"Mechanic's hands": a misleading cutaneous sign of the antisynthetase syndrome.
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Biomedical subjects
Publications and source records attributed to J Cadranel.
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Diagnostic probability of community-acquired pneumonia (CAP) depends on data related to age and clinical and radiological findings. The critical evaluation of data in the literature leads to the following conclusions: 1) the prevalence of CAP in a given population with acute respiratory disease is 5% in outpatients and 10% in an emergency care unit. This could be as low as 2% in young people and even higher than 40% in hospitalized elderly patients; 2) the collection of clinical data is linked to the way the patient is examined and to the expertise of the clinician. The absolute lack of "vital signs" has a good negative predictive value in CAP; presence of unilateral crackles has a good positive predictive value; 3) there is a wide range of X-ray abnormalities: localized alveolar opacities; interstitial opacities, limited of diffused. The greatest radiological difficulties are encountered in old people with disorders including chronic respiratory or cardiac opacities and as a consequence of the high prevalence of bronchopneumonia episodes at this age; 4) among patients with lower respiratory tract (LRT) infections, the blood levels of leukocytes, CRP and procalcitonine are higher in CAP patients, mainly when their disease has a bacterial origin. Since you have not a threshold value reliably demonstrated in large populations with LRT infections or acute respiratory disease, presence or absence of these parameters could only be taken as a slight hint for a CAP diagnosis.
INTRODUCTION: Ocular metastases are rare in patients with lung cancer, and exceptionally indicate the condition. EXEGESIS: We report 2 patients with symptomatic ocular metastases indicating lung adenocarcinoma, involving the choroid in the first case and the optic disc in the other, associated with other metastases. No improvement of visual acuity was observed after chemotherapy and radiotherapy. DISCUSSION: Ocular metastases may indicate lung cancer, and are usually associated with other metastatic sites. The global prognosis is poor but an early treatment should result in improvement of visual prognosis.
INTRODUCTION: Soon after the introduction of antiretroviral therapy for HIV infection, some patients may develop an inflammatory immune reconstitution syndrome, in the presence of clinically unsuspected infection. CASE REPORT: We describe a 31 year old patient, who presented with a lymphoid interstitial pneumonia associated with HIV infection. Unexpectedly, 15 days after the beginning of antiretroviral therapy, he developed a worsening of his respiratory function due to Pneumocystis infection. CONCLUSION: The appearance or aggravation of pulmonary symptoms, after highly active antiretroviral therapy has been initiated should lead to suspicion of an opportunist infection. Specific sampling must be considered.
Polymyositis is characterised by an inflammatory reaction in skeletal muscle with a variable degree of muscular weakness and associated with skin lesions in the case of dermatomyositis. Involvement of the muscles of deglutition and the diaphragm may lead to inhalation pneumonia and acute or chronic respiratory failure, often hypercapnic. The other respiratory manifestations are diffuse interstitial pneumonitis (DIP), usually non-specific, and very occasionally pulmonary arterial hypertension. The development of DIP during polymyositis is a grave prognostic factor, respiratory involvement being one of the main causes of morbidity and mortality. The onset of DIP is acute in between 30 and 47% of cases. Anti-synthetase antibodies (particularly anti-JO-1) are positive in about 75% of cases. Treatment is usually with a combination of immunosuppressants and corticosteroids without any immunosuppressants therapy having shown a superiority.
AIDS related mortality has fallen sharply in industrialised countries since 1996 following the introduction of highly active antiretroviral therapy. This has been accompanied by an increase in the proportion of deaths attributable to non-AIDS defining solid tumours, especially lung cancer. The risk of developing lung cancer seems to be higher in HIV infected subjects than in the general population of the same age, partly because the former tend more frequently to be smokers and, especially, intravenous drug users. The carcinogenic role of the antiretroviral nucleoside drugs and their interaction with smoking needs to be examined. Interestingly, there is no clear relationship between the degree of immunosuppression and the risk of lung cancer, so the reason for the increased risk is unknown. The mean age of HIV infected patients at the time of lung cancer diagnosis is 45 years and most are symptomatic. Lung cancer is diagnosed when locally advanced or metastatic (stage III-IV) in 75-90% of cases, similar to patients with unknown HIV status. Adenocarcinoma is the most frequent histological type. The prognosis is worse in HIV infected patients than in the general lung cancer population. Efficacy and toxicity data for chemotherapy and radiation therapy are few and imprecise. Surgery remains the treatment of choice for localised disease in patients with adequate pulmonary function and general good health, regardless of immune status. Prospective clinical trials are needed to define the optimal detection and treatment strategies for lung cancer in HIV infected patients.
INTRODUCTION: The diagnosis of diffuse intra-alveolar haemorrhage (DAH) is suggested by the combination of haemoptysis, anaemia and pulmonary infiltrates. Broncho-alveolar lavage produces macroscopically haemorrhagic fluid and/or haemosiderin laden macrophages. The diagnostic approach should allow distinction between immune mediated and other causes on account of the therapeutic implications. BACKGROUND: The main immunological causes are small and medium vessel vasculitis (Wegener's granulomatosis, microscopic polyangeitis), lupus and Goodpasture's syndrome. Other immune disorders are only rarely involved. The association of DAH with an acute glomerulonephritis, indicating the pulmonary-renal syndrome, extra-thoracic involvement and immunological abnormalities suggest an immune aetiology. Immunosuppressant treatment should be started as soon as possible with corticosteroids often combined with intravenous cyclophosphamide. Plasmapharesis is indicated for Goodpasture's syndrome and poorly responding lupus. Aggravating factors such as hypervolaemia and disorders of haemostasis should be searched for and treated. Hospital mortality is close to 20%. VIEWPOINT AND CONCLUSION: Immune mediated DAH is a disorder whose rarity justifies the establishment of a national registry with the aim of developing standardised diagnostic and therapeutic strategies.
Bronchioloalveolar carcinoma is one of the four histological subtypes of adenocarcinoma and its incidence is increasing. It grows in a lepidic fashion along the alveolar septa without invading alveolar walls. The strict histological definition requires complete surgical resection to exclude any evidence of invasion. This definition is thus only applicable in practice to isolated operable pulmonary nodules. For other types high-resolution lung CT-scan is necessary to evaluate pulmonary involvement because of the high frequency of multifocal disease at initial presentation and because of the presence of ground glass opacities, which can be one of the first manifestations of CBA on CT. Therapeutic management does not differ from non-small cell lung cancer. Solitary nodules are treated by surgical resection with a good prognosis whereas multifocal disease is rarely respectable. Diffuse and/or pneumonic forms are treated with systemic chemotherapy with a generally poor prognosis. However, the recent discovery of the particular sensitivity of this form of adenocarcinoma to EGFR (Epidermal Growth Factor Receptor) tyrosine kinase inhibitors offers new possibilities for management.
OBJECTIVE AND DESIGN: The presence of increased numbers of tumor-infiltrating neutrophils is associated with poorer outcome in patients with adenocarcinoma of the bronchioloalveolar (BAC) subtype. We evaluated the role of inflammatory environment on C-X-C chemokine tumor production. MATERIALS: Bronchoalveolar lavage from 31 consecutive patients with adenocarcinoma of the BAC subtype as well as tumor and normal pulmonary tissue samples. A549 BAC cell line. Peripheral blood mononuclear cells (PBMC), polymorphonuclear neutrophils (PMN) and alveolar macrophages (AM). METHODS: Elisa measurements and immunohistochemical studies of ENA-78, IL-8, IL-1beta and TNF-alpha. RNA isolation, reverse transcription, and PCR amplification of ENA-78 and IL-8. RESULTS: C-X-C peptides were expressed by tumor cells of all the tumor specimens tested. ENA-78 and IL-8 were also expressed by AM. To better understand the regulation of the C-X-C production, BAC cell line was cultured alone or with inflammatory cells. PBMC upregulated both tumor ENA-78 and IL-8 mRNA expression and protein release whereas AM only upregulated ENA-78 mRNA expression and protein release; PMN had no effect. Anti-human IL-1beta antibodies (ab) inhibited the A549 ENA-78 and IL-8 production stimulated by PBMC-CM. Anti-human TNF-alpha ab inhibited A549 ENA-78 production stimulated by AM-CM. IL-1beta and TNF-alpha were expressed in vivo by inflammatory cells, although TNF-alpha was also expressed by tumor cells. CONCLUSIONS: This work emphasizes the role of the host inflammatory response in promoting tumor growth in vivo.
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BACKGROUND: Pneumocystis jerovici pneumonia (PJP) remains a frequent opportunistic infection in HIV infected patients which markedly upregulates HIV replication by mechanisms so far poorly elucidated. PJP triggers the production of proinflammatory mediators with activating effects on HIV. However, anti-inflammatory factors with inhibiting effects on HIV are normally produced in parallel. We postulated that an imbalance of mediators normally controlling HIV replication could underlie its marked increase during PJP. METHODS: The production of tumour necrosis factor alpha (TNFalpha), interleukins IL-6 and IL-10, and beta-chemokine by bronchoalveolar lavage (BAL) cells recovered from HIV infected patients with and without PJP was compared. The pulmonary viral load was determined and correlations with cytokine and chemokine production were examined. RESULTS: TNFalpha and IL-6 release was similar in patients with and without PJP but IL-10 and beta-chemokine release was markedly lower in the PJP group (IL-10: p<10(-2), RANTES, MIP-1alpha and MIP-1beta: p<0.001). The pulmonary viral load was markedly higher in patients with PJP (p<0.001) and correlated negatively with levels of MIP-1alpha, RANTES and IL-10 in BAL fluid cells (p<0.05). CONCLUSION: Pulmonary IL-10 and beta-chemokine production is markedly defective in HIV infected patients with PJP, while pulmonary TNFalpha and IL-6 levels are normal. The resulting excess of these latter factors, which are known to upregulate HIV replication, might contribute to the increase in pulmonary viral load and to the more rapid HIV disease progression observed in patients with PJP.
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The aim of this study was to determine the significance of isolation of Aspergillus fumigatus from cultures of respiratory specimens in nongranulocytopenic patients. The medical records of patients with respiratory specimens positive for Aspergillus fumigatus who were admitted to an adult pneumology ward were reviewed during a 2-year period. A total of 80 respiratory specimens from 76 patients yielded Aspergillus fumigatus. Forty-eight patients were colonized with Aspergillus fumigatus, whereas the 28 (37%) remaining patients had pulmonary aspergillosis, manifest as aspergilloma ( n=19 patients), chronic necrotizing pulmonary aspergillosis ( n=7 patients), and bronchial aspergillosis ( n=2 patients). The presence of typical hyphae in direct examination of bronchoscopic specimens was more likely to be found in infected than in colonized patients ( P=0.04). No immunological test was positive in colonized patients, whereas anti- Aspergillus antibodies were detected in 55% of infected patients ( P<0.001). Pulmonary tuberculosis was the most common underlying lung disease in patients with aspergilloma, but it was not found in any patient with chronic necrotizing pulmonary aspergillosis ( P=0.006). Anti- Aspergillus antibodies were more likely to be detected in patients with aspergilloma (78%) than in patients with chronic necrotizing pulmonary aspergillosis (14%) ( P=0.007). The analysis of predisposing factors, in conjunction with immunological tests and examination of bronchoscopic specimens, is helpful in distinguishing between colonization and infection with Aspergillus fumigatus, as well as for differentiating between aspergilloma and chronic necrotizing pulmonary aspergillosis.