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Reactive arthritis from Blastocystis hominis.

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25 1
LETTERS
Table 1. Patterns of peripheral reactivity of SLE patient sera and normal control sera with
autoantibodies to DNA, lamins, and nuclear pore complexes, using HEp-2 cells as substrate*
Reactivity pattern
Diagnosis
Broad peripheral (n = 10)
Thin peripheral (n = 4)
SLEt
3 SLE criteria (n = 1)
SLE (n = 2)
Rheumatoid arthritis
(n = 1)
Pol ymyositis
Speckled peripheral
(n
=
DNA binding
activity,
mean %
(range)
Strong lamin
reactivity,
no. (%)
Nuclear pore
complex
reactivity
76.1 (48-100)
9 (5-16)
I (10)
4 (100)
No
No
0 (0)
Yes
0 (0)
No
I1
1)
Negative (n = 10)
Normal controls
3.5 (2-6)
* Filter-binding assay; normal range 0-28%.
t Includes sera supplied by the Centers for Disease Control as reference sera for peripheral and
homogenous patterns and for antibodies to native DNA (20). SLE = systemic lupus erythematosus.
establish molecular identity of autoantigens. Further, as
other autoantibodies to nuclear envelope-associated antigens are identified, it is likely that fluorescent patterns
similar to those reported here will be described. Definite
antigenic specificity characterization should be performed
using specific assays.
Jean-Luc Senkcal, MD
Notre-Dame Hospital
Montreal, Quebec, Canada
Yves Raymond, PhD
Institut du Cancer de MontrPal
Montreal, Quebec, Canada
1. Beck JS: Variations in the morphological patterns of autoimmune nuclear fluorescence. Lancet I: 1203-1205, 1961
2. Casals SP, Friou GJ, Teague PO: Specific nuclear reaction
pattern of antibody to DNA in lupus erythematosus sera. J Lab
Clin Med 62:625-631, 1963
3. Casals SP, Friou GJ, Myers LL: Significance of antibody to
DNA in systemic lupus erythematosus. Arthritis Rheum 7:379390, 1964
4. Rothfield NF, Stollar BD: The relation of immunoglobulin class,
pattern of antinuclear antibody and complement-fixing antibodies to DNA in sera from patients with systemic lupus erythematosus. J Clin Invest 46:1785-1794, 1967
5. Nakamura RM, Peebles CL, Rubin RL, Molden DP, Tan EM:
Autoantibodies to nuclear antigens: screening assays, Autoantibodies to Nuclear Antigens (ANA): Advances in Laboratory
Tests and Significance in Systemic Rheumatic Diseases. Chicago, American Society of Clinical Pathologists Press, 1985
6. Reichlin M: Antinuclear antibodies, Textbook of Rheumatology. Third edition. Edited by WN Kelley, ED Harris Jr, S
Ruddy, CB Sledge. Philadelphia, WB Saunders, 1989
7. McKeon FD, Tuffanelli DL, Fukuyama K, Kirschner MW:
Autoimmune response directed against conserved nuclear envelope proteins in a patient with linear scleroderma. Proc Natl
Acad Sci USA 80:4374-4378, 1983
8. Reeves WH, Chaudhary N, Salerno A, Blobel G: Lamin B
autoantibodies in sera of certain patients with systemic lupus
erythematosus. J Exp Med 165:75&762, 1987
9. Guilly MN, Danon F, Brouet JC, Bornens M, Courvalin JC:
Autoantibodies to nuclear lamin B in a patient with thrombopenia. Eur J Cell Biol 43:266-272, 1987
10. Lassoued K, Guilly MN, Danon F, AndrC C, Dhumeaux D,
Clauvel JP, Brouet JC, Seligmann M, Courvalin JC: Antinuclear
autoantibodies specific for lamins. Ann Intern Med 108:829-833,
1988
11. Wesierska-Gadek J, Penner E , Hitchman E, Sauermann G:
Antibodies to nuclear lamins in autoimmune liver disease. Clin
Immunol Immunopathol49:107-115, 1988
12. Tan EM: Autoantibodies to nuclear lamins. Ann Intern Med
108:897-898, 1988
13. Dagenais A, Bibor-Hardy V, SenCcal JL: A novel autoantibody
causing a peripheral fluorescent antinuclear antibody pattern is
specific for nuclear pore complexes. Arthritis Rheum 31:13221327, 1988
14. Ginsberg B, Keiser H: A millipore filter assay for antibodies to
native DNA in sera of patients with systemic lupus erythematows. Arthritis Rheum 16: 199-207, 1973
15. Weinstein A, Bordwell B, Stone B, Tibbets C, Rothfield NF:
Antibodies to native DNA and serum complement (C3) levels:
application to diagnosis and classification of systemic lupus
erythematosus. Am J Med 74:206-216, 1983
16. Raymond Y,Gagnon R: Lamin B shares a number of distinct
epitopes with lamins A and C and with intermediate filament
proteins. Biochemistry 27:2590-2597, 1988
17. Raymond Y,Chauvette M: Minor lamin polypeptides from rat
liver nuclei can be cross-linked into heteropolymers by disulfide
bridges. Biochem Cell Biol66:1295-1302, 1988
18. Lucian0 A, Rothfield NF: Patterns of nuclear fluorescence and
DNA-binding activity. Ann Rheum Dis 32:337-341, 1973
19. SenCcal JL: Screening sera undiluted is necessary to detect the
peripheral pattern on the HEp-2 ANA substrate (abstract). Clin
Res 35:567A, 1987
20. Tan EM, Fritzler MJ, McDougal JS, McDuffie FC, Nakamura
RM, Reichlin M, Reimer CB, Sharp GC, Schur PH, Wilson MR,
Winchester RJ: Reference sera for antinuclear antibodies. I.
Antibodies to native DNA, Sm, nuclear RNP, and SS-B/La.
Arthritis Rheum 25:1003-1005, 1982
Reactive arthritis from Blastocystis hominis
To the Editor:
Blastocystis hominis was described and named by
Brumpt (1) in 1912. The microorganism was classified as a
252
fungus by earlier investigators ( I ,2); however, recent examination of its morphology, its ultrastructure, and its culture
characteristics have supported its reclassification as a protozoan (3). Although it is considered a harmless intestinal
commensal (4), there have been several reports of diarrhea
having been caused by this organism (4-7). We describe here
a patient with reactive inflammatory polyarthritis caused by
B hominis.
The patient, a 46-year-old white woman, visited
India in early August 1987, and stayed for 12 days. She drank
only purified water and avoided raw fruits and vegetables.
Two days after leaving India, while in London, she ate p a t 6
which she thought was “bad.” The next day, she had 5-10
loose bowel movements, which got worse when she ate or
drank anything. The stool was watery, but there was no
blood or mucus. She also had intestinal cramps and flatulence, which were relieved by bowel movement. She had
taken an unknown “preventive” medication, which was
given to her by her family doctor, before her trip. With the
onset of the diarrhea, she took diphenoxylate, but experienced no relief. The diarrhea continued unchanged for 2
weeks; by the third week, she was having fewer bowel
movements per day. She had no other symptoms at that
time.
In early September 1987, severe, constant pain suddenly developed over the patient’s left sacroiliac joint. The
next day, a similar pain developed over the right sacroiliac
joint. The pain was constant, and remained unchanged by
activity or rest. One day later, redness and “matting” of the
left eye developed, which lasted 2 days and spontaneously
resolved. Two days later, painful swelling of the right
metatarsophalangeal (MTP) joints developed. This pain increased with standing. She was admitted to the hospital on
September 7, 1987, because of constant pain in the sacroiliac
joint bilaterally and in the toes of her right foot. On the day
of admission, she had a temperature of 101”F, as well as
aching and stiffness of the left knee, without swelling.
The patient said she experienced fatigue 24 hours
daily, and had lost a significant, but unknown, amount of
weight. Review of systems was unremarkable. Medical
history, family history, and social history contributed no
information pertinent to the diagnosis. Her only medications
were estrogen and progesterone, which she had taken for an
unknown number of years. She had no known allergies.
On physical examination, she looked ill. Her temperature was 102°F. Results of examination of the head, eyes,
ears, nose, throat, neck, chest, heart, and abdomen were
within normal limits. Specifically, there were no aphthous
ulcerations, skin rashes, or evidence of conjunctivitis. Results of examination of the joints showed 3+ effusion of the
left knee, with 2+ pain on motion and 2+ tenderness. She
had no warmth or redness. She had 4+ swelling and tenderness about the right first MTP joint, with some extension
toward the other MTP joints on the right foot. Fabere
maneuver (flexion, abduction, external rotation, extension)
for hip arthritis gave positive findings bilaterally. Results of
neurologic examination were within normal limits.
Laboratory tests showed an erythrocyte sedimentation rate (ESR) of 89 mm/hour, a hemoglobin value of 12
mg/dl, a white blood cell (WBC) count of 8,800/mm3 with a
LETTERS
left shift, normal urinalysis findings, and normal blood
chemistry. Results of tests for rheumatoid factor, antinuclear antibody, and HLA-B27 were negative. Aspiration of
the patient’s left knee yielded 30 ml of clear yellow fluid,
with a WBC count of approximately 3,000/mm3 and a protein
level of 4.1 mg/dl. No crystals were seen, and cultures for
bacteria and fungi showed no growth. Findings on radiographs of the knee, foot, and sacroiliac joints were within
normal limits. A bone scan revealed increased uptake of
radiotracer in the left knee and right first toe. Stool samples
were found to be ‘‘loaded’’ with organisms, which were
identified as B hominis.
The patient was given metronidazole, 250 mg 3 times
daily, and indomethacin, 75 mg twice daily. The patient had
to discontinue taking the indomethacin because of headache
and nausea.
When seen on September 16 (day 5 of metronidazole
(treatment), the patient was still having 5 loose bowel
movements daily, which were watery and brownish, without
blood or mucus. She had a daily temperature of 100°F. She
had mild diminution of the pain and swelling in her left knee,
although the pain was still moderately severe. She continued
to have swelling and pain of the right first toe, and similar
problems developed (to a lesser degree) in the left second
and third toes. Moderate swelling of the right ankle also
developed, without pain or stiffness. The treatment was
switched to naproxen, 750 mg twice daily, in a therapeutic
trial. Her ESR was 106 mm/hour.
The patient was evaluated on September 23, 1987, at
which time she had finished a full course of metronidazole,
and no longer had diarrhea or high temperature. The Blustocystis organism was not present in the patient’s stool
samples. The patient had less pain and swelling of the left
knee and the right first toe, but had stiffness and soreness of
the left knee. The right first toe remained inflamed and
painful with activity. She noted sausaging of the left second
and third toes. She had no difficulty with the right ankle or
the sacroiliac joints. There was 2+ swelling and I + tenderness of the left knee, without heat. Findings on examination
of her ankles were normal. She had 2+ swelling and tenderness of the right first MTP joint, and 2+ swelling, without
tenderness, of the left second and third toes. ESR was 77
mm/hour.
Over the next week, the patient’s symptoms persisted. She did not think that the naproxen was beneficial, so
therapy was changed to sulindac, 300 mg twice daily.
The patient was reevaluated on November 4, 1987,
having continued the sulindac therapy. She had no recurrence of her abdominal symptoms or diarrhea. She had been
afebrile. She was quite active. She had had continued
resolution of the swelling and pain in the left knee (then only
minimally present). The right first toe symptoms continued
to resolve, having only mild pain and swelling noted primarily with walking. Sausaging of the left second and third toes
was unchanged. She had increased swelling of the right ankle
but no other associated symptoms. Results of physical
examination confirmed these findings. The patient said that
she had an episode of painful aphthous ulceration of the
lower lip 1 week previously, lasting 2-3 days. Her ESR was
253
LETTERS
60 mm/hour. Sulindac was stopped, and she was given
meclofenamate sodium monohydrate, 100 mg 4 times daily.
On November 25, 1987, she had slight swelling and
pain of her right ankle, but all other joints were normal. She
had no gastrointestinal symptoms, and the ESR was 10
mm/hour.
She was reevaluated on January 13, 1988, at which
time she was totally asymptomatic, and joint examination
results were normal. The ESR was 4 mm/hour. She has since
not taken the meclofenamate for more than 1 year and has
had no recurrence of symptoms.
The characteristics of reactive arthritis after enteric
infection include the onset of arthritis predominantly during
the second or third week after the onset of diarrhea. The
arthritis is asymmetric, additive or migratory, predominates
in the lower extremities, and may involve the lower back or
sacroiliac joints; fever is present in most cases (8). Laboratory findings include an elevated ESR and inflammatory
synovial fluid with negative results of cultures (8). Our
patient’s symptoms met all of the above features. In addition, the patient’s stools were loaded with B hominis. After
treatment with metronidazole, the diarrhea resolved, stool
test results were negative for B horninis, and the arthritis
subsequently resolved on treatment with nonsteroidal antiinflammatory agents. The ESR became normal. Despite
stopping treatment, symptoms have not recurred for over 1
year.
Reactive arthritis has been reported in association
with a number of enteric bacterial pathogens including
Shigella pexneri, Salmonella species, Yersinia enrerocolitica, Campylobacterjejuni, and Brucella species (8). These
reactive enteric-arthritic syndromes demonstrate an HLAB27 negative linked predisposition, except for that caused by
Brucella species (8). Our patient was negative for HLA-B27.
B hominis, an intestinal protozoan, has been increasingly implicated as a pathogen in diarrheal disease. We are
not aware of any report of reactive arthritis after enteric
infection with B hominis and believe this to be the first such
report. The relative numbers of the organism are associated
with the severity of symptoms (9). When 2-5 organisms are
present per preparation, the result is reported as rare; 1
organism per 5-10 microscopic fields is reported as few;
1 organism per 2-3 microscopic fields to 1-2 organisms per
microscopic field are reported as moderate, and “several”
organisms in every microscopic field are reported as many
(9). The specimen from our patient was described as being
“loaded” with B hominis (per microscopic field), which was
more than “several.” Whether the numbers of the organism
represent a predisposing factor in reactive arthritis is not
known.
Our patient had reactive inflammatory polyarthritis
after enteric infection with B hominis. The disease resolved
on treatment with metronidazole and nonsteroidal antiinflammatory drugs. An absolute cause and effect cannot be
proven because other enteric pathogens are not present in
the stool when the reactive arthritis appears, and because B
hominis is not a usual major pathogen. Nonetheless, B
hominis should be considered as a possible pathogenic agent
in patients with enteritis and arthritis. The diagnosis is easily
made by stool examination, and the treatment may be
curative.
Sharad Lakhanpal, MD, FACP
Stanley B. Cohen, MD
Roy M. Fleischmann, MD
St. Paul Medical Center
Dallas, TX
1. Brumpt E: Blastocystis hominis n. sp. et formes voisines. Bull
SOCPathol Exot 5:725-730, 1912
2. Knowles R, Das Gupta BM: On the nature of Blastocystis
hominis. Indian J Med Res 12:31-38, 1924
3. Zierdt CH, Rude WS, Bull BS: Protozoan characteristics of
Blastocystis hominis. Am J Clin Pathol48:495-501, 1967
4. Sheehan DJ, Raucher BG, McKitrick JC: Association of Blastocystis hominis with signs and symptoms of human disease. J Clin
Microbiol 24548-550, 1986
5. Vannatta JB, Adamson D, Mullican K: Blastocystis horninis
infection presenting as recurrent diarrhea. Ann Intern Med
102:495-496, 1985
6. Gallagher PG, Venglarcik JS 111: Blastocystis hominis enteritis.
Pediatr Infect Dis 4556-557, 1985
7. Diaczok BJ, Rival J: Diarrhea due to Blastocystis hominis: an old
organism revisited. South Med J 80:931-932, 1987
8. Good AE, Utsinger PD: Enteropathic arthritis, Textbook of
Rheumatology. Second edition. Edited by WN Kelley, ED
Hams Jr, S Ruddy, CB Sledge. Philadelphia, WB Saunders, 1985
9. Malkani K: Blastocystis hominis. Tex Prevent Dis News 46:l-2,
1986
Felty’s syndrome: response to cyclosporin A with
disappearance of neutrophil autoantibodies
To the Editor:
Felty’s syndrome (FS) consists of frequently severe
rheumatoid arthritis (RA) and neutropenia and is usually
associated with splenomegaly, other systemic features, and
cutaneous and pulmonary infections. Different mechanisms
for the pathogenesis of neutropenia have been suggested
(1,2): diminished neutrophil production, excessive neutrophi1 margination due to circulating immune complexes,
increased neutrophil destruction by autoantibodies, and destruction by enlarged spleen. Neutrophil-bound immunoglobulins and immune complexes have been detected in
patients with FS, and serum from these patients usually
suppresses granulopoiesis in vitro.
Although splenectomy is the primary therapy for FS,
it has proven efficacious only in a few patients. Furthermore,
a decrease in neutrophil-bound IgG has been described in
those patients who did respond to splenectomy (3). Lowdose corticosteroids are usually ineffective and may predispose to infections. Prolonged treatment with lithium has not
proved beneficial. High-dose testosterone may induce remission, but its androgenic side effects preclude its use in female
patients. Gold salts and D-penicillamine have yielded good
results in small series of patients, although there is commonly a late response. Evidence favoring an immune mechanism in the pathogenesis of most cases of FS has served as
the rationale for trials using immunosuppressive drugs, and
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