Adult respiratory distress syndrome in polymyositis patients with the anti–jo‐1 antibody

Clawson, Kevin; Oddis, Chester V.

doi:10.1002/art.1780381020

Cited by 50 publications

(30 citation statements)

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“…Pulmonary symptoms may dominate the clinical picture, and a chronic decline in pulmonary function or rapidly progressive ILD can be fatal (13)(14)(15). Aggressive therapy is warranted in patients with interstitial pneumonitis, particularly in those with presumed active and treatable alveolitis as demonstrated on high-resolution computed tomography.…”

Section: Discussionmentioning

confidence: 99%

Treatment of antisynthetase‐associated interstitial lung disease with tacrolimus

Wilkes

Sereika

Fertig

et al. 2005

Arthritis & Rheumatism

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217

107

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Objective. To assess the efficacy of tacrolimus in patients with anti-aminoacyl-transfer RNA synthetase (anti-aaRS)-associated interstitial lung disease (ILD) and idiopathic inflammatory myopathy (IIM).Methods. Ninety-eight patients with anti-aaRS autoantibodies were identified in our IIM cohort of 536 patients. The medical records of 15 patients with antiaaRS-associated ILD treated with tacrolimus between 1992 and 2003 were retrospectively reviewed. Pulmonary parameters of response included forced vital capacity, forced expiratory volume in 1 second, and diffusing capacity for carbon monoxide. Manual muscle testing results, serum creatine kinase (CK) levels, and the daily corticosteroid dosage were used to assess improvement in myositis. Random coefficient modeling considering polynomials of time was used to assess the clinical response to tacrolimus.Results. All patients, except for 1, who had pure ILD, had definite or probable IIM. Two patients received tacrolimus for fewer than 3 months, and their data were not analyzed. For the remaining 13 patients, the mean age at onset of ILD was 46.9 years, and the mean duration of pulmonary disease was 14.7 months. Twelve patients had anti-histidyl-transfer RNA synthetase autoantibody (anti-Jo-1) and 1 had anti-alanyltransfer RNA synthetase autoantibody (anti-PL-12). Patients received tacrolimus for an average of 51.2 months. A significant improvement was observed in all pulmonary parameters measured. The serum CK level declined significantly, and 10 patients had either an improvement in muscle strength or maintained normal muscle strength. A statistically significant reduction in the corticosteroid dosage was also observed. Conclusion. Tacrolimus is a well-tolerated and effective therapy for managing refractory ILD and myositis in anti-aaRS-positive patients.The idiopathic inflammatory myopathies (IIMs) are a group of heterogeneous disorders characterized by skeletal muscle weakness and the presence of inflammatory infiltrates on muscle biopsy. The most common autoantibody in IIM targets the anti-aminoacyltransfer RNA synthetase (anti-aaRS) specific for histidine (anti-Jo-1); other antibodies are directed against the aaRS for threonine (PL-7), alanine (PL-12), glycine (EJ), asparagine (KS), and isoleucine (OJ). The "antisynthetase syndrome," which is seen in many patients with anti-aaRS autoantibodies, is characterized by myositis, fever, ILD, inflammatory arthritis, and Raynaud's phenomenon.ILD is a frequent manifestation of polymyositis (PM) and dermatomyositis (DM), and in patients with antisynthetase autoantibodies, the prevalence has been reported to exceed 50% (1-9). Corticosteroids remain the empirical first-line therapy for myositis-associated ILD, but additional immunosuppressive agents are often necessary, including azathioprine, cyclophosphamide, cyclosporine, and tacrolimus. In a previous pilot trial, tacrolimus, a relatively specific inhibitor of lymphocyte proliferation, showed promise in patients with refractory myositis and ILD who were positive for an...

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Section: Discussionmentioning

confidence: 99%

Treatment of antisynthetase‐associated interstitial lung disease with tacrolimus

Wilkes

Sereika

Fertig

et al. 2005

Arthritis & Rheumatism

Self Cite

217

107

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“…Although other forms of lung involvement have also been reported, such as ARDS [11] or organizing pneumonia [10], fibrosing alveolitis is predominant in AA-associated ILD. Its onset is often acute, and the response to corticosteroids is moderate with frequent relapse of the myositis when immunosuppression is tapered off.…”

Section: Discussionmentioning

confidence: 99%

“…Fifty to 100% of patients with AAs, particularly anti-Jo-1, have been shown to develop fibrosing alveolitis [3,[6][7][8][9]. Other primary lung manifestations associated with myositis and anti-Jo-1 include organizing pneumonia [10], acute respiratory distress syndrome (ARDS) [11] and capillaritis with diffuse alveolar haemorrhage [12]. Fever, Raynaud's phenomenon, arthritis and mechanic's hands have all been found to have a strong association with myositis accompanied by ILD, are manifestations of the "anti-synthetase syndrome" [3,9].…”

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confidence: 99%

Pulmonary fibrosis with predominant CD8 lymphocytic alveolitis and anti-Jo-1 antibodies

Sauty

Rochat²,

Schoch³

et al. 1997

Eur Respir J

103

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Interstitial lung disease (ILD) is a complication of polymyositis (PM) and dermatomyositis (DM). It often manifests itself in association with myositis-specific antisynthetase autoantibodies, among which anti-Jo-1 antibodies are the most commonly encountered. In contrast, ILD associated with anti-Jo-1 antibodies without muscle involvement is rare and not well characterized. We report four patients presenting with ILD associated with anti-Jo-1 antibodies. Histological findings of transbronchial biopsies disclosed a pattern consistent with nonspecific interstitial pneumonitis, a CD8+ lymphocytosis was found in bronchoalveolar lavage. Only one of these patients developed an "antisynthetase syndrome" with PM, after nearly 2 yrs of severe ILD. The clinical conditions of all four cases showed stabilization or improvement when cyclosporine was added to their immunosuppressive treatment. These cases confirm that a CD8+ lymphocytic interstitial lung disease may be the first, and sole manifestation of autoimmune disease associated with anti-Jo-1 antibodies. Furthermore, they suggest that this form of interstitial lung disease apparently has a poor response to steroids and cytotoxic drugs, but may respond to moderate doses of cyclosporine and azathioprine in addition to low doses of steroids.

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“…The diagnosis of PM/DM-related ILD does not pose a diagnostic challenge in patients with established disease or in newly diagnosed patients with typical disease manifestations. However, PM/DM may not be suspected as the underlying cause of ILD when lung involvement is the sole manifestation [20,38,41] or when muscle weakness is obscured by incapacitating dyspnoea [20,38,42]. Rarely, in patients with amyopathic DM, the ILD may also create diagnostic difficulties due to the absence of muscle weakness [43].…”

Section: Polymyositis/dermatomyositismentioning

confidence: 99%

Occult connective tissue diseases mimicking idiopathic interstitial pneumonias

Toya²,

2007

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In patients with interstitial lung disease (ILD), the diagnosis of idiopathic interstitial pneumonia is usually made after excluding, among other conditions, connective tissue diseases (CTDs). Although in most patients with a CTD and respiratory symptoms, the systemic nature of the disease is obvious, the ILD-related manifestations in CTDs may often dominate the clinical picture or precede systemic findings and thus mimic idiopathic interstitial pneumonia.With the exception of systemic lupus erythematosus, all CTDs may imitate chronic idiopathic interstitial pneumonias. In this setting, clues to an underlying CTD may be entirely absent or include subtle findings from various systems, including skin, vascular and musculoskeletal system or internal organs. Since nonspecific interstitial pneumonia is a relatively frequent histological pattern in CTDs, biopsy reports of nonspecific interstitial pneumonia should also prompt a search for an underlying CTD.Ultimately, diagnosis of a CTD requires confirmation with immunological testing; interpretation of the various laboratory tests should always be carried out in conjunction with clinical findings.The present article reviews specific clinical aspects of connective tissue disease-related interstitial lung disease that may help differentiate it from idiopathic interstitial pneumonia, especially when interstitial lung disease is the predominant or sole manifestation of an occult connective tissue disease.

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Adult respiratory distress syndrome in polymyositis patients with the anti–jo‐1 antibody

Cited by 50 publications

References 8 publications

Treatment of antisynthetase‐associated interstitial lung disease with tacrolimus

Treatment of antisynthetase‐associated interstitial lung disease with tacrolimus

Pulmonary fibrosis with predominant CD8 lymphocytic alveolitis and anti-Jo-1 antibodies

Occult connective tissue diseases mimicking idiopathic interstitial pneumonias

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