~~~

~

Several groups of cases of fasciitis and myositis with eosinophilia are reported. The common features are inflammation into fascia and/or perimysium, and/or muscle fibers; eosinophilia in blood and/or in muscle biopsy. The following classification of 24 cases is suggested: at one end of the spectrum are fasciitis with eosinophilia: diffuse fasciitis (Shulman syndrome): 10 cases (3with hematological complications); 2 cases of diffuse fasciitis with muscle atrophy; 3 cases of restricted fasciitis. Relapsing perimyositis with eosinophilia belong to the same spectrum, either diffuse (5 cases) with myalgias, or localized (2 cases). Other cases are focal myositis or multiple myositis, polymyositis with eosinophilia. The relationship among these cases is discussed. There is a continuum among the different groups. The pathophysiology remains unknown. Key words: eosinophil fasciitis perimyositis polymyositis Shulman syndrome MUSCLE & NERVE 131385-395 1990

FASCIITIS, PERIMYOSITIS, MYOSITIS, POLYMYOSITIS, AND EOSINOPHILIA G. SERRATRICE, MD, J.F. PELLISSIER, MD, H. ROUX, MD, and P. QUILICHINI, MD

T h e syndrome described by Shulman,lg diffuse fasciitis with eosinophilia, is now well acknowledged and more than 100 cases have been reported in the literature. However, besides the forms corresponding exactly to true eosinophilic fasciitis, the course as well as the clinicopathologic characteristics allow the differentiation of several cases. In this article, 24 cases are reported, with the following common features: inflammation in muscle biopsy, localized in fascia and/or perimysium, and/or muscle fibers; and eosinophilia in blood and/or in muscle biopsy. In spite of several differences, these cases can be classified in a continuum, around the so-called Shulman syndrome, that is true fasciitis with eosinophilia. These cases show the spectrum of eosinophilia and fasciitis, perimyositis, myositis and polymyositis. Some of them are close to the primary hypereosinophilic ~yndrome,~.'' a systemic disease which is close to eosinophilic leukemia, but they differ from secondary eosinophilic syndromes, especially parasitic infestations (trichinosis, cysticercosis, echinococco-

From the Clinique des maladies du systeme nerveux et de I'appareil locomoteur. Faculte de medecine- Marseilles, France Address reprint requests to Dr. Serratrice. Clinique des maladies du systeme nerveux et de I'appareil locomoteur, CHU Timone, 13005 Marseilles, France. Accepted for publication June 15, 1989 CCC 0148-639W90/050385-011 $04.00 0 1990 John Wiley & Sons, Inc.

Fasciitis and Myositis with Eosinophilia

sis), Hodgkin's disease, allergic diseases or vasculitis. CASE REPORTS

The 24 cases have been classified into four groups: 1. Fasciitis with Eosinophilia. Included in the 15 cases are several varieties. The example of typical Shulman syndrome is Case 1. Case 1, A 30-year-old woman complained of a 4-month history of pain in her four limbs after unusual physical exertion of the upper limbs. She complained more particularly of painful fingers and wrists and of contractures of fingers along with pain on wrist flexion. On the medial face of both arms, the skin was indurated. She had a slight hyperthermia (37.5") and asthenia. On clinical examination skin changes were present on the forearms, predominantly on the right side. Both forearm muscles were indurated. Calves were slightly painful on pressure. Pain was increased by muscular contraction. Laboratory investigations yielded the following data: erythrocyte sedimentation rate, 35 mm; creatine kinase, 28 units (normal: 50); erythrocytes, 4.6 million; leukocytes, 9900 with 9% eosinophila. There were no nuclear antibodies. A skin biopsy showed dermis and hypodermis fibrosis with several inflammatory cells, mainly lymphocytes and histiocytes, but only a few eosinophils. The muscle biopsy showed fibers of

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385

A

B

C

normal size but inflammatory cells, mainly lymphocytes and plasma cells, with rare eosinophils, especially in the fascia, which were unusually thickened and into the perimysium and endomysium (Fig. 1A). The histoenzymologic study was normal. Acid phosphatase was positive for histiocytes. The patient was given 40 mg/day corticosteroid therapy and has not been reexamined. Table 1 shows the other cases of fasciitis with eosinophilia. Some are typical, others unusual. 2. Perimyositis (7 Cases)

Case 6. A 47-year-old man had a 4-week history of pain in the lower limbs. The onset corresponded to a digestive episode with diarrhea and hyperthermia. Examination showed firm muscles with induration into calves along with limited dorsiflexion of foot and limited flexion of knees. Painful calf induration impaired walking. The skin was thickened. Erythrocyte sedimentation rate was 25 mm and leukocytes, 9800 with 20% eosinophils. Parasitic investigations were negative. Electromyogram showed spontaneous activity and short polyphasic potentials. A biopsy of a calf specimen showed inflammatory infiltrates, mainly of eosinophils, into the perimysium and less significantly into the endomysium (Fig. 2). Clinical and biological data were quickly improved by indomethacin therapy. After three months without any clinical signs nor treatment, a relapse occurred with a 45mm erythrocyte sedimentation rate, and 27% eosinophils. A further muscle biopsy showed inflammatory cells, especially lymphocytes, without eosinophils. There was a good response to indomethacin and there has been no relapse since then. Table 2 is a summary of a number of similar cases. In the same group, 2 cases of restricted perimyositis are unusual. Case 21. A 35-year-old man had pain in the upper limbs and complained of heavy limbs. He reported a previous history of acute poliomyelitis at the age of two resulting in a global atrophy of the left lower limb necessitating the use of crutches. Later, muscular hypertrophy developed slowly in both upper limbs. At the age of 30, he had moderate and diffuse muscular weakness. On examination, the muscles of the left upper limb

were painful on pressure. The muscles of the arms and forearms were found to be hypertrophic. There was a weakness in the deltoid, brachioradialis, trapezius, biceps brachialis muscles on the left side. Hemogram data were: 7130 leukocytes with 15% eosinophils; erythrocyte sedimentation rate, 55 mm; creatine kinase, 118 units. Investigations for parasites were negative. A muscle biopsy of the left biceps brachialis showed a significant perivascular eosinophilic infiltrate into the perimysium. In comparison, a biopsy performed on the right in the same conditions was normal. A muscle CT scan was normal, also. Case 22. A 30-year-old man had suffered for a year from a right hypertrophic and edematous forearm. The right leg was slightly swollen. Erythrocyte sedimentation rate was 11 mm. Leukocytes, 10300; eosinophils, 16%. Muscle biopsy showed a moderate inflammation into the dermis with fibrosis, lymphocytes, and plasma cells. The perimysium was edematous with lymphocytic and plasma cell infiltrates without eosinophils. Muscle fibers were normal. There was a relapse in the left forearm 6 months later.

3. Multiple Eosinophilic Myositis (1 Case)

Case 23. In a 49-year-old patient a painless swelling of the left temporal muscle had developed during the night. Shortly afterward, a firm mass was observed in the temporal and masseter muscles that became painful. A biopsy of a mass specimen showed degeneration, regeneration, necrosis of muscle fibers and multinucleated giant cells. Electromyogram was normal; erythrocyte sedimentation rate was 34 mm. A 60 mglday corticosteroid therapy did not improve the masseter swelling. Later, the patient suffered from arthralgia. Laboratory investigations gave the following results: hemogram, 24% eosinophils; positive latex and Waaler-Rose tests; creatine kinase, 111 units; normal capillaroscopy; bone marrow, 8% eosinophils. Two months later, a firm mass was observed in the right brachioradialis muscle and the biopsy showed fiber necrosis with macrophagic reaction and interstitial inflammatory nodular or diffuse infiltrates of lymphocytes, histiocytes and plasma cells with rare eosinophils (Fig. 3 ) . The masses disappeared completely after three months of corti-

FIGURE 1 (opposite). Fasciitis with eosinophilia. (A): Inflammatory infiltrate in the endomysium with lymphocytes, macrophages and rare eosinophilic polymorphs; Case 1. (H & E x360). (6) Fasciitis with lymphocytes and macrophages; Case 4. (H & E x225). (C) Diffuse fasciitis with all types of inflammatory cells; Case 13. (H & E ~90).

Fasciitis and Myositis with Eosinophilia

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387

30

72

32

25

60

66

66

53

50

46

4a

35

20

50

25

F

F

F

F

M

F

M

M

F

M

M

M

F

M

M

1

2

3

4

5

6

7

8

9

10

11

12

13

14

15

0

0

0

0

0

+

0

0

t

0

Exertion

Lower & upper limbs Lower & upper limbs

0

Upper limbs Upper limbs

Upper limbs

Upper limbs

Upper limbs Lower limbs Lower limbs Lower limbs Lower & upper limbs Lower & upper limbs Lower & upper limbs Lower limbs

Pain

M = male; F = female; Age in years: N = normal.

Arre

Sex

Case

Forearms lower limbs

0

0

t

0

1-3

10-20

8-12

+

0

5-10 20-30

0

Masticatory Forearms paraspinal Forearms thigh Forearms

0

6-20

12-36

110-130

75-150

120-1 32

70- 80

43-80

0

0

Forearms

0

0

+ 0

t

t

+

0

t

+

Forearms legs

Forearms lower limbs Forearms lower limbs Forearms lower limbs

Forearms

Leas

Forearms

30

35

N

N

-

N 40

70

N

N

N

N

-

50

14

19

25

8

14

20

N

44

MYOgenic

N

MyOgenic

N

N

MyOgenic N

N

-

5-30

i)

27

24

6-12

Forearms Legs

N

EMG

N

9

12- 65

Forearms

Creatine kinase

N

Blood eosinophilia, 96

Joint contractures

Sedimentation rate

Skin induration

Raynaud’s phenomenon

Table 1. Typical Shulman’s syndromes and variations.

40 mg

Fasciitis

FasciitisEosinophils

FasciitisEosinophils FasciitisEosinophils

3 localized relapses

40 mg

30 mg

60 mg

improvement

Improvement

Unknown

2 relapses 20 mg

20 mg

No improvement

Chronic course

Improvement, Anemia = erythrocyte Improvement, erythrocytes 1, 8 Death, pancytopenia

Improvement, relapse

Improvement

Improvement

Unknown

Unknown

Course

60 mg

60 mg

100 mg

Fasciitis

FasciitisType I I fiber atrophy Fasciitisperifascicular atrophy FasciitisEosinophils FasciitisEosinophils

80 mg

40 mg

40 mg

0

60 mg

40 mg

Corticotherapy

FasciitisEosinophils

FasciitisEosinophiis

Fasciitis

FasciitisEosinophils Fasciitis

Fasciitis

Biopsy

L

4

=

+

35

M

20

M

0

0

0

60

F

19

Male; F = Female; age in years; N = Normal

0

0

0

Upper& lower limbs Thigh

0

30

F

18

Legs

+

0

0

Wrists

0

52

F

518 3

5

N

N

N

1

32/60

15130

Myogenic

Myogenic

EMG

18

20

%

Blood eosinophilia.

15140

30160

+

17

Legs

Legs

0

47

M

16

Pain

Exertion

Sedirnentation rate

Joint contractures

Age

Sex

Case

Skin induration

Table 2. Diffuse relapsing perimyositis.

Perimyositis, eosinophils Perimyositis, eosinophils into the dermis

Perirnyositis, eosinophils Perirnyositis, eosinophils Perirnyositis, eosinophils

Biopsy

Corticotherapy 20 mg Corticotherapy 60 rng

30 mg

Corticotherapy 30 mg Corticotherapy

lndomethacin

Treatment

Improvement

Unknown

Improvement, relapse Improvement, relapse Improvement

Course

A

B

FIGURE 2. Perimyositis. (A) Numerous eosinophilic polymorphs in the perimysium; Case 14. (H & E septum infiltrated with histiocytic cells and eosinophils; Case 17. (H & E x360).

390

Fasciitis and Myositis with Eosinophilia

x900).

(B)lnterfascicular

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A

B FIGURE 3. Multiple myositis with eosinophilia and polyrnyositis-with eosinophils. (A) Muscle fiber necrosis and endomysial inflammatory infiltrates with histiocytic cells, plasma cells, lymphocytes and rare eosinophils; Case 23. (H & E x360). (6)Massive inflammatory cell infiltrate and edema in an interfascicularseptum; Case 23. (H & E x90).

Fasciitis and Myositis with Eosinophilia

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391

costeroid therapy and laboratory tests were normal. Later on masses developed again in the trapezius and biceps brachii. 4. Eosinophilic Polymyositis (1 Case)

Case 24. For 18 months, a 46-year-old woman had been complaining of myalgias and asthenia. On examination both proximal and distal muscle wasting was observed. She was unable to kneel down or to stand up on heels or toes and a Gower’s sign was noted. Lower limbs were edematous with the following biological results: erythrocyte sedimentation rate, 25 mm; normal hemogram; creatine kinase, 2045 units; bone marrow, 4% eosinophils. Electromyogram was myogenic and neurogenic with spontaneous activity. A muscle biopsy showed necrosis, macrophagia and regeneration of muscle fibers. There were infiltrates of lymphocytes, plasma cells and eosinophils into the perimysium and the endomysium. Investigations for parasites were negative. A 100 mglday corticosteroid therapy was ineffective. Creatine kinase level decreased to 829 units but the clinical features did not improve. DISCUSSION

Cases of fasciitis with eosinophils are now well documented and their sympltomatolo y has been reported in several recent reviews. 142’ The original descriptions by Shulman in 1975” are still quite accurate, the main characteristics being: the frequency of onset after physical exertion, scleroderma-like cutaneous alterations, blood eosinophilia and hypergammaglobulinemia, thickening

~~~

~

Table 3. Classification of the 24 cases Group 1

Group 2

Group 3 Group 4

392

Fasciitts with eosinophilia Diffuse fascittis (Shulman’s syndrome) Cases 1, 2, 3, 4, 5, 14, 15 Diffuse fasciitis with hematologic complications Cases 6, 7, 8 Diffuse fasctitis with muscle fiber atrophy Cases 9, 10 Restricted fasciitis Cases 11, 12, 13 Relapsing eostnophrlic perimyositis Diffuse relapsing perimyositis Cases 16, 17, 18, 19,20 Restricted perimyosttis Cases 21, 22 Focal myositis or multiple myosttis with eosinophilia Case 23 Polymyositis with eosinophilta Case 24

Fasciitis and Myositis with Eosinophilia

of the fascia, and diffuse and perivascular inflammation. They were termed “diffuse eosinophilic fasciitis” or “fasciitis with eosinophils.” Since 1975, other features of the syndrome have been acknowledged: intramuscular eosinophils in some cases, extension of the inflammation into other muscles, l 7 severe hematologic in the course of a disease which had been considered as benign until then. Moreover, there has been descri tions of relapsing eosinophilic perimyositisIg2’ or localized eosinophilic myositis? Thus the description of the clinicopathologic manifestations of eosinophilic fasciitis is advancing. The report of the 24 cases mentioned above shows the heterogeneity of these cases and their relationship. The following classification is suggested, as shown in Table 3 . Various forms are included (Table 1). Cases 1 , 2, 3 , 4,5, 6, 7,8, 14, and 15, with 5 women and 5 men ranging between 25 and 72 years, should be considered as true eosinophilic fasciitis. Eosinophilic fasciitis seemed to have been induced by exercise in 3 cases. T h e first symptoms were cutaneous induration, peau d’orange and edema. The skin changes usually started with stiffness and swelling of the forearms, rarely of the legs. Raynaud’s phenomenon was present in six cases. Joint contractures, especially in elbows, wrists and ankles, developed in nine cases. The results of laboratory investigations are summarized in Table 1 . Erythrocyte sedimentation rate was raised in 5 cases. Peripheral blood eosinophilia, with more than 7% differential counting, was present in all the patients. Serum creatine kinase was usually normal. The electromyographic examination, performed in seven patients, was normal in five and myogenic in two. Muscle biopsies showed an inflammatory reaction into the fascia with eosinophils in five cases, and without eosinophils in others. There was a good response to corticotherapy except in one hematologic case. These cases of Shulman’s syndrome suggest two comments: As regards the cutaneous clinical data, fasciitis with eosinophilia could be a variant of s ~ l e r o d e r m afor ~ ~some ~ ~ ~authors, whereas it is a distinct syndrome for others.16 We think that there are very significant distinguishing features between eosinophilic fasciitis and scleroderma. In eosinophilic fasciitis, onset after physical exertion is frequent, skin induration is localized to the forearms, sparing the hands, Raynaud’s phenomenon is rare, nail-fold capillaroscopy is normal, visceral

Group 1: Typical Shulman’s Syndromes.

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May 1990

involvement uncommon, blood hypereosinophilia constant as well as fascia inflammation. With such differentiating features, Shulman’s syndrome may be clearly identified as a disease entity distinct from scleroderma. Moreover the course of eosinophilic fasciitis is usually benign except in some hematologic forms whereas life expectancy is shortened in scleroderma. Among the hematologic cases of our series (cases 6, 7, and 8) a patient died of pancytopenia which had a double origin: central, with a medullary hypoplasia of the granulous and megakaryocytic cells, and peripheral, with aplastic anemia by antibodies. A case of association between eosinophilic fasciitis and pancytopenia has been reported.6 Other cases were associated with aplastic anernia8’l2 thrombocytopenic pur ura, myeloid leukemia,’* and Hodgkin’s disease.‘ The prognosis is rather poor in cases where Shulman’s syndrome is associated with hematologic disorders. It has been demonstrated2‘ that the coexistence of thrombocytopenia and aplastic anemia are due respectively to antiplatelet antibodies and circulating inhibition of erythroid stem cells. Another subgroup of Shulman’s syndrome with atrophy of muscle fibers was illustrated by cases 9 and 10: type I1 fiber atrophy in one case and perifascicular atrophy, pathognomonic of dermatopolymyositis, in the other. The last subgroup could be termed “restricted” or “localized”fasciitzs with blood and muscle eosinophilia. The clinical signs were relapsing swelling and induration in several muscles: forearm in case 1 1, forearm, paraspinal and masticatory muscles in case 12, thigh muscles in case 1 . The findings of muscle biopsy were similar to those obtained in muscle biopsy performed in cases of Shulman diffuse fasciitis with muscle eosinophilia. We did not find any report of similar cases in the literature.

Group

2:

Relapsing

Eosinophilic

Perimyositis.

There are two subgroups: diffuse forms (cases 16, 17, 18, 19, 20) and restricted forms (cases 21, 22). We observed five cases of diffuse relapsing eosinophilic perimyositis (Table 2), three females and two males ranging between 30 and 60 years, induced by exertion in one case. Patients complained of diffuse pain, especially in lower limbs; skin induration and joint contractures were present in two cases, blood eosinophilia in two other cases. The most significant differential data was the muscle biopsy. Fascia were normal but there was an inflammation of the perimysium with

Fasciitis and Myositis with Eosinophilia

eosinophils (Fig. 2). Cases 16 and 17 had a relapsing course. Similar cases have been reported2’ since the first description.” Myalgias are predominant in lower limbs. There is no evidence of muscle weakness or of systemic involvement. Parasitic investigations through muscle biopsy or serology are negative. Such cases must be classified separately for several reasons. Anatomically, fascia and perimysia are different: fascia wrap fascicles whereas the perimysium surrounds the muscle fibers. Pathological changes are limited to the presence of eosinophils in the perimysium. The symptomatology is characterized by diffuse pain with inconstant blood eosinophilia. A relapsing but benign course is frequent. As suggested by Sladek et a1,21 this illness should be considered as a new form in the spectrum of eosinophilic disorders of unknown etiology. The second subtype of perimyositis is “restricted” perimyositis. In these cases, muscle pain and weakness were localized in one arm (in case 21), in one forearm and a leg (in case 22) with a relapsing course for this last case. Multiple relapsing focal eosinophilic myositis was observed in case 23, with an unusual pseudotumor of muscle and eosinophils in muscle, bone marrow and blood. A similar case has been reported2 described as a soft-tissue mass in the sternocleidomastoid muscle, without parasitic infection. The muscle was infiltrated by eosinophils, lymphocytes and plasma cells. In one case the muscles of mastication were involved. This entity has been acknow1edged by veterinary pathologists’0922in dogs and called “masticator myopathy.” It has been described in the skeletal muscles of cattle, sheep, horses, pigs and monkeys. There are eosinophilic infiltrates in muscles and peripheral blood eosinophilia. Investigations for parasites were negative in these animal cases. The origin is not determined.

Group 3: Focal Eosinophilic Myositis.

Group 4: Eosinophilic Polymyosltis. This is illustrated by case 24 with a high level of serum creatine kinase and typical electromyogram. Muscle biopsy showed inflammation with eosinophils, necrosis, and regeneration. Eosinophilic polymyositis has rarely been except in parasitic infection such as trichinosis and cysticercosis. Cases of eosinophilic polymyositis are associated with systemic symptoms, peripheral blood eosinophilia, multiple organ involvement (pancarditis,

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393

Table 4. Pathological changes. ~~~~

~

Cases

Inflammation

++ ++ ++ F ++ F ++ F ++ ++ F ++ ++ ++ F ++ ++ F ++ ++

1 2 3

4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23

+F

Muscle fibers

Perimysium

Fascia Cell type LPE LPE LPE LP LP LPHE LP LH LH LH E LE LPE LH E

Inflammation

+

+ +

+ + + + Type II atrophy Perifascicular atrophy LPE

++

LH

++ ++ ++ ++ ++ ++ ++

E LPE E

F = Fibrosls; L

=

Hypodermis FLHE

FLHP FLE F F F

FLE F F F FLH

F

E

LH

E

FE

LP

FLHE

F

FLP

FLP

E LH

E LP LHPE Necrosis-Regeneration Necrosis-Regeneration

LPE

24

Lymphocytes; P = Plasma cells; H = Histiocytes; E = Eosinoohils

pulmonary infiltrates, multiple mononeuropathy, embolic strokes). Clinical features of polymyositis and severe course have been described and variously termed hypereosinophilic syndrome, eosinophilic leukemia, and eosinophilic collagen d i ~ e a s e . ~The , ’ ~ boundaries of eosinophilic polymyositis are now clearly defined. Some cases are close to true eosinophilic leukemia; a rapidly fatal course is frequent in spite of corticosteroid therapy. Although different, these cases should be viewed as a continuum: 1) true diffuse fasciitis with blood eosinophilia, without muscle eosinophils; 2) diffuse fasciitis with muscle eosinophils; 3) diffuse fasciitis with hematologic complications; 4) diffuse fasciitis with muscle fiber atrophy; 5 ) restricted fasciitis; 6) diffuse relapsing perimyositis; 7) restricted perimyositis; 8) multiple myositis with eosinophilia; 9) eosinophilic polymyositis. The pathology is slightly different depending on the cases but, strictly speaking, there is some overlapping (Table 4) in the involvement of fascia and perimysium. The extension of the alteration remains unclear in some cases. Thus in case 6 corresponding to a typical fasciitis of Shulman type,

394

Dermis FLHE

Cell type

+ +

Skin

Fasciitis and Myosttts with Eosinophilia

the inflammation was very marked in the fascia but there was also a moderate extension to the perimysium. In six cases there was a fibrosis of dermis and hypodermis. Conversely, in perimyositis, fascia were usually normal, except in case 18; and there was a dermis-hypodermis inflammation in cases 17, 20, 22. Similar findings have been reported“ in which the anatomical substrate of eosinophilic fasciitis was not confined to the fascia but involved also mysia and the muscle itself. Finally, the pathophysiology of eosinophilic fasciitis remains unknown. Neurotoxicity of eosinophils has been described by Gordon.’ Further studies demonstrated that the so-called “Gordon phenomenon,” that is weakness and incoordination, induced by cerebral injection in rabbits, depended on the presence of eosinophils in the inoculum. As regards fascia and muscle, an eosinophil-derived toxin might cause the damage. The human eosinophil granule contains several cationic protein^."^ The major basic protein is the probable cause of endothelial damage in multiple organs with involvement of the hypereosinophilic syndrome. But in our cases vasculitis is unlikely to have been the case of fasciitis and myositis.

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REFERENCES

1. Ackerman SJ, Loegering DA, Venge P: Distinctive cationic proteins of the human eosinophil granule: Major basic protein, eosinophil cationic protein, and eosinophil-derived neurotoxin. J Immunol 1983; 1312977-2982. 2. Agrawal BL, Giesen PC: Eosinophilic myositis. An unusual course of pseudo-tumor and eosinophilia. J A M A 1981; 246: 70- 7 1. 3. Bjelle A, Henriksson KG, Hofer PA: Polymyositis in eosinophilic fasciitis. Eur Neurol 1980; 19: 128- 137. 4. Chusid MJ, Dale DC, West BC: The hypereosinophilic syndrome: Analysis of fourteen cases with review of the literature. Medicane 1975; 54:l-27. 5. Fredens K, Dahl R, Venge P: T h e Gordon phenomenon induced by the eosinophil cationic protein and eosinophil protein X. J Allergy Clin Zmmunol 1982; 70:361-366. 6. Fu TS, Soltani K, Sorensen LB: Eosinophilic fasciitis. J A M A 1978; 240:451-453. 7. Gordon MH: Studies of the aetiology of lymphadenoma. Bristol, UK: John Wright and Sons Ltd, 1932: p p 7-76. 8. Hoffman R, Dainiak N , Sibrack L: Antibody-mediated aplastic anemia and diffuse fasciitis. N Engl J Med 1979; 300~718-721. 9. Huang KW, Chen XH: Pathology of eosinophilic fasciitis and its relation to polymyositis. CanadJ Neurol Sci 1987; 14:632-637. 10. Hulland TJ: Muscle, in Jubb KVK, Kennedy PC (eds): Pathology of domestic animals, cd 2. New York, Academic Press Inc, 1970: p p 453-494. 11. Layzer RB, Shearn MA, Satya-Murtis S: Eosinophilic polymyositis. A n n Neurol 1977; 1:65-71. 12. Littlejohn J O , Keystone EC: Eosinophilic fasciitis and aplastic anemia. J Rheumatol 1980; 7:730-732. 13. Michaels RM: Eosinophilic fasciitis complicated by Hodgkin’s disease. J Rheumatol 1982; 9:473-476.

Fasciitis and Myositis with Eosinophilia

14. Michet CH Jr, Doyle JA, Ginsburg WW: Eosinophilic fasciitis. Report of 15 cases, Mayo Clin Proc 1981; 56:27-34. 15. Odeberg B: Eosinophilic leukemia and disseminated eosinophilic collagen disease. A disease entity? Acta Med Scand 1965; 77:129- 140. 16. Kozboril MB, Maricq HR, Kodnan GP: Capillary microscopy in eosinophilic fasciitis: A comparison with systemic sclerosis. Arlhritis Rheum 1983; 26:617-622. 17. Schumacher RH: A scleroderma-like syndrome with fasciitis, myositis and eosinophilia. Ann Znt Med 1975; 84:49. 18. Serratrice G, Pellissier JF, Cros D, Gastaut JL, Brindisi G: Relapsing eosinophilic perimyositis. J Rheum,utol 1980; 73199-205. 19. Shulman IE: Diffuse fasciitis with eosinophilia: A new syndrome. Transactions of the Association of American Physicians. 1975; 88~70-86. 20. Sibrack LA, Callen JP: Diffuse fasciitis with eosinophilia, in Cutaneous aspects of internal disease. Callen JP (ed) Chicago: Yearbook Medical Publishers, 1980, p p 55-60. 21. Sladek GD, Vasey FB, Sieger B, Behnke DA, Germain BF, Espinoza LR: Relapsing eosinophilic myositis. J Rheumatol 1983; 10:467-470. 22. Smith AT, Jones TC, Hunt RD: Veterinary pathology, ed 4. Philadelphia, Lea & Febiger, 1972, p p 1046- 1091. 23. Stark RJ: Eosinophilic polymyositis. Arch NeuroE 1979; 3 6 ~ 7 12- 722. 24. Torres VM, George WM: Diffuse eosinophilic fasciitis. A new syndrome or variant of scleroderma? Arch Dermatol 1977; 113:1591- 1593. 25. Urbano-Marques A: Eosinophilic fasciitis evolving into scleroderma, letter. A n n Intern Med 1983; 99:412. 26. Weltze M, Salvado A, Rosse W: Humoral suppression of hematopoiesis in eosinophilic fasciitis. Blood 1978; 52:218.

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Fasciitis, perimyositis, myositis, polymyositis, and eosinophilia.

Several groups of cases of fasciitis and myositis with eosinophilia are reported. The common features are inflammation into fascia and/or perimysium, ...
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