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Prevention by chloroquine of hexosamine cartilage depletion by e-prostaglandins.

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LETTERS
Reflex sympathetic dystrophy syndrome of the
knee after meniscectomy
To the Editor:
Dr. Hong Joon Kim et a1 (1) in reporting 3 cases
of reflex sympathetic dystrophy of the knee following
meniscectomy pointed out that this had not previously
been reported. We have recently seen a further case.
Prompted by the reports of Eisinger et a1 (2) and
Acquaviva et a1 (3), this unit has been involved in a pilot study examining the use of calcitonin in the reflex
sympathetic dystrophy syndrome. During the last 18
months we have had the opportunity to study 14 patients with reflex sympathetic dystrophy. One had involvement of the knee that had developed after meniscectomy, and another developed reflex sympathetic
dystrophy of the foot following arthroscopy of the ipsilateral knee.
A 36-year-old woman slipped, twisting her left
knee in March 1977 and was seen by an orthopedic surgeon 6 months later. Radiographs revealed no abnormalities. She did not improve with physiotherapy, and a
meniscal injury was suspected but was not confirmed on
arthrography in December 1977. In May 1978 a tom
medial meniscus was removed at arthrotomy. Postoperatively she failed to improve as anticipated, experiencing considerable pain and swelling. The knee
was aspirated, and the results demonstrated no hemorrhage or infection. Despite physiotherapy and nonsteroidal antiinflammatory drugs, she continued to have
constant pain and diffuse tenderness involving the patella and adjacent femur and tibia. Radiographs 4
months after surgery showed patchy osteoporosis of the
distal femur, patella, and proximal tibia. A 9 9 m Tdi~
phosphonate scan in December 1978 showed increased
uptake in the affected knee only. Results of laboratory
investigations including blood count, erythrocyte sedimentation rate, rheumatoid factor, serum calcium, and
alkaline phosphatase were normal or negative. To date,
her response to treatment including calcitonin and peripheral sympathetic blockade with intravenous guanethidine has been disappointing, and she remains considerably disabled.
This patient appears identical to the 3 patients
described by Dr. Hong Joon Kim et al. She has now
been followed for 18 months and, like their patients, has
not developed evidence of specific inflammatory joint
disease, and her symptoms remain localized to the affected knee. Neither during the course of the present
study nor in reviewing the diagnostic index covering all
patients attending this department during the last 7
years has reflex sympathetic dystrophy involving the
knee previously been observed. Characteristically, the
reflex sympathetic dystrophy syndrome involves the distal extremity, usually of the upper limb. Considering the
frequency of meniscectomy, this must be an unusual
complication.
V. M. MARTIN,MB, MRCP
Whittington Hospital
Department of Rheumatology
and Rehabilitation
St. Mary’s Wing
Highgate Hill
London N19 5NF, England
REFERENCES
Kim HJ, Kozin F, Johnson RP, Hines R: Reflex sympathetic dystrophy syndrome of the knee following meniscectomy: report of three cases. Arthritis Rheum 22:177181, 1979
Eisinger J, Acquaviva PC, DOmezon Y, Recordier AM:
Traitement des algodystrophies par la calcitonine: resultats
preliminaires. Marseille-Medical 1 10:373-376, 1973a
Acquaviva PC, Eisinger J, Schiano A, Serratrice G: Calcitonin and algodystrophy: a review of 90 patients, Bone
Disease and Calcitonin. Edited by JA Kanis. Symposium
Proceedings, 1976, pp 143-146
Prevention by chloroquine of hexosamine
cartilage depletion by E-prostaglandins
To the Editor:
We read with great interest the paper by Fulkerson et a1 (1) showing that prostaglandins (PG) E l and
E2 cause a significant loss of hexosamine from cartilage
matrix compared to controls, and that this effect is prevented by chloroquine. However, we would like to suggest another interpretation of the effects of this antimalarial drug. Manku and Horrobin (2,3) have
demonstrated that chloroquine and other antimalarial
drugs such as quinine and mepacrine exert an antagonist effect on PGE action in a rat isolated vascular mesenteric bed preparation. This was also observed by Ok-
LETTERS
78 1
pako (4) on in vitro PGE2-induced contractions of the
rat stomach strip. We have personally observed a nonselective antagonism of chloroquine (5) on several agonist-induced contractions, including the effect of PG in
the guinea pig isolated ileum. In vivo chloroquine is
also able to antagonize PG actions. It suppresses cardiac
rhythm disturbances induced by PG in the rat (6). It is
able to promote closure of patent ductus arteriosus in
premature infants, a condition known to persist when
high levels of PG are achieved (2).
On the basis of these results, Manku and Horrobin (2) suggested that binding sites for chloroquine including those to nucleic acids might be binding sites for
PG. Actually they have shown that PG can block the
binding of chloroquine to DNA. But more important is
the fact that chloroquine might interfere with PG membrane binding sites which trigger cyclic-AMP production. The results of Teitz and Chrisman (7) cited by Fulkerson et a1 (1) are easily explained by this hypothesis.
The intraarticular injection of PG in the rabbit knee induces a synovitis that is not prevented by systemic salicylate, since it is not due to stimulation of PG synthetase
but is abolished by systemic chloroquine because of its
PG antagonist effect.
We propose a similar interpretation of the results
of Fulkerson et a1 (1). If chloroquine is truly a PG antagonist, it is not surprising that the in vitro effects of
PGE on cartilage slices are abolished by this drug.
However, in our interpretation the main effect of
chloroquine must take place at the membrane binding
sites for PG. An additional action on DNA-dependent
RNA synthesis is still possible, but it would not be necessary for obtaining the inhibition of the stimulation of
hexosamine cartilage depletion by PGE.
J.P. FAMAEY,
MD
J. FONTAINE,
PhD
Laboratory of Pharmacology
Rheumatology Unit
School of Medicine and Institute of Pharmacy
University of Brussels
Belgium
REFERENCES
1. Fulkerson JP, Landenbauer-Bellis IM, Chrisman OD: In
vitro hexosamine depletion of intact articular cartilage by
E-prostaglandins: prevention by chloroquine. Arthritis
Rheum 22:1117-1121, 1979
2. Manku MS, Horrobin DF: Chloroquine, quinine, procaine,
quinidine and clomipramine are prostaglandin agonists
and antagonists. Prostaglandins 12:789-80 1, 1976
3. Horrobin DF, Manku MS, Karmazyn M, Ally AI, Morgan
RO, Karmali RA: Quinacrine is a protaglandin antagonist.
Biochem Biophys Res Commun 76:1188-1193, 1977
4. Okpako DT: Interactions of aminoquinolines and mepacrine with prostaglandin E2 in tissues of rats and guinea
pigs. Gen Pharmacol 9:25-28, 1978
5. Famaey JP, Fontaine J, Reuse J: An analysis of the inhibitory effects and of possible prostaglandins antagonism of
chloroquine in the guinea pig isolated ileum. J Pharm
Pharmacol29:761-762, 1977
6. Swift A, Karmazyn M, Horrobin DF, Manku MS, Karmali
RA, Morgan RO, Ally AI: Low prostaglandin concentrations cause cardiac rhythm disturbances: effect reversed by
low levels of copper or chloroquine. Prostaglandins
15:651-657, 1978
7. Teitz CC, Chrisman OD: The effect of salicylate and
chloroquine on prostaglandin-induced articular damage in
rabbit knees. Clin Orthop 108:264-274, 1975
Renal disease in rheumatoid arthritis
To the Editor:
The association of renal disease with rheumatoid
arthritis (RA) has been debated for many years. A recent review (1) and case report (2) have suggested that a
membranous glomerulonephritis (GN) occasionally occurs in the course of the joint disease. The nature of the
relationship has been difficult to clarify, since agents
used in the treatment of RA have themselves been implicated in the production of proteinuric renal disease.
In fact, Samuels ( 1 ) hypothesized that the GN might be
pathogenetically linked to the rheumatoid disease and
that gold or penicillamine treatment could produce the
nephrotic syndrome in only appropriately predisposed
patients. Most patients studied who developed proteinuria in the course of rheumatoid disease had also taken
some potentially nephrotoxic therapy before the detection of proteinuria. Those with well documented RA
had long-standing joint disease before the renal disease
became manifest.
Case report. We have recently seen a 40-year-old
man who came to the New York Veterans Administration Medical Center complaining of pain and swelling
in his right ankle and right temporomandibular joint.
He had experienced a symmetrical but migratory pain
in his shoulders and hands and morning stiffness of 1hour duration for 1 year before admission. Physical examination revealed moderate synovitis of the metacarpophalangeal and proximal interphalangeal joints
bilaterally and reduced range of motion in both shoulders. His laboratory data consisted of a latex fixation titer of 1:2560 and sheep cell agglutination at 1:320. His
hematocrit (HCT) was 47.3% and white blood cell count
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chloroquine, prostaglandin, hexosamine, prevention, cartilage, depletion
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