British Journal of Rheumatology 1994;33:787-792
LETTERS TO THE EDITOR
Systemic Lupus Erythematosus Following Interferon
Therapy
SIR—The occurrence of autoimmune disease related to
interferon (IFN) therapy has been reported previously
[1]. SLE has been described occasionally following IFN
therapy [2-4]. Schilling described a patient treated with
a-2a IFN (Roferon A, Roche) who developed SLE.
Metha reported a patient treated with a-2b IFN (Intron,
Schering-Plough) who developed SLE and finally Oberg
published a case of SLE induced by a-2a IFN (Roferon,
Roche).
We present two cases of chronic myeloid leukemia
treated with IFN who subsequently developed SLE. Both
patients fulfilled the ARA criteria for SLE [5].
Case 1 was a 31-yr-old Caucasian woman with no per-
sonal or family history of connective tissue disease who
was admitted for surgery on her left parotid gland because
of a mixed parotidal tumour. Physical examination
revealed a palpable spleen. Blood tests revealed a leuko-
cytosisof94.0 x lO'/l (band forms 12%, neutrophils 56%,
lymphocytes 10%, eosinophils 10%, metamyelocytes 8%,
myelocytes 12%, basophils 0%), haemoglobin was
12.9 g/dl and platelets 780 x lO'/l. The leucocyte alkaline
phophatase (LAP) score was 4 (normal 20-40), serum lac-
tic dehydrogenase was 883 U/l. Cytogenetic studies
yielded a Philadelphia chromosome in 100% of meta-
phases. Treatment with busulphan (4 /p day) and alpha-2b
IFN (Intron, Schering AG, 10 x 10* U/day) was initiated.
Twenty weeks later the patient developed fever, arthri-
tis in the PIP joints of both hands, photosensitivity and
alopaecia. ANA were 1/156 with a homogenous pattern.
DNA antibodies were negative. LAP was 44 u/l. Forty
weeks later the patient developed autoimmune haemo-
lytic anaemia with positive Coomb's test for IgG and
complement. She was treated with corticosteroids, her
ANA titre was 1/640. Six months later an allogenic bone
marrow transplant was performed. She died of cardiac
arrest 13 days after the transplant.
Case 2 was a 15-yr-old white female with no personal or
family history of connective tissue disease who developed
marked asthenia. Blood tests showed: white cell count,
156 x 109/l with neutrophils, 54%; lymphocytes, 6%;
monocytes, 1%; eosinophils, 1%; metamyelocytes, 16%;
myelocytes, 14%; promyelocytes, 2%; blast cells, 2%;
nucleated red cells, 1%; haemoglobin, 9.8 g/dl; platelets,
498 x 109/l the LAP score was 3, the Philadelphia chro-
mosome was present in 100% of metaphases.
Busulphan (4 mg/day) and a-2b IFN (Intron, Schering
AG 10 x 106 U/day) were initiated. One month later the
patient complained of mild fever, headache, alopaecia
photosensitivity, mouth ulcers and pain in the PIP and
DIP joints of both hands. ANA antibodies were 1/320 with
a homogenous pattern. IFN therapy was not interrupted.
The white cell count was 4 x 10* but cytogenetic response
was partial (50% Philadelphia negative metaphases).
SLE is a prototype of autoimmune disease character-
ized by development of antibodies to multiple nuclear and
cytoplasmatic antigens. Interestingly enough elevated
levels of y-IFN have been found in active SLE [6]. In SLE
patients the levels of ct-IFN correlated with ANA and
anti-DNA antibodies, and inversely correlated with
complement levels. All of these are indicators of disease
activity. In addition elevated levels of a-IFN indicated
clinical disease activity [7].
787
SLE might be a side-effect of IFN treatment. Animal
models of lupus had the disease exacerbated after 7-IFN
therapy. Furthermore monoclonal antibodies blocking
IFN receptors produced an improvement in the lupus
symptoms with a decrease in anti-DNA antibodies [8].
We could not confirm that SLE developed as a result of
IFN therapy because the ANA status of our patients was
not determined prior to treatment. However cohort stud-
ies of haematological patients treated with recombinant
IFN-a 2a (Roferon-A, Roche) have shown that a minority
of patients developed positive ANA during treatment
after being followed for 22 months (range 3-62 months).
None developed full blown SLE [9]. Other studies showed
Downloaded from http://rheumatology.oxfordjournals.org/ at Florida Atlantic University on July 29, 2015
the development of SLE in three of 125 patients treated
with Y-2b IFN (Intron A, Schering-Plough) [10].
We conclude that IFN therapy may exacerbate, cause or
induce SLE in a minority of patients.
A. FLORES,* A. O u v ^ t E. FELIU,* X. TENA
*Haematology Service and fRheumatology Section, Hos-
pital Universitario 'Germans Trias i Pujol', Cta Canyet sn,
Badalona 08917, Spain
Accepted 28 February 1994
Correspondence to: A. Ohve\
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Measuring the Effects of Yoga in Rheumatoid Arthritis
SIR—RA is a complex disease which requires the broad
skills of a multidisciplinary team for effective manage-
ment. Increasing attention is now given to the patient's
role with the team, with emphasis on self-help and a
greater degree of control by the patients of their disease
and its treatment. A logical extension of this process is the
use of less conventional methods of management in con-