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Rheumatology 2001; 40: 712-714
© 2001 British Society for Rheumatology
Letters to the Editor |
Gold-induced pneumonitis: computed tomography findings in a patient with rheumatoid arthritis
Departments of Rheumatology and
1Radiology, Wrexham Maelor Hospital, Croesnewydd Road, Wrexham LL13 7TD, UK
SIR, Pneumonitis is a rare adverse effect of treatment with gold. It can cause diagnostic difficulty and can be fatal if unrecognized. We describe here a case and the findings on the computed tomography (CT) scan.
A 77-yr-old lady was diagnosed to have rheumatoid arthritis (RA) when she presented with an 8-month history of pain and swelling affecting the small joints of her hands, wrists, knees, ankles and both shoulders, with early morning stiffness. On examination she had synovitis and restricted movements in her metacarpophalangeal and proximal interphalangeal joints and her wrists, as well as synovitis with effusion in both her knees. She was negative for rheumatoid factor. After initial treatment with steroid pulses, she was commenced on gold (sodium aurothiomalate) injections at a standard dose of 50 mg intramuscularly weekly, following a test dose of 10 mg.
Her RA responded well to treatment, but after a cumulative dose of 560 mg of gold she was admitted on an emergency basis with a 2-week history of progressively increasing shortness of breath on exertion and generally feeling unwell. She did not have any history of cough, expectoration, haemoptysis, orthopnoea, paroxysmal nocturnal dyspnoea or chest pain. On examination, she was comfortable at rest and was not cyanosed, but appeared pale and was apyrexial. Chest auscultation revealed bilateral basal inspiratory crackles and she had an ejection systolic murmur but no pedal oedema, and her jugular venous pressure was normal. Her arthritis was quiescent with no evidence of active synovitis.
Laboratory investigations showed her haemoglobin to be 10 g/dl, the white cell count was 17.6x109/l, with neutrophilic leucocytosis and no eosinophilia, and platelets were 240x109/l. Urea was 22.1 mmol/l and creatinine was 215 mmol/l, which later improved to 7.5 and 92 mmol/l respectively. C-reactive protein was 140 mg/l. Chest radiograph revealed widespread ill-defined shadowing predominantly in the middle and lower zones of both lungs (Fig. 1
). High-resolution CT showed ground glass opacities, which were more obvious in the upper zones. The predominant lung changes involved the middle and lower zones with thickening of the peribronchovascular interstitium and interlobular septa (Fig. 2). The pulmonary function test was consistent with a restrictive lung defect. Echocardiogram showed a mild mitral regurgitation with normal left ventricular function.
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She received three pulses of intravenous methylprednisolone of 500 mg each and the gold injections were discontinued. She responded well and was much improved symptomatically 10 days after the first pulse of methylprednisolone. The repeat CT scan 10 months later showed almost complete resolution, with some heterogeneity of lung density in the posterior aspect of the lower lobes (Fig. 3
). At this time, she was on no specific medication and had not received any maintenance steroid treatment.
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Gold-induced pneumonitis is an uncommon disorder with an incompletely understood pathogenesis. Although first described in 1948 [1], it was brought to wider medical attention only in 1976 [2]. The rarity of the disorder is borne out by the fact that in a review of 47 years of experience with gold therapy in 1019 RA patients, not a single case was described [3].
Gold pneumonitis is a hypersensitivity reaction, as suggested by the clinical and pathological characteristics of the disease. It is also supported by the fact that the syndrome recurred when patients were rechallenged with gold [2]. Release of lymphokines from the lymphocytes of patients with gold-induced pneumonitis after incubation of the lymphocytes with gold salts has been demonstrated, suggesting that cell-mediated immunity may play a role [4].
There is no way to predict its occurrence in individual patients, but there is some evidence for the role of genetic factors, with a significantly increased frequency of HLA-B40 in patients with gold pneumonitis compared with the normal population [5]. It has also been found that patients with RA and gold-induced pneumonitis express two extended human leucocyte antigen haplotypes, HLA-A3 B35 Dwl BfF C4A3,2(BO) and HLA-B40 with a C4 null allele, at a higher frequency than controls [6].
The initial presentation of gold-induced pneumonitis is characterized by progressive dyspnoea and dry cough and is usually accompanied by malaise and weakness [7]. Clinical examination reveals that the patient is tachypnoeic and has basal crepitations. The chest radiograph shows diffuse interstitial and/or alveolar infiltrates with patchy consolidation [8]. CT scans show alveolar opacities along the bronchovascular bundles [9].
There are no characteristic laboratory findings. The plasma viscosity is usually high. Arterial blood gas analysis reveals type 1 respiratory failure with hypoxia and hypocarbia, and the pulmonary function test confirms restrictive defect [8]. Analysis of bronchoalveolar lavage fluid shows an increased number of lymphocytes as opposed to increased polymorphonuclear leucocytes in patients with rheumatoid interstitial lung disease [10, 11]. Pathologically, the changes are non-specific and include interstitial infiltration with plasma cells and lymphocytes, interstitial and alveolar wall fibrosis and intra-alveolar desquamation of mononuclear cells [2, 4, 12–14].
The response of gold hypersensitivity pneumonitis to corticosteroid administration has been prompt and dramatic in most cases [7], although there is no uniformity in the dose and the duration of the treatment. Gold has to be discontinued in all cases [15]. The dose of glucocorticoids and the duration of therapy can be guided by the clinical response of the patient [8]. Relapses have occurred following discontinuation of steroids in some cases [2].
Although uncommon, gold pneumonitis must be considered in patients on chrysotherapy when they develop pulmonary symptoms. It can be fatal or lead to irreversible pulmonary fibrosis if not recognized and treated promptly.
Notes
References
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- Winterbauer RH, Wilske KR, Wheelis RF. Diffuse pulmonary injury associated with gold treatment. N Engl J Med1976; 294:919–21.[Abstract]
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Hakala M, van Assendelft AHW, Ilonen J, Jalava S, Tiilikainen A. Association of different HLA antigens with various toxic effects of gold salts in rheumatoid arthritis. Ann Rheum Dis1986; 45:177–82.
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