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Acute pneumonitis starting 2 hours after intramuscular gold administration in a patient with rheumatoid arthritis
  1. A Hafejee,
  2. M J Burke
  1. Department of Rheumatology, Burnley General Hospital, Casterton Avenue, Burnley, Lancashire BB10 2PQ, UK
  1. Correspondence to:
    Dr A Hafejee

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Gold salts have been used for the treatment of rheumatoid arthritis (RA) for over 50 years.1 Their use is limited by the incidence of adverse reactions, including pneumonitis. Most case reports describe pneumonitis developing after a cumulative dose of several hundred milligrams.2 Only four cases of lung disease have been reported with a cumulative dose of <100 mg.3

Here we report a case of gold pneumonitis, starting only 2 hours after the first maintenance dose of 20 mg was administered.


A 54 year old woman with RA had been followed up since 1984, her arthritis being well controlled with chloroquine. In 1997 her disease had flared up, and alternative disease modifying drugs were introduced—sulfasalazine, then methotrexate (both of were stopped because of adverse side effects), and finally, leflunomide. The last of these caused leucopenia and hypertension (controlled with bendrofluazide and ramipril) and hence was discontinued. Subsequently, her disease became more active again with prolonged joint stiffness, hand synovitis, and erythrocyte sedimentation rate (ESR) 102 mm/1st h.

Treatment was started with gold injections, with a test dose of 10 mg (no adverse effects noted), followed a week later by a dose of 20 mg. About 2 hours afterwards she complained of dizziness, nausea, then she developed a cough and breathlessness. She was admitted to hospital later that day. On examination she was apyrexial, tachypnoeic, cyanosed (oxygen saturation 79% on air), pulse 110/minute, blood pressure 80/46, heart sounds normal, and had no signs of heart failure.

Investigations showed haemoglobin of 103 g/l with normal white cell and platelet counts. C reactive protein was 115 mg/l and troponin-I (a marker for myocardial infarction) was normal at 0.1 μg/l. Arterial blood gases on air showed a type 1 respiratory failure pattern. A chest x ray examination showed bilateral lower zone alveolar shadowing. An echocardiogram showed a normal ejection fraction.

After high dose oxygen treatment, intravenous hydrocortisone 100 mg, and intramuscular adrenaline 0.5 mg 1:1000, some improvement was seen clinically, oxygen saturation rising to 90% and blood pressure to 116/69. She was admitted to the high dependency unit and treatment started with pulse methylprednisolone 1 g daily, nasal continuous positive airway pressure ventilation, and required parenteral nutrition. On the day after her admission, she developed a generalised macular rash. Over the next 7 days her clinical condition improved (serial chest x ray examinations over this period showed clearing of the previous alveolar shadowing), and her treatment was changed to a reducing regimen of oral steroids. She was discharged, continuing frumil once daily and prednisolone 5 mg daily. Her arthritis was inactive and blood pressure 110/70. The ESR was 22 mm/1st h.

During her admission, it was considered that owing to the severity of her illness she was not fit enough to have other investigations—for example, computed tomography chest scan, bronchoalveolar lavage, and pulmonary function tests.

The gold was discontinued and her arthritis remains in remission.


Gold pneumonitis is a potentially fatal complication of gold salt treatment. This case illustrates two important points in management:

  • Some of the early symptoms could have been confused with a nitritoid reaction. Indeed, hypertensive patients with RA who are taking angiotensin converting enzyme inhibitors (in this case ramipril) show a higher frequency of such reactions4 even if long term gold treatment is established. This combination should be avoided where possible.

  • The clinical picture started to develop after only 2 hours of gold administration with just a 30 mg cumulative gold dose. Most case reports have suggested higher cumulative dose exposure2,5,6 and longer duration of treatment. To our knowledge such a florid onset has not been previously reported.