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Arthritis After Jejunoileostorny
To the Editor:
In view of the recent emphasis of the safety
of jejunoileostomy versus jejunocolostomy, we
would like to bring to your attention the occurrence of arthritis following jejunoileostomy
for the treatment of obesity.
A 33-year-old housewife with lifelong obesity
and no known prior liver disease underwent jejunoileostomy in March 1970, as part of a
drastic effort to lose weight. At the time of
surgery she was 5 feet 6 inches tall and weighed
295 pounds. After surgery she lost weight
steadily and finally stabilized at a weight of 170
Immediately after surgery she developed
severe watery diarrhea (20 to 30 stools/day).
One episode of hypocalcemic carpopedal spasm
and tetany occurred within 4 months after
In November 1970, five months after
surgery, an acute polyarthritis involving the
wrists, shoulders and knees occurred. Physical
examination demonstrated arthritis of the right
ankle, hip, left shoulder, both elbows and several distal interphalangeal joints. Hepatomegaly was also noted.
Aspiration of the right knee yielded 8 ml of
clear synovial fluid, which formed a good mucin
clot, contained no crystals and had 260 white
blood cells/cu mm. Serum tests for antigammaglobulins and antinuclear antibodies were
negative; uric acid was 5.2 mg%. X-rays of the
hands, knees, feet, sacroiliac joints and cervical
spine were negative. Sulfobromophthalein retention was 10.4%. Other liver function tests
were normal. Liver biopsy, in April 1971,
demonstrated moderate centrolobular fatty
metamorphosis and mild periportal inflammation. A moderate number of polymorphonuclear
cells were seen around bile ducts. No fibrosis or
alcoholic hyaline was identified.
Aspirin, indomethacin and phenylbutazone
were used to treat the arthritis, with generally
good, though variable, response. At present the
patient’s arthritis occasionally interferes with
her tasks of daily living.
Several operative procedures have been
proposed for the therapy of intractable obesity,
initially jejunocolostomy (1) and, more recently, end-to-end jejunoileostomy (2). Hepatic
dysfunction (3), as well as malabsorption of fats
and electrolytes (4), have been observed as undesirable complications of all types of intestinal
bypass surgery. Shagrin et a1 (5) have recently
described arthritis in 23% of patients undergoing jejunocolostomy, but this has not yet been
described in patients with jejunoileostomy.
It is possible that the arthritis in the present
patient was coincidental to her jejunoileostomy.
However, the temporal relationship of arthritis
to surgery, its similarity to the arthritis of
Whipple’s disease (6) and the lack of resemblance to other known types of joint disease
suggest that the arthritis was causally related to
the surgery. Further support for a relationship
is gained from the observation of recurrent arthralgia in 10 of 150 patients with jejunoileostomy (7).
T h e pathophysiology of arthritis that occurs
in association with enteric disorders is obscure.
T h e well-known, extraintestinal manifestations
of inflammatory bowel disease suggest systemic
responses via unknown mechanisms, such as:
reabsorption of intraluminal toxins through
damaged intestinal epithelium; immunologic
reactions; and systemic effects of hormones of
enteric origin. With intestinal bypass surgery,
the large blind loop may function in a manner
parallel to that of other forms of bowel disease.
In support of this suggestion, it is noted that the
arthritis of one of Shagrin’s patients improved
with tetracycline therapy, and that musculoskeletal symptoms abated after reanastomosis
in a second patient.
These empiric observations stimulate specu-
Arthritis and Rheumatism,Vol. 15, No. 6 (November-December 1972)
lation regarding the role of intestinal stasis,
malabsorption and bile salt metabolism in the
pathogenesis of arthritis associated with intestinal disease, and may yield clues to the systemic and musculoskeletal complications of gastrointestinal inflammatory disease.
consecutively in a general medical clinic. This
incidence of 8% is lower than the 16% in
Bolzan and co-workers’ study, but still higher
than expected. As in their study, the bulge sign
was unilateral in more than half of our cases.
After the bulge signs were found, studies revealed factors-felt io possibly contribute to the
cause of the small effusions in 10 of 12 patients.
T o measure the small amounts of synovial fluid
Division of Rheumatology necessary to produce a bulge, we have aspirated
Department of Medicine the knees of patients with the sign. In 13 paHarborview Medical Center tients the sign could not be demonstrated after
University of Washington the knee was aspirated. T h e volume of synovial
Seattle, Washington fluid removed from each patient ranged from
2.6 to 8.0 ml with a mean of 4.9 (versus 6.5 ml
for Bolzan et af in 13 similiar patients).
We feel that the bulge sign is a valuable
1 . Payne JH, DeWind LT: Surgical treatment of
of detecting small increases of synovial
obesity. Am J Surg 118:141-147, 1969
most often reflect some knee joint
2. Salmon PA: The results of small intestinal byabnormality.
These small effusions would usupass operations for the treatment of obesity.
ally be missed by using other methods of knee
Surg Gynecol Obstet 132:965-979,1971
3 . Drenick EJ, Simmons F, Murphy JF: Effect on examination. Bolzan et al take a different view.
hepatic morphology of treatment of obesity by On the basis of a single examination and withfasting, reducing diets and small bowel bypass. N out the help of knee joint roentgenograms they
Engl J Med 282:829-834,1970
conclude that in patients with no joint symp4. Lewis LA, Turnbull RB, Page IH: Effects toms the sign identifies an upper range of norjunocolic shunt on obesity, serum lipoproteins, mal for knee joint fluid. They propose that
lipids and electrolytes. Arch Intern Med
persons with a heavy physique have larger knee
117:4-16, 1966
joint fluid volumes, and, thus, show bulge signs.
5 Shagrin JW, Frame B, Duncan H: Polyarthritis
h e evidence presented for these conclusions
in obese patients with intestinal bypass. Ann Inseems rather weak. First, the data supporting
tern Med 75:377-380, 1971
6 Maize1 H, Ruffin .JM, Dobbins W D 111: Whip- their opinion could easily have been weighted
ple’s disease: A review of 19 patients from one by the fact that the several physicians particihospital and a review of the literature since 1950. pating in the study agreed about the presence of
Medicine (Baltimore) 49:175-205, 1970
a bulge sign only 41% of the time when more
7 DeWind LT: Personal communication, 1971
than one examined the same patient. Second, if
the bulge sign was related to physique, it should
be bilateral, but it was found to be unilateral in
Bulge Sign
the majority of patients. While in some inTo the Editor:
stances a small bulge sign (estimated 3 to 4 ml)
I would like to add our experience with the may merely identify the upper range of normal
bulge sign to that of Bolzan and co-workers (1) fluid volume for the knee, we feel that other
and compare our findings with theirs. In factors are likely important in most cases, essomewhat similar studies (2,3) we found the pecially those with larger bulge signs (indicatbulge sign to be present in 12 of 150 patients ing 5 to 10+ ml). These factors include miniwithout ,joint symptoms who were examined mal knee trauma, minimal inflammation and
Arthritis and Rheumatism,Vol. 15, No. 6 (November-December 1972)
body fluid balance. Because these conditions are
relatively common, the bulge sign is detectable
relatively frequently. Early or mild knee joint
pathology may not be excluded on one examination, and followup is often necessary to make
a correct diagnosis.
I have performed this maneuver on almost
every general medical and rheumatologic patient examined since 1960 (we started calling it
the bulge sign in 1961) and have noted the sign
to be present and diagnostically useful in many
conditions in which knee effusions occur. T h e
bulge sign is most helpful in evaluatinp; mild or
early cases of rheumatoid arthritis, SLE and
related disorders, polymyalgia rheumatica,
developing or resolving acute gout and pseudogout, as well as degenerative arthritis, torn
meniscus, chondromalacia patellae and after
minimal knee trauma. It may be present after
vigorous physical activity even without specific
knee injury. One patient with mild chondromalacia patellae, followed since 1960, frequently has bulge signs for a few days (sometimes unilateral, sometimes bilateral) after
strenuous use of the knees. Even a seemingly
asymptomatic bulge sign might be related to an
underlying disease. For example, in 1 patient
with untreated interval gout who never had
knee pain, a 5 ml knee effusion was aspirated
when a bulge sign was unexpectedly found, and
a small number of urate crystals were observed
in the centrifuged sediment. Interestingly, the
bulge sign was absent after 2 months of
probenecid therapy and may, therefore, have
been related to the gout. In this light it would be
interesting to know whether any synovial fluids
from 3 patients with interval gout studied by
Bolzan et a1 contained monosodium urate crystals. T h e bulge sign can also be elicited in some
patients with body fluid abnormalities such as
congestive heart failure, nephrotic syndrome
and Cushing’s disease with leg edema. As these
conditions are treated the bulge sign becomes
smaller or disappears.
In most patients who have been followed, the
bulge signs frequently varied in size over a
period of time ranging from days to several
weeks, whether or not a relatable disease was
present. In order to better interpret the bulge
sign in patients without joint symptoms, a prospective follow-up study is necessary after initial thorough evaluation of the patients. Some
quantitation of the amount of fluid in the knee
should be included. The volume of fluid could
be measured by knee aspiration, estimation of
the fluid present after gaining experience or
even simply recording whether the bulge sign
was small, moderate or large. T h e Sudbury
study of chronic disease provides an excellent
opportunity for such a study.
Mayo Clinic
Rochester, Minn 55901
1. Bolzan JA, O’Sullivan JB, Cathcart ES: Unexpected prevalence of knee joint effusions in the
population of Sudbury. Arthritis Rheum
2. Hunder GG, Polley HF: Clinical study of small
effusions of the knee. Arthritis Rheum 7:318, 1964
3. Hunder GG, Polley HF: Detecting small effusions of the knee. Postgrad Med 40:689-692.
The Quantitation of Rheumatoid Factors
To the Editor:
W e have encountered difficulties, both
theoretic and experimental, in our attempts to
quantitate rheumatoid factors (RF’s) by the
technic of Torrigiani and Roitt (1 ). We feel that
these difficulties cast doubt on the validity of
some quantitative technics. Following their
method we were unable to: a) absorb all RF’s
in contrast to published claims (1); b) demonstrate unequivocally that non-RF immunoglobulins were not absorbed; c) show, by an
unexceptionable method, that absorbed RF’s
were eluted completely and in a native state and
d) quantitate the eluted RF’s by a radial immunodiffusion technic.
Arthritis and Rheumatism,Vol. 15, No. 6 (November-December 1972)
Table 1. Absorption of Agglutinating Antibodies by Insoluble Rabbit Cohn Fraction Il-Test Results
Latex test
SCAT titer
28 1
< 20
Ripley titer
< 20
< 20
< 20
< 20
< 20
< 20
< 20
Butler and Vaughan (2) described the use of
rabbit IgG immunoabsorbents prepared with
benzidine to absorb rheumatoid sera. Only part
of the R F hemagglutinating activity for human
I@-coated cells was removed. In contrast,
Torrigiani and Roitt (1) claimed that all RF’s
reacting in the SCAT, human and rabbit F I I
latex tests could be removed under specified
conditions. W e could not confirm this claim,
and experiments under modified conditions
were also unsuccessful. At the same time, tests
were made on several rabbit IgG immunoabsorbents under similar experimental conditions
to detect the removal from serum or denaturation of non-RF IgM antibodies, by titration of
anti-blood group A activity. T h e test was of
limited value because only major losses of activity were detectable. However, loss of non-RF
antibody was not detected using immunoabsorbents made with benzidine, o-dianisidine
a n d glutaraldehyde cross-linking reagents
(Table 1). Immunoabsorbents prepared with
agarose, acrylamide and ethyl chloroformate
absorbed or denatured IgM antibodies nonspecificall y.
It has been claimed that all the immunoglobulins removed by IgG immunoabsorbents
< 20
2 10240
2 10240
< 20
Anti-A titer
< 20
< 20
< 20
< 20
< 20
< 20
< 20
< 20
from the sera of normal individuals and patients
with various conditions are thereby proved to
have R F antiglobulin activity (1, 3-5). It seems
desirable to seek confirmation by other methods. IgM RF’s are unusually labile, particularly during concentration (1, 6). Eluates from
immunoabsorbents have been shown (2) to
contain active 19s RF’s and also proteins of
higher molecular weight (S > 19), which may
represent aggregated or complexed RF’s. Preparations containing denatured or complexed
antibodies may give anomalous results by
quantitative radial immunodiffusion.
Further difficulties are encountered in the
immunologic quantitation of serum proteins in
the presence of antiglobulins. Spurious measurements of human serum IgA were made
on human sera containing anti-goat IgM antibodies (7). When fluorescent rabbit antibody
was used to detect specifically human PIC it
was necessary to block RF containing sites with
aggregated normal rabbit IgG, because, otherwise, any fluorescent rabbit IgG antibody
could have been bound at these sites as antigen,
regardless of its specificity as antibody (8). T h e
ability of some RF’s to react with insoluble
rabbit IgG precludes their measurement by
Arthritis and Rheumatism, Vol. 15, No. 6 (November-December 1972)
rabbit antisera, particularly those made monospecific by the addition of human IgG (l),
and the choice of species for the production of
antisera for measuring RF’s may be difficult.
Similar obstacles may be experienced with radioimmunoassay technics employing rabbit antisera for the measurement of RF’s, such as that
of Franchimont and Suteanu (9).
In summary, we feel that several published
technics for the measurement of RF’s fail to
overcome the objections listed above and are
consequently unsatisfactory.
D. J. LEA, P H D
Oswestry, SALOP, UK
1. Torrigiani G, Roitt IM: Antiglobulin factors in
sera from patients with rheumatoid arthritis and
normal subjects: Quantitative estimation in different immunoglobulin classes. Ann Rheum Dis
2. Butler VP, Vaughan .JH: The reaction of rheumatoid factor with animal gamma-globulins:
quantitative considerations. Immunology
3. Torrigiani G, Ansell BM, Chown EEA, et al:
Raised I& antiglobulin factors in Still’s disease.
Ann Rheum Dis 28:424-7,1969
4. Torrigiani G, Roitt IM, Lloyd KN, et al: Elevated IgG antiglobulins in patients with seronegativerheumatoid arthritis. Lancet 1:14-16, 1970
5. Howell FA, Chamberlain MA, Perry RA, et al:
I@ antiglobulin levels in patients with psoriatic
arthropathy, ankylosing spondylitis and gout.
Ann RheumDis31:129-131,1972
6. .James K, Felix-Davies D, Stanworth DR: Studies
on the isolation of rheumatoid factor. Ann Rheum
Dis 20:369-85, 1961
7. Leikola .J, Vyas GM: Human antibodies to
ruminant IgM concealing the absence o f IgA in
man.,J LabClinMed77: 629-38,1971
8. Bonomo L, Tursi A, Gillardi U, et al: Immune
complexes in rheumatoid synovitis: A mixed
staining immunofluorescencestudy. Immunology
9. Franchimont P, Suteanu S: Radioimmunoassay
of rheumatoid factor. A r t h r i t i s Rheum
Philosophic Aspects of Drug Therapy
in Rheumatoid Arthritis
70the Editor:
Dr. Willkens (and others) might be surprised
to find that I am in complete accord with his
general philosophy, and that I, in fact, expressed much the same point of view in a previous article (1). As a practicing rheumatologist, with the bulk of my work being the care
of the private patient, I am keenly aware of the
many-faceted problems of drug therapy in
rheumatic diseases, and especially in rheumatoid arthritis. Calculated risks must be taken if
we are not to resort to the safe refuge of therapeutic nihilism.
With two qualifications, we may give drugs,
with varying quantitative and qualitative degrees of side effects, a) patient acceptance and
b) reasonable vigilance and precautionary testing by the physician. These qualifications
would be met by many antirheumatic drugs,
such as: aspirin with its gastric ulceration
and blood loss; phenylbutazone with its bone
marrow depression and other toxic manifestations; chrysotherapy with its renal, skin and
other toxic side effects; and even small-dose
cortiocosteroid therapy.
However, to most laymen, blindness is a
catastrophe second only to death itself, and
hence, visual impairment would be considered
an unacceptable side effect. In my editorial on
chloroquine (2), I emphasized this point and
stated, “Perhaps a physician should at least feel
somewhat obligated to tell his patient that a
planned course of therapy with antimalarials
m a y . . . possibly result in serious irreversible
damage to the eyes with visual impairment.”
Furthermore, the literature strongly implied
that retinopathy was an inevitable side effect of
chloroquine in some patients who received
doses that were, at that time, recommended for
rheumatoid arthritis. In a Letter to the Edit o r ( 3 ) , I underlined this point, referring to
Arthritis and Rheumatism,Vol. 15, No. 6 (November-December 1972)
Arden and Kolb (4) who gave “an overall instance of retinal changes attributable to antimalarial therapy in rheumatoid arthritis of
1 3 % . . . . In the group who had taken more
than 8 g/kg body weight, the incidence was
40% . . . ”! (They emphasized that doses of this
size were not rare, since they were given to 1 of
7 patients.) One should be reminded that the
large deposits of chloroquine in the liver make
meaningful prophylactic ophthalmologic
examinations impossible. If it were possible (as
suggested by Dr. Paul Young et al, from
Asheville, NC, at the annual meeting of the
June 1972) to pick out the retinopathy-prone
and give chloroquine only to those who do not
have this susceptibility, chloroquine therapy
might assume a more rational basis for the
treatment of rheumatoid arthritis.
T h e same considerations apply to immunosuppressive therapy, which certainly has no
place in the routine treatment of rheumatoid
arthritis, but which should be used only in an
experimental or investigative clinical setting.
Such therapy carries with it a potential side
effect which, in my view, is wholly unacceptable
to most laymen-ie, cancer. Furthermore, this
side effect is as yet not preventable by vigilant
surveillance or frequent and intensive laboratory tests.
T o reiterate, I a m in accord with Dr. Willkens; I cannot subscribe to the ostrich-like
views of therapeutic nihilism and fateful inevitability. I agree most heartily with an aggressive approach to treatment, especially in
the patient with severe classic rheumatoid
arthritis whose prognosis, without treatment,
is hopeless. Most patients not only accept,
but want and plead for this aggressive therapy. I would exclude only those therapies
whose side effects are unacceptable to the
patient or are likely to be inevitable (especially undetectable in the preventive or abortive
Permit me to quote the last few lines of my
article (l), previously referred to, “If it were
true, as stated by some, that the disease cannot
be altered by drugs, one would be hard pressed
to justify the administration of any drug other
than pure analgesics. Pity the rheumatoid if
such an attitude were to prevail”!
Clinical Professor of Medicine
Ohio State University
College of Medicine
Columbus Medical Center
Research Foundation
121 1 Dublin Road
Columbus, Ohio
1. Rothermich NO: An updated look at antirheumatic drugs. Med Clin North Am 51:1213-1222,
2. Rothermich NO: Coming catastrophes w i t h
chloroquine? Ann Intern Med 61 : 1203-1205,
3. Rothermich NO: Letter to the editor. JAMA
4. Arden GB, Kolb H: Antimalarial therapy and
early retinal changes in patients with rheumatoid
arthritis. Br Med J 1:270, 1966
Mycoplasmas and Rheumatoid Arthritis
To the Editor:
Continuing impetus to the search for mycoplasmas in synovial fluids and tissues from
patients with rheumatoid arthritis has been
provided by several recent reports by Jansson
and her colleagues (1-5). During the past several years we have continued to attempt to isolate mycoplasmas from a variety of patient
specimens including synovial fluids, synovial
biopsy or surgical specimens, and cell strains established from synovial tissues using sensitive
technics. T h e results have been uniformly negative (6).
T h e methodology described by Jansson (1-5,
and personal communication) was applied to
the study of ten specimens in our laboratory.
Arthritis and Rheumatism,Vol. 15, No. 6 (November-December 1972)
T h e specimens included: nine synovial fluids
(six from patients with rheumatoid arthritis,
one from a patient with degenerative joint disease, one from a patient with Reiter's syndrome
and one from a patient with chronic synovitis of
undetermined etiology) and one synovial tissue
specimen obtained at operation from a patient
with rheumatoid arthritis. All specimens were
inoculated into two tubes of brain heart infusion
broth containing 1% heat inactivated chicken
egg yolk at p H 7.2 and 7.8 and onto two agar
plates containing 1% egg yolk at pH 7.2 and
7.8. All cultures were incubated anaerobically
at 37" C. At 10- and 20-day intervals, subcultures were made from the broth cultures to fresh
broth tubes and agar plates. A total of three
subcultures were made following the original
isolation attempt. Agar blocks were stained by
Dienes' method at 10- and 20-day intervals. All
of the results were negative, with one exception.
At the third, 10-day subculture of a specimen
derived from the synovial fluid of a patient with
rheumatoid arthritis, two or three morphologically suggestive colonies were observed. Five
separate attempts to transfer these colonies
failed and we conclude that they were probably
T h e broth and agar media adequately supported the growth of several laboratory mycoplasma strains (M granularurn, M hominis 1
and M hyorhinis). We were unable, however,
to demonstrate the growth of a T-strain mycoplasma (T3J in spite of its growth using standard methods.
T h e artifacts produced by the egg yolk additive were particularly bothersome, and, subjectively, synovial cells appeared to survive
somewhat better in this media, producing yet
another interfering artifact.
These results are at variance with those reported by Jansson et al (1-5).
from human sources. J Clin Pathol 24:53-56,
Jansson E, Vainio U, Snellman 0, et al: Search
for mycoplasma in rheumatoid arthritis. Ann
Rheum Dis 30:413-418,1971
Jansson E, Makisara P, Vainio K, et al: An 8year study on mycoplasma in rheumatoid arthritis. Ann Rheum Dis 30:506-508, 1971
Jansson E, Vainio U, Tuuri S: Cultivation of a
mycoplasma from the bone marrow in systemic
lupus erythematosus disseminatus. Acta Rheumato1 Scand 17:223-226, 1971
Jansson E, Makisara P, Vainio K, et al: Further
studies on mycoplasma in rheumatoid' arthritis.
Acta Rheumatol Scand 17:227-235,1971
Sharp JT: Mycoplasmas and arthritis. Arthritis
Rheum 13:263-271,1970
Mycoplasmas and Rheumatoid Arthritis
To the Editor:
Because of the number of investigators who
have an active interest in, or research programs
on, mycoplasmas in relation to human arthritis,
the following brief note would seem indicated.
On reading the published papers of .Jamson
et a1 (1-4), we attempted to confirm their
findings. We took synovial fluid from 10 patients with rheumatoid a r t h r i t i s and 2
nonrheumatoid subjects and inoculated cultures
in the manner described by <Jansson.We attempted to follow their procedures precisely and
passaged the cultures blindly for three passages.
We were unable to demonstrate any mycoplasma1 colonies when we tested this passage
broth on agar in the manner they indicated. We
have no explanation for the difference between
these results from Vancouver, BC, Canada and
those from Finland.
University of British Columbia
Department of Medicine
Vancouuer General Hospital
Vancouver 9, Canada
Baylor College of Medicine
Houston, Texas 77025
1. Jansson E: Isolation of fastidious mycoplasma
Arthritis and Rheumatism, Vol. 15, No. 6 (November-December 1972)
Jansson E: Isolation of fastidious mycoplasma
from human sources. ,J Clin Pathol 24:53-56,
Jansson E, Vainio U , Snellman 0, et al: Search
for rnycoplasma in rheumatoid arthritis. Ann
Rheum Dis 30:413-418,1971
Jansson E, Vainio U, Tuuri S: Cultivation of a
mycoplasma from the bone marrow in systemic
lupus erythematosus disseminatus. Acta Rheumatol Scand 17:223-226, 1971
Jansson E, Marisara P, Vainio K, et al: Further
studies on mycoplasma in rheumatoid arthritis.
Acta Rheurnatol Scand 17:227-235. 1971
mice, the antibody response shown by some patients a n d t h e u l t r a s t r u c t u r e of t h e isolates (1,2). This resembled that of Mycoplasma
arthritidis strain PG 6 grown under identical
conditions. T h e difference was that the isolate
investigated was growing mostly inside the
growth medium components where it seemed to
be multiplying.
Minerua Foundation
Institute for Medical Research
Hels ink 2, Finland
Mycoplasmasand RheumatoidArthritis
To the Editor:
Dr. Denys K. Ford and 3 other famous mycoplasmatologists have been unable to isolate
mycoplasmas from synovial fluid of patients
with rheumatoid arthritis.
Certainly these tiny microorganisms are not
easily isolated because of their size and somewhat atypical appearance. In addition, often
only a few colonies were seen in first culture
passages. Therefore, a large view-field microscope (Leitz Orthoplan) was used with a special condensor (Achr 0.70/L4) which corrects
the thickness of the agar block preparations.
T h e cultures on solid medium were stained in
situ with 10% Dienes stain and every plate was
also examined using 1000-fold magnification.
T h e materials originating from the growth
medium components are much more coarse,
with a definite border-line. They show a large
variation both in size and shape, and often stain
deep violet with Dienes stain. T h e fastidious
microorganisms from rheumatoid arthritis are
very fragile, grow in solid medium on different
levels and, especially in later passages, tend to
take on a lilac hue.
If the organisms recovered were artifacts, the
following findings would remain unexplained:
their ability to metabolize arginine and kill
1. .Jamson
E, Eklund H, Vainio K, et al: Scanningbeam electron microscopy of mycoplasma isolated
from rheumatoid arthritis. J Clin Pathol
24:808-809,197 1
2. von Bonsdorff C-H, Jansson E, Vainio U, et al:
Ultrastructure of a mycoplasma recovered from
the bone marrow in systemic lupus erythematosus. Ann Rheum Dis (in press)
Hemarthrosisin Chondrocalcinosis
To the Editor:
Pseudogout, first described clinically by Zitnan and Sitaj (1,2) in 1958 and further clarified
in the laboratory by McCarty et a1 ( 3 ,4 ) , is being recognized more frequently (5). T h e syndrome is characterized by chondrocalcinosis
and the demonstration of intracellular and
extracellular calcium pyrophosphate crystals
in synovial fluid during the acute attack. T h e
most common clinical picture is that of recurrent attacks of acute symptoms, although
chronically painful joints have also been described (6,7). Recently, we have seen 2 patients with chondrocalcinosis who presented
with acute hemarthrosis in which the synovial
fluid contained many white cells with characteristics of calcium pyrophosphate.
Case 1
M F , a 67-year-old housewife, was admitted
Arthritis and Rheumatism,Vol. 15, No. 6 (November-December 1972)
to the Long Island College Hospital for epis- her right knee. Although she had had some
taxis due to erosion of a vessel of the nasal previous mild pain in the knee in the past, she
mucosa. She had no history of hypertension or never had swelling. There was no history of
bleeding disorder. T h e epistaxis was treated trauma and she had taken no medication.
with cauterization and did not recur. Her past Physical examination was negative except for
history was unremarkable, except for occasion- her right knee, which was swollen, warm and
al aching of her left knee. T h e complete blood tender. Fifty milliliters of grossly bloody fluid
count was normal; bleeding time, 3 minutes was aspirated within 24 hours of the onset of
(normal up to 5 minutes); clotting time, 8.5 symptoms. Compensated polarized light
minutes (normal 6-1 5 minutes); prothrom- microscopy revealed many intracellular crystals
bin time, 11.4 seconds (control 10.5 seconds) having characteristics of calcium pyrophosphate. An x-ray of the right knee revealed
and platelets, 250,000.
T w o days after admission, her knee became chondrocalcinosis. T h e bleeding time was 2.5
acutely swollen and painful. T h e uric acid was minutes (normal up to 5 minutes); prothrom5.6 mg% (normal 2.5 to 7 mg%) and the latex bin time, 12.7 seconds (control, 11.5 seconds);
fixation test for rheumatoid arthritis was neg- platelets, 185,000 and fibrinogen normal. T h e
ative. An x-ray of the left knee showed chon- patient was treated with rest and ice packs.
drocalcinosis, and the synovial fluid, which T h e pain and swelling subsided rapidly and she
was aspirated within 12 hours of onset, had a has since remained well.
T w o patients with chondrocalcinosis prewhite cell count of 50,000 with numerous intracellular crystals which had a weakly positive sented with acute hermarthrosis unrelated to
birefringence. She was treated with oxyphen- trauma. There was no evidence of a bleeding
butazone (400 mg/day) for 3 days and the knee disorder by history or indicated by the limited
improved rapidly. After discharge she re- number of tests done. Neither had taken asmained well for 4 weeks. She again developed pirin. X-rays of the symptomatic knees revealed
an acutely swollen and extremely painful knee. chondrocalcinosis, and the bloody fluid conThere had been no trauma and she had taken tained many white blood cells with intracellular
no medication of any sort (specifically aspirin). crystals characteristic in appearance to calciNinety milliliters of grossly bloody fluid, um pyrophosphate seen with compensated
aspirated 16 hours after the onset of symptoms, polarized light microscopy. This would seem
did not clot on standing. Compensated polar- to suggest that hemarthrosis was related to
ized light microscopy revealed many white pseudogout and that pseudogout should be
blood cells with intracellular crystals having considered in the differential diagnosis of
hemarthrosis. T h e crystals can easily be
characteristics of calcium pyrophosphate.
T h e following tests were again normal: identified in a hemorrhagic effusion. McCarty
bleeding time, clotting time, prothrombin time et a1 (3) noted in 1962 that 2 patients with
and platelet count. T h e knee was treated with pseudogout had a hemorrhagic effusion. We
ice packs and bed rest. During the remainder are not aware of any other reports. If, indeed,
of her workup, a hypernephroma was found hemarthrosis is related to calcium pyrophosand treated. T o date, she has had two attacks phate crystals, we do not know the mechanism.
of synovitis associated with many crystals, but
no hemarthrosis.
Department of Internal Medicine
Case 2
Division of Rheumatology
Long Island College Hospital
HF, a 70-year-old housewife came for treatBrooklyn, N Y 11201
ment of a sudden onset of pain and swelling of
Arthritis and Rheumatism,Vol. 15, No. 6 (November-December 1972)
1. Zitnan D, Sitaj S: Mnohopocetna Familiarha
Kalcifikaciz artikularynch chrupick. Bratislavske
Lekarske Listy 28:217, 1958
2. Zitnan D, Sitaj S: Chondrocalcinosis articularis,
Section I. Clinical and Radiological Study. Ann
3. McCarty DJ, Kohn NN, Faires, JS: The significance of calcium pyrophosphate crystals in the
synovial fluid of arthritic patients: The Pseudogout Syndrome I. Clinical Aspects. Ann Intern
Med 56:711-737, 1962
4. Kohn NN, Hughes RE, McCarty DJ, et al: The
significance of calcium phosphate crystals in the
synovial fluid of arthritic patients: The Pseudogout Syndrome 11. Identification of crystals
Ann Intern Med 56:738-745, 1962
5. McCarty DJ: On the crystal deposition diseases.
6. Moskowitz RW, Katz D: Chondrocalcinosis and
(Pseudogout syndrome),
analysis of twenty-four cases. Am J Med
7. Reginato MA, Valenzuela RF, Martinez CV, et
al: Polyarticular and familial chondrocalcinosis.
Arthritis Rheum 13:197-213, 1970
Abstracts of papers submitted for presentation at the ARA scientific sessions in
Los Angeles must be postmarked no later than Friday, March 2, 1973. Abstract
forms will be mailed to all ARA members in advance. Others may obtain forms by
Arthritis and Rheumatism. Vol. 15, No. 6 (November-December 1972)
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