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Timing of therapy in vasculitis-associated multiple myelomaComment on the article by Hasegawa et al.

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LETTERS
and chemical embolization of the liver mass was performed.
Although the patient experienced a slight improvement of his
muscular symptoms, he died a few months later.
Despite the fact that D M is associated with different
neoplasms in -5-20% of cases (2), the association with
hepatocarcinoma is very rare (3). The etiology of D M remains
unknown. Multiple viral infections could play an important
role as a trigger (4). Coxsackie B, adenovirus, human immunodeficiency virus, echovirus, human T cell leukemia/lymphoma
virus type I (S), and hepatitis B virus have been implicated (2).
We know that HCV is associated with vasculitis as cryoglobulinemia (6), and in their recent report, Weidensaul and
colleagues described an association between H C V and PM.
HCV infection is a well-known risk factor for the development
of hepatocarcinoma.
The rarity of an association between hepatocarcinoma
and DM led us to speculate that H C V could play an important
role in the pathogenesis of D M in our patient. We agree with
the suggestion by Weidensaul et al that HCV-induced autoantibodies or circulating immune complexes could contribute
to the pathogenesis of PM (1) or, as in our patient, DM.
Anti-Jo-1 antibody is the most common of a group of anticytoplasmic aminoacyl-transfer R N A (tRNA) synthetase enzymes
directed against histidyl-tRNA synthetase. The viruses that
could cause myositis, perhaps including HCV, interact with
aminoacyl-tRNA synthetase, which is the target of several
myositis-specific antibodies (2). H C V could start the lesion of
myositis and antibody production. We would emphasize that
anti-Jo-1 antibodies have not been reported to be associated
with DM secondary to malignancy, whereas these antibodies
have been found in hepatitis C associated with PM and
interstitial lung disease (1),the latter condition being absent in
our patient. We believe studies for the detection of HCV
should be considered in all patients with D M o r PM.
Albert Gomez, M D
Roser Solans, M D
Carmen Pilar Simeon, M D
Albert Selva, M D
Fernando Garcia, M D
Vicencs Fonollosa, M D
Miguel Vilardell, M D
Hospital General I Universitan de la Val1 d 'Hebron
Barcelona, Spain
1. Weidensaul D, Imam T, Holyst M-M, King PD, McMurray RW:
Polymyositis, pulmonary fibrosis, and hepatitis C. Arthritis Rheum
38:437-439, 1995
2. Plotz PH, Miller FW: Inflammatory muscle disease. In, Rheumatology. Edited by JH Klippel, PA Dieppe. London, Mosby-Year
Book Europe Ltd, 1994
3. Horie Y, Yamada M, Nakai K, Kawasaki H, Hirayama C, Matsui K,
Kdmbe N, Shimao S: Combined hepatocellular-cholangiocarcinoma
associated with dermatomyositis. J Gastroenterol Hepatol 4:lOl104, 1989
4. Venables P, Brookes S: Retroviruses: potential aetiological agents
in autoimmune rheumatic disease. Br J Rheumatol 31%-846,
1992
5. Sherman MP, Amin RM, Rodgers-Johnson PEB, Morgan OSC,
Char G, Mora CA, Iannone R, Collins GH, Papsidero L, Gibbs CJ
Jr, Poiesz BJ: Identification of human T cell leukemiailymphoma
virus type I antibodies, DNA, and protein in patients with polymyositis. Arthritis Rheum 38:690-698, 1995
6. Misiani R, Bellavita P, Fenili D: Hepatitis C virus infection in
395
patients with essential mixed cryoglobulinemia. Ann Intern Med
1175733577. 1992
Timing of therapy in vasculitis-associated multiple
myeloma: comment on the article by Hasegawa et al
To the Editor:
We read with great interest the case report by Hasegawa et al ( l ) , who described a patient with multiple myeloma
whose condition declined due to systemic necrotizing vasculitis. W e had a similar finding in a 67-year-old female patient
who was admitted to the hospital with small painful lesions,
disseminating progressively on her legs. She denied any medication intake. O n admission, her vital signs and physical
examination results were normal except for multiple purpuric
lesions and ulcers on the legs. Laboratory studies disclosed a
hemoglobin concentration of 11.9 gm/dl, an erythrocyte sedimentation rate of 1.50 mm/hour, and serum globulin and
albumin concentrations of 4.8 gm/dl and 3.7 gmidl, respectively. A skeletal survey showed no lytic lesions. Serum antinuclear antibody, antibodies to double-stranded DNA, hepatitis B surface antigen and antibody, hepatitis C antibody, and
cryoglobulin were undetectable. C3 and C4 levels were normal.
The serum IgG level was found to be high (2,450 mg/dl;
normal 720-1,680). A monoclonal spike of IgGK light chain
and 61.5% atypical plasma cells were detected by serum
immunoelectrophoresis and bone marrow aspiration, respectively. Histologic findings on skin biopsy revealed vascular
thickening with thrombus plaques in the lumen of the dermal
vessels and polymorphonuclear and mononuclear cell infiltration on light microscopy, confirming a diagnosis of leukocytoclastic vascuhtis coexisting with IgGK-type multiple myeloma.
Immunoflorescence studies showed C3 positivity in dermal
vessels; IgG, IgA, and IgM were negative.
Oral prednisone, 40 mg/day, was instituted for progressive vasculitic lesions. Chemotherapy for myeloma was postponed and vancomycin was started due to purulent discharge
of leg ulcers infected with methicillin-resistant Staphylococcus
aureus. Unfortunately, she developed renal failure and died 3
weeks after diagnosis, due to intractable septic shock despite
supportive measures and broad-spectrum antibiotic therapy.
Though the precise mechanisms are not clearly defined, probably due to the unique differences among paraprotein structures, cutaneous manifestations of myelomatous disorders are most commonly associated with IgA monoclonal
protein (2-5). Leukocytoclastic vasculitis coexisting with IgGtype multiple myeloma, as observed in our patient, is infrequent, with only 2 reports in the literature to date (6,7);
necrotizing vasculitis simulating polyarteritis nodosa is even
more rare (1).
It is noteworthy that in both our patient and the patient
described by Hasegawa and colleagues, multiple myeloma was
progressive despite corticosteroid therapy for vasculitic manifestations; one would expect that this therapy in the doses
given would also lead to suppression of the neoplastic plasma
cell clone. It might be suggested that vasculitis-associated
myeloma indicates an additional poor prognostic sign, and it
remains to be determined, by further experience, whether
LETTERS
396
intensive and prompt treatment of multiple myeloma should
be initiated even if the disease is indolent.
Arzu Topeli, M D
Hacettepe University School of Medicine
Ankara, Turkey
Ibrahim Bariqta, M D
Ismail Celik, M D
Emin Kansu, MD, FACP
Hacettepe University Institute of Oncology
Ankara, Turkey
1. Hasegawa H, Ozawa T, Tada N, Taguchi Y, Ohno K, Chou T,
Watanabe T, Kuroda T, Nakano M, Usuda H, Ernura I, Arakawa
M: Multiple myeloma-associated systemic vasculopathy due to
crystalglobulin or polyarteritis nodosa. Arthritis Rheum 39:330334, 1996
2. Highet AS: Urticaria1 vasculitis and IgA myeloma. Br J Dermatol
102:355-357, 1980
3. McMillen JJ, Krueger SK, Dyer GA: Leukocytoclasticvasculitis in
association with immunoglobulin A myeloma. Ann Intern Med
105~709-710,1986
4. Means RT Jr, Greer JP, Sergent JS, McCurley T L Leukocytoclastic
vasculitis and multiple myeloma (letter). Ann Intern Med 106:329,
1987
5. Yiannias JA, el Azhary RA, Gibson LE: Erythema elevatum
diutinum: a clinical and histopathologic study of 13 patients. J Am
Acad Dermatol 2638-44, 1992
6. Kois JM, Sexton FM, Lookingbill DP: Cutaneous manifestations of
multiple myeloma. Arch Dermatol 127:69-74, 1991
7. Case Records of the Massachusetts General Hospital (case 301995). N Engl J Med 3332362-868, 1995
for PAN (1). If we had been aware of the crystalglobulininduced vasculopathy associated with multiple myeloma, we
would have initiated early intensive chemotherapy and administered plasma exchange for the crystalglobulinemia. While
some authors have reported an unfavorable outcome of such
treatment in cases of crystalglobulin-induced vasculopathy,
others suggest that it may be efficacious (2-4).
Leukocytoclastic vasculitis may be induced by activation of the complement system by the paraprotein itself, by
immune complexes, o r by cryoglobulin ($6). Obstructive vasculopathy, which is rare in multiple myeloma, is induced by
intravascular deposition of a crystalline substance composed of
paraprotein. This may lead to a systemic vasculopathy with
clinical features that mimic those of PAN. There is an apparent
relationship between the paraprotein and the vasculopathies,
i.e., leukocytoclastic vasculitis and crystalglobulin-induced
vasculopathy.
It is important for clinicians to be aware of the clinical
and morphologic features of the vasculopathies associated with
multiple myeloma. Prompt and intensive treatment of the
multiple myeloma may lead to a favorable outcome in some
cases.
Hisashi Hasegawa, M D
Masaaki Nakano, M D
Masaaki Arakawa, M D
Niigata University School of Medicine
Niigata, Japan
1. Lightfoot RW Jr, Michel BA, Bloch DA, Hunder GG, Zvaifler NJ,
Reply
To the Editor:
We were interested in the description by Dr. Topeli
and colleagues of their patient with leukocytoclastic vasculitis
associated with multiple myeloma, whose case resembled that
of our patient. We agree that the development of vasculitis in
a patient with multiple myeloma may indicate a poor prognosis. Indeed, each of these patients died within a year of
diagnosis. In our opinion, intensive chemotherapy should be
administered in such cases even if multiple myeloma is inactive, although this was not done in our patient.
Our patient was initially diagnosed, early in his clinical
course, as having a vasculopathy as an incidental complication
of polyarteritis nodosa (PAN). His clinical and pathologic
features met the American Collage of Rheumatology criteria
2.
3.
4.
5.
6.
McShane DJ, Arend WP, Calabrese LH, Leavitt RY, Lie JT, Masi
AT, Mills JA, Stevens MB, Wallace SL: The American College of
Rheumatology 1990 criteria for the classification of polyarteritis
nodosa. Arthritis Rheum 33:1088-1093, 1990
Cummings FJ, Park CH, Bogaars HA, Kalderon AE, Melnicoff I,
Kaplan SR, Diamond I, CalabresiP: Successful therapy of crystalcryoglobulinemia. Med Pediatr Oncol 7:181-190, 1979
Mills LE, Brettman LR, Jentoft JE, Viner ED: Crystallo-cryoglobulinemia resulting from human monoclonal antibodies to albumin. Ann Intern Med 99:601-604, 1983
Ball NJ, Wickert W, Mam LH, Thaell JF: Crystalglobulinemia
syndrome: a manifestation of multiple myeloma. Cancer 71:12311234, 1993
McMillen JJ, Krueger SK, Dyer GA: Leukocytoclasticvasculitis in
association with immunoglobulin A myeloma. Ann Intern Med
105~709-710,1986
Means RT Jr, Greer JP, Sergent JS, McCurley T L Leukocytoclastic
vasculitis and multiple myeloma (letter). Ann Intern Med 106:329,
1987
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