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Effect of heat on crystals.

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LETTERS
637
conditions with diverse etiologies suggests their nonspecific nature.
The most striking finding in all biopsies was the
presence of inclusions within the muscle fiber (Figure
1). These inclusions were cristae-like and have not been
reported before. They superficially appear similar to
mitochondrial aggregates, but on closer examination do
not show the outer limiting membrane that surrounds
the mitochondrial cristae. The significance of these inclusions is not clear.
Though the clinical expression of muscle involvement in Behqet’s disease is rare, the myopathology
of this disease appears to be quite common.
RIDAFRAYHA,MD, FACP
Associate Professor of Medicine
American University of Beirut
Beirut, Lebanon
REFERENCES
Figure 1. Cristae-like inclusions found within the muscle fiber.
Proximal muscle tissue was studied by conventional light microscopy, histochemistry, high resolution
light microscopy, and electron microscopy. Although no
viral-like particles could be identified, we were impressed by the different myopathologic alterations present. High resolution light microscopy revealed alterations in the muscle in 3 patients, whereas electron
microscopy revealed alterations in the muscle of all patients. These alterations suggest involvement of the
muscle fibers (4). The varying degrees of myofilamentous disarray and loss seen in our material is consistent with similar observations by others (5).
Other findings included the aggregation of mitochondria and lysosomes in subsarcolemmal sites. The
demonstration of central nuclei in regions devoid of
contractile material is similar to that noticed in the patient of Arkin et a1 (1). The presence of these nuclei in
1. Arkin CR, Rothschild BM, Florendo NT, Popoff N: Behqet
syndrome with myositis: a case report with pathologic findings. Arthritis Rheum 23:600-604, 1980
2. Shishido A, Yamanouchi K: Virological studies on etiology
of BehGet’s disease. Presented at the International Symposium on Behqet’s Disease, Istanbul, September 1977
3. ODuffy JD: Neuro involvement in 7 patients with Behqet’s
disease. Am J Med 61:170-178, 1976
4. Afifi AK, Frayha RA, Bahuth NB, Tekian A: The myopathology of Behqet’s disease: histochemical, light, and
electron microscopic study. J Neurol Sci, in press
5 . Garcin R, Lapresle J, Hewitt J: Determinations muscularies au cours d’une maladie de Behqet (ou grande aphtose
de Touraine): etude clinique; documents histologiques et
ultra-structuraux concernant la biopsie musculaire. Rev
Neurol 117:345-361, 1967
Effect of heat on crystals
To the Editor:
The irreversible structural alteration of monosodium urate crystals induced by heat recently reported
by Dr. Neil S . Mandel (1) has been well recognized (but
not previously published) by our laboratory. We performed similar experiments on the effects of heat
(200°C for 3 hours) on 3 crystalline samples: monosodium urate monohydrate, a synthetic mixture of calcium pyrophosphate dihydrate triclinic and calcium
pyrophosphate tetrahydrate orthorhombic, and calcium
apatite. Our x-ray diffraction patterns were recorded on
flat plates with a crystal-to-plate distance of 75 mm,
LETTERS
638
1. MSU.H20
2
MSU.Hz0
3
CPPDCT)
REFERENCES
25OC
2OO'"C
+
3 hf
25'C
CPPT(O1
4 . CPPDCT)
+
200°C
3 hi
CPPT(0)
APATITE
25'C
6. APATITE
200'C
3 hr
7
zoo°C
5 hr
5
APATITE
I
I
2.5 3
I
l
4
610
l
I
l
l
106 4
I
I
3 2.5
A
Figure 1. Demonstration of alteration in monosodium urate monohydrate (MSU) crystal structure and the crystal structure of hydrated
calcium pyrophosphates (CPPD), and enhancement of calcium apatite diffraction pattern (APATITE).
thereby giving higher original magnifications than those
from the Guinier cameras used by Mandel.
As shown in Figure 1, we confirm the alteration
in monosodium urate monohydrate crystal structure
and demonstrate further that the crystal structures of
hydrated calcium pyrophosphates are also changed. In
contrast, the calcium apatite diffraction pattern was enhanced, i.e. heating reinforced the crystal lattice. Further annealing of the apatite crystals of 200°C for 5
hours produced sharper x-ray diffraction patterns, although the d spacings were unchanged.
These studies indicate that hydrated crystals
such as monosodium urate monohydrate (2) and calcium pyrophosphate dihydrate (3,4) are sensitive to
structural change by heat whereas calcium apatite,
which has an anhydrous lattice (5), is not.
It should be emphasized that even without structural alteration, heat may affect the surface composition
of crystals in ways which may not be detectable by powder x-ray diffraction analysis, but which may be critical
in terms of the effect of crystals on chemotactic and
other inflammatory activity (6). Therefore, we reiterate
Dr. Mandel's caution that results of biologic experiments in which crystals were previously heated to destroy pyrogens must be critically reassessed.
PEI-TAKCHENG,PhD
K. P. H. PRITZKER,MD, FRCP(C)
Mount Sinai Hospital
Toronto, Canada
1. Mandel NS: Structural changes in sodium urate crystals on
heating. Arthritis Rheum 23:772-776, 1980
2. Mandel NS, Mandel GS: Monosodium urate monohydrate, the gout culprit. J Am Chem SOC98:2319-2323,
1976
3. Mandel NS: The crystal structure of calcium pyrophosphate dihydrate. Acta Cryst B31: 1730-1734, 1975
4. Cheng P-T, Nyburg SC, Pritzker KPH: Alpha-calcium disodium pyrophosphate tetrahydrate. Acta Cryst B36:92 1924, 1980
5. Young RA: Biological apatite vs hydroxyapatite at the
atomic level. Clin Orthop 113:249-262, 1975
6. Pritzker KPH, Zahn CE, Nyburg SC, Luk SC, Houpt JB:
The ultrastructure of urate crystals in gout. J Rheumatol
5:7-18, 1978
Parasitic rheumatism
To the Editor:
I read with great interest the abstract by Bocanegra et a1 (1) concerning 2 patients with arthritis associated with parasitic infection. Evidence of abnormal
humoral immunity to parasites was present, with circulating immune complexes in serum and synovial fluid,
and IgG and C3 deposits in synovium. These patients
had developed acute polyarthritis during the course of
Strongyloides stercoralis and Taenia saginata infections.
These data are very fascinating and confirm my
own observation (2) of an 85-year-old white man who
developed a rheumatic disease which mimicked polymyalgia rheumatica. Pain and stiffness of the pelvis and
shoulder girdle persisted for several months. The
erythrocyte sedimentation rate was >40 mm/hour
(Westergren), with a marked hypereosinophilia (3 1%).
Many Rhabditoides Strongyloides stercoralis larva were
identified in the bile. Our diagnosis was "joint manifestation of S stercoralis infection due to an immunoallergic mechanism." To our knowledge, this is the first
such case in the literature.
After specific antiparasitic treatment with thiabendazole only, the patient quickly improved and was
completely cured in one month. Post-treatment peripheral blood eosinophilia and the erythrocyte sedimentation rate returned to normal levels.
In 1975 we proposed the following criteria for
the diagnosis of parasitic rheumatism (3):
1. Clinical features of monarthropathy, pauciarthropathy, or polyarthropathies of an inflammatory type
2. History of a stay in an endemic parasitic
country
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