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We read with interest the recent review by Abraham et al.1 Other uncommon conditions of the liver have been described in association with rheumatic diseases.
One case report detailed the presence of rheumatoid nodules in a patient with active rheumatoid arthritis complicated by amyloidosis and chronic renal failure.2 Postmortem findings disclosed numerous nodules scattered throughout the liver of maximum diameter 5 mm. Histological examination of these showed a central zone of cell necrosis with surrounding histiocytes in a palisade arrangement with peripheral fibrosis and a chronic inflammatory cell infiltrate. These nodules were identical to subcutaneous nodules found in the same patient near joints.
Landas et al reported another distinct histopathological entity involving the liver in patients with rheumatoid arthritis who had been treated with gold compounds.3 Each of these patients was biopsied after their gold treatment had been stopped for at least 3 months and before they started treatment with methotrexate. Twenty three of 41 (56%) patients had well formed lipogranulomas in the lobules compared with a 5% incidence in the control biopsy group. In 20 of these cases pigment was noted in the lipogranulomas and in seven patients it was found in lipid droplets in portal triads. The black to brown pigment was confirmed as gold in three cases by energy dispersive spectroscopy. The presence of gold pigment in the liver did not appear to have any serious immediate pathological consequences or other long term effects as judged in 12 patients who were followed up over a period of 10 years.
Spontaneous rupture of the liver has been reported in association with rheumatoid arthritis and systemic lupus erythematosus.4,5 This condition has been described in rheumatoid arthritis complicated by extra-articular features and high titre rheumatoid factor. Petterson et al have also described spontaneous liver rupture in a patient with mild seronegative inflammatory arthritis.6 A generalised necrotising arteritis may also complicate many of the rheumatoid and connective tissue diseases. Hepatic involvement may be part of the arteritis, with resultant nodular regenerative hyperplasia and hepatic rupture occurring as a consequence.
Hepatic involvement therefore can occur not only as part of the disease process but also as Abraham et al1 point out as a result of drug treatment.
We thank Drs Sandhu and Jawad for highlighting additional hepatic pathologies associated with rheumatoid arthritis. Our review was specifically aimed at highlighting liver involvement primarily due to autoimmune rheumatic disease and not as a result of pharmacotherapy.
The presence of hepatic rheumatoid nodules or gold pigmented lipogranulomas is of histopathological interest but has not definitively been associated with an adverse clinical outcome in rheumatoid arthritis. Spontaneous rupture of the liver and hepatic necrotising arteritis are rare, but nevertheless life threatening, complications of autoimmune rheumatic disease.
We reiterate that the physician should remain vigilant to liver pathology using serum liver enzyme markers and clinical examination for hepatomegaly.