases of this syndrome. It was associated with cough, sputum, sometimes haemoptysis, febrile episodes and deterioration of general health. The diagnostic criteria and treatment were defined by the American Thoracic Society. The pathophysiological hypothesis proposed by Reich and Johnson was that voluntary suppression of the cough led to congestion of the bronchi and secondary infection with atypical mycobacteria. Currently it is thought more likely that the following factors are involved: progressive increase in dilatation of small bronchi, delayed diagnosis, morphological abnormalities of the thorax, hormonal factors, immune deficiency, genetic neutrophil dysfunction, and even heterozygous forms of cystic fibrosis.
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PMID:[The Lady Windermere syndrome: clinical and bacteriological data and progress in seven cases]. 2268 89

No guidelines are in place for the follow-up and management of pulmonary nodules that are incidentally detected on CT in the pediatric population. The Fleischner guidelines, which were developed for the older adult population, do not apply to children. This review summarizes the evidence collected by the Society for Pediatric Radiology (SPR) Thoracic Imaging Committee in its attempt to develop pediatric-specific guidelines.Small pulmonary opacities can be characterized as linear or as ground-glass or solid nodules. Linear opacities and ground-glass nodules are extremely unlikely to represent an early primary or metastatic malignancy in a child. In our review, we found a virtual absence of reported cases of a primary pulmonary malignancy presenting as an incidentally detected small lung nodule on CT in a healthy immune-competent child.Because of the lack of definitive information on the clinical significance of small lung nodules that are incidentally detected on CT in children, the management of those that do not have the typical characteristics of an intrapulmonary lymph node should be dictated by the clinical history as to possible exposure to infectious agents, the presence of an occult immunodeficiency, the much higher likelihood that the nodule represents a metastasis than a primary lung tumor, and ultimately the individual preference of the child's caregiver. Nodules appearing in children with a history of immune deficiency, malignancy or congenital pulmonary airway malformation should not be considered incidental, and their workup should be dictated by the natural history of these underlying conditions.
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PMID:The incidental pulmonary nodule in a child. Part 1: recommendations from the SPR Thoracic Imaging Committee regarding characterization, significance and follow-up. 2565 69

Pneumonia is the leading cause of death after acute spinal cord injury and is associated with poor neurological outcome. In contrast to the current understanding, attributing enhanced infection susceptibility solely to the patient's environment and motor dysfunction, we investigate whether a secondary functional neurogenic immune deficiency (spinal cord injury-induced immune deficiency syndrome, SCI-IDS) may account for the enhanced infection susceptibility. We applied a clinically relevant model of experimental induced pneumonia to investigate whether the systemic SCI-IDS is functional sufficient to cause pneumonia dependent on spinal cord injury lesion level and investigated whether findings are mirrored in a large prospective cohort study after human spinal cord injury. In a mouse model of inducible pneumonia, high thoracic lesions that interrupt sympathetic innervation to major immune organs, but not low thoracic lesions, significantly increased bacterial load in lungs. The ability to clear the bacterial load from the lung remained preserved in sham animals. Propagated immune susceptibility depended on injury of central pre-ganglionic but not peripheral postganglionic sympathetic innervation to the spleen. Thoracic spinal cord injury level was confirmed as an independent increased risk factor of pneumonia in patients after motor complete spinal cord injury (odds ratio = 1.35, P < 0.001) independently from mechanical ventilation and preserved sensory function by multiple regression analysis. We present evidence that spinal cord injury directly causes increased risk for bacterial infection in mice as well as in patients. Besides obvious motor and sensory paralysis, spinal cord injury also induces a functional SCI-IDS ('immune paralysis'), sufficient to propagate clinically relevant infection in an injury level dependent manner.
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PMID:Spinal cord injury-induced immune deficiency syndrome enhances infection susceptibility dependent on lesion level. 2675 88