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Hepatitis C as another possible cause of porphyria cutanea tarda and systemic lupus erythematosusComment on the article by Kutz and Bridges.

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LETTERS
352
might be a precipitating factor for AAU among Japanese
patients with AS, but not in persons who are otherwise
healthy.
We agree that in those of our patients who had AAU,
the onset of AS was earlier than in those who had not
developed AAU; however, this difference was not statistically significant (Student’s t-test). We also compared the age
at onset of AS between DR8-positive and DR8-negative
patients. No significant difference in the age at onset was
observed between these 2 groups. In our study, the only
significant difference observed was in the association of
HLA-DR8 in patients with versus those without AAU.
There was only 1 patient who was positive for DR8 but did
not have AAU. Since the number of DR8-positive AS
patients with the early-onset type of the disease in our study
population was not large enough to enable statistical analysis, it was difficult to conclude whether DR8 had any relation
to the age of onset of AS. More studies with more patients
are needed in order to support the hypothesis that HLADR8 is specifically associated with the early-onset type
of AS.
With regard to the LMP2 genes, it is difficult to
comment about which class I1 specificity occurs with the
LMP;! gene for linkage disequilibrium, since this has not
been studied in a Japanese population. This might be a useful
area for further investigation.
In conclusion, this first study with a small number of
Japanese AS patients indicated a significant association of
HLA-DR8 among patients who later developed AAU. A
firm conclusion can be reached only when further studies
reconfirm the same observation.
S. M. Monowarul Islam, MD
Jiro Numaga, MD
University of Tokyo School of Medicine
Tokyo, Japan
Hiroo Maeda, MD
Saitama Medical School
Saitama, Japan
Fatal postpartum vasculitis in systemic lupus
erythematosus
To the Editor:
In their interesting case report, Rubin et al describe a
pregnant systemic lupus erythematosus (SLE) patient who
developed pulmonary vasculitis leading to death in the early
postpartum period (1). Although the authors stated that this
was an unreported complication of pregnancy in SLE, we
have reported an almost identical case (2). Both our patient
and the patient described by Rubin and coworkers became
acutely dyspneic and died within 24 hours following vascular
collapse and progressive hypoxemia. At autopsy, acute
inflammation with abundant nuclear debris and fibrinoid
necrosis were unexpectedly found within the walls of pulmonary arteries of varying sizes. Other arteries showed
older lesions with intimal fibrosis and organized and rechanellized thrombi. Interestingly, in both cases, the abovedescribed acute abnormalities were restricted to the lung,
and renal damage attributable to SLE was not found at either
autopsy. Similarities also included the presence of Raynaud’s phenomenon, malar rash and anti-Ro/SS-A antibodies, treatment with low-moderate daily doses of prednisone
throughout pregnancy, and the administration of supplementary hydrocortisone during delivery. Onset of the fatal
complication occurred at different times: our patient had
noted exertional dyspnea and substernal tightness on exertion, relieved by rest, since 4 months prior to the beginning
of her pregnancy, whereas the patient described by Rubin et
a1 reported mild dyspnea beginning in the latter part of her
pregnancy.
Zulman et a1 described an SLE patient who also
developed progressive dyspnea, chest pain, and fever leading to death, within the first week postpartum. Autopsy of
the lung showed no evidence of pulmonary emboli but did
reveal focal vasculitis with fibrinoid necrosis and vascular
occlusion (3).
SLE patients may be particularly vulnerable to complications in the postpartum period. Acute fatal pulmonary
vasculitis, although rare, is one of the catastrophic events
that may develop. In our patient (2), this complication
occurred after 10 years of relatively mild SLE and following
an uncomplicated pregnancy.
Osvaldo Hubscher, MD
Alicia Eimon, MD
Roberto M. Arana, MD
CEMIC
Buenos Aires, Argentina
Rubin LA, Geran A, Rose T H , Cohen H: A fatal pulmonary
complication of lupus in pregnancy. Arthritis Rheum 38:71&714,
1995
Hubscher 0, Eimon A, Elsner B, Arana RM: Fatal post-partum
pulmonary vasculitis in systemic lupus erythematosus. Clin
Rheumatol3:547-550, 1984
Zulman J, Talal N, Hoffman G , Epstein W: Problems associated
with the management of pregnancies in patients with SLE. J
Rheumatol7:37-49, 1980
Hepatitis C as another possible cause of porphyria
cutanea tarda and systemic lupus erythematosus:
comment on the article by Kutz and Bridges
To the Editor:
Kutz and Bridges describe a patient whose condition
they believe represents the rare complication of hydroxychloroquine-induced porphyria cutanea tarda (PCT) in systemic lupus erythematosus (SLE) (1). However, the literature they cite as evidence for hydroxychloroquine induction
of PCT predates the era of diagnostic techniques for hepatitis
C virus, and therefore should be accepted with caution.
Current medical literature shows strong epidemiologic evidence for chronic hepatitis C viral infection as the major
etiologic factor in acquired or sporadic PCT (2-10). It has
been recommended that all patients presenting with PCT be
screened for hepatitis C infection (7-10). In addition, there
has been evidence presented (1 1-14) which shows that
hepatitis C viral infection can induce high-titer antinuclear
LETTERS
353
antibodies, other autoantibodies including anti-DNA in low
titer, and clinical immunologic disorders which in combination may cause a patient to meet the American College of
Rheumatology (ACR) 1982 criteria for SLE (15).
Kutz and Bridges’ patient had findings that were
suggestive of chronic hepatitis C viral infection, yet they do
not mention whether she was screened or otherwise evaluated for this disease. In our opinion, hepatitis C infection is
an important part of the ditferential diagnosis of apparent
SLE with liver disease, and of acquired or induced PCT. We
think the anecdotal information the authors have presented
could be explained by occult chronic hepatitis C viral infection.
The case presented by Kutz and Bridges should be accepted as
evidence for the rare event of hydroxychloroquine-induced
PCT in the setting of SLE only if hepatitis C infection has
been ruled out. Since the treatment for chronic hepatitis C
virus infection is different from that for SLE, and since it is
possible for patients with chronic hepatitis C infection to
meet ACR criteria for SLE, we propose that hepatitis C
testing should be considered in the evaluation for SLE with
abnormal liver-associated enzyme levels or liver disease, as
well as for acquired or drug-induced PCT.
Karen Nepveu, MD
Bonita Libman, MD
University of Vermont College of Medicine
Burlington, VT
DC, Bridges AJ: Bullous rash and brown urine in a
systemic lupus erythematosus patient treated with hydroxychloroquine. Arthritis Rheum 38:44&443, 1995
Fargion S, Piperno A, Cappellini MD, Sampietro M, Fracanzani
AL, Romano R, Caldarelli R, Marcelli R, Vecci L, Fiorelli G:
Hepatitis C virus and porphyria cutanea tarda: evidence of a
strong association. Hepatology 16:1322-1326, 1992
Herrero C, Vincente A, Bruguera M, Ercilla MG, Barrera JM,
Vidal J, Teres J, Mascaro JM, Rodes J: Is hepatitis C virus
infection a trigger of porphyria cutanea tarda? Lancet 341:788789, 1993
DeCastro M, Sanchez J , Herrera JF, Chaves A, Duran R,
Garcia-Buey L, Garcia-Monzon C, Sequi J , Moseno-Otero K:
Hepatitis C virus antibodies and liver disease in patients with
porphyria cutanea tarda. Hepatology 17551-557, 1993
F e n i C, Baicchi U, LaCivita L, Greco F, Longombardo G,
Mazzoni A, Carrecia G, Bombardieri S, Pasero G, Zignego AL,
Manns MP: Hepatitis C virus-related autoimmunity in patients
with porphyria cutanea tarda. Eur J Clin Invest 23:851455,
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Jasmer RM, Larson MS, Weilbaecher KN: Porphyria cutanea
tarda and hepatitis C virus infection in a patient with acute liver
failure. West J Med 161513-515, 1994
Lacour JPH, Bodokh I, Castanet J, Bekri S, Ortonne JP:
Porphyria cutanea tarda and antibodies t o hepatitis C virus. Br
J Dermatol 128:121-123, 1993
Murphy A, Dooley S, Hillary I S , Murphy GM: HCV infection
in porphyria cutanea tarda. Lancet 341:1534-1535, 1993
Castanet J, Lacour JPH, Bodokh I, Bekri S, Ortonne JP:
Porphyria cutanea tarda in association with human immunodeficiency virus infection: is it related to hepatitis C virus infection? Arch Dermatol 130:664-665, 1994
Koester G, Feldman J, Bigler C: Hepatitis C in patients with
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The letter by Drs. Nepveu and Libman illustrates
two important points: 1) hepatitis C viral infection may
precipitate PCT; and 2) hepatitis C viral infection may
induce autoantibodies and cryoglobulinemia, mimicking systemic lupus erythematosus.
Although not mentioned in the case report, our
patient had serologic testing for hepatitis A, B, and C on 2
different occasions after the onset of PCT, with negative
results. This suggests that there is a very low likelihood that
hepatitis C infection precipitated the PCT in this patient.
PCT may be familial, sporadic, or acquired (1).
Patients who develop PCT often have underlying liver
disease secondary to toxic factors such as alcohol, increased
liver iron, or medications (2). Hepatitis C infection is only
one of a number of infections involving the liver that are
associated with PCT; others include hepatitis B infection and
human immunodeficiency virus (3,4). The mechanism underlying the association between liver disease and PCT is
unclear; however, an effect on cellular porphyrin rnetabolism is suspected.
In our patient, there was a strong temporal relationship between the institution of hydroxychloroquine treatment and the onset of PCT. The relationship between
hydroxychloroquine and PCT is also supported by the
results of controlled studies in humans, although hepatitis C
infection could have been present in the patients studied ( 5 ) .
In addition, patients with PCT and hepatitis C infection
usually have chronic elevations found on liver function tests,
whereas patients with PCT that is not associated with
hepatitis C infection typically have normalization of their
transaminase levels after treatment (6). As stated in our
report, our patient had normal liver function prior to hydroxychloroquine therapy, and after treatment, the transaminase
levels normalized.
Hepatitis C infection may cause arthralgia, and in a
small number of patients, autoantibodies may be found (7,8).
Most patients with hepatitis C infection have negative or
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