Refer to: Dermatomyositis-Medical Staff Conference, University of California, San Francisco. West J Med 124:316-322, Apr 1976

Medical Staff Conference

Dermatomyositis These discussions are selected from the weekly staff conferences in the Department of Medicine, University of California, San Francisco. Taken from transcriptions, they are prepared by Drs. David W. Martin, Jr., Associate Professbr of Medicine, and H. David Watts, Assistant Professor of Medicine, under the direction of Dr. Lloyd H. Smith, Jr., Professor of Medicine and Chairman of the Department of Medicine. Requests for reprints should be sent to the Department of Medicine, University of California, San Francisco, CA 94143.

DR. SMITH: * One of the most puzzling disorders with which we must occasionally be concerned is that which is categorized uneasily as "polymyositis" or "dermatomyositis." We have such a case for presentation today. The discussion will be by Dr. Lawrence M. Tierney, Jr., Assistant Chief of Medicine at the Fort Miley Veterans Administration Hospital. The case will be presented by Leon

Axel.t Case Summary A 59-year-old white man was admitted to the University of California Medical Center for evaluation of dermatomyositis. The patient's illness began three years previously when dysphagia, weakness and generalized edema developed. Results of evaluation by his private physician showed abnormal levels of serum enzymes including elevated lactic dehydrogenase, serum glutamic-oxaloacetic transaminase and creatine phosphokinase. A cine-esophagram showed hypomotility with Lloyd H. Smith, Jr., MD, Professor and ment of Medicine. tLeon Axel, Medical Student.


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aspiration. He was referred to the University of California Medical Center for evaluation. His past medical history was remarkable only for coronary artery disease. On physical examination, the patient appeared chronically ill. An erythematous maculopapular rash over the trunk and upper extremities, penorbital edema and a reddish discoloration of the upper eyelids were noted. There was pitting edema of upper and lower extremities with some tenderness to palpation and pronounced proximal weakness. Laboratory data included hemoglobin of 11 grams per liter, leukocyte count of 11,600 per cu mm with a normal differential, erythrocyte sedimentation rate of 60 mm per hour, creatine phosphokinase of 880 iu per hour, lactic dehydrogenase of 645 iu per liter and aldolase of 22 Iu per liter. Alpha fetoglobulin and carcinoembryonic antigen determinations were negative. Findings on muscle biopsy and electromyography were interpreted as consistent with myositis. Treatment was started with high dose steroids, and there was mild improvement in strength and levels of enzymes and the erythrocyte sedimenta-


tion rate returned to normal. Persistent dysphagia necessitated tracheostomy and use of a nasogastric feeding tube. The patient was discharged to a rehabilitation hospital two months after admission. Continuing dysphagia and aspiration led to use of a gastrostomy tube for feeding. There were multiple steroid complications including vertebral compression fractures, cataracts and skin infections. One year ago therapy with methotrexate was started, 20 mg per week given intravenously. Coinciding with tapering of the steroid dosage, there was a gradual, mild increase in the patient's strength. One month before this admission, an erythematous rash developed over the entire body. Administration of methotrexate was discontinued. The patient experienced progressive weakness and was referred back to the University of California Medical Center for reevaluation. On physical examination, vital signs were found to be normal. A dusky rash over the patient's face and upper trunk was noted. Small bilateral cataracts were seen to be present. Stool specimens were guaiac positive. Periungual telangiectasias and pronounced proximal muscle weakness were found on examination of the extremities; there was weakness of the neck flexors as well. Findings on laboratory studies showed hematocrit reading, leukocyte count and differential to be within normal limits. Erythrocyte sedimentation rate was 6 mm per hour and serum muscle enzyme levels were only slightly elevated. Results on upper gastrointestinal series showed the presence of an active duodenal ulcer. Myopathy consistent with inflammatory or steroid causes was shown on an electromyogram. A skin biopsy of the upper extremities gave findings consistent with dermatomyositis. Administration of methotrexate was begun without any evidence of hypersensitivity reaction and the patient was discharged on a regimen of steroids and weekly intravenous injections of methotrexate. His condition has been stable since, except for one episode of mild bleeding from the duodenal ulcer. DR. TIERNEY:* Though the case we have just heard about surely provides a textbook picture of dermatomyositis, this term will be used interchangeably with polymyositis during this talk. Comments about the case will be made where *Lawrence M. Tierney, Jr., MD, Assistant Chief of Medicine, Fort Miley Veterans Administration Hospital.

relevant. In reviewing the literature on this subject, one finds a great deal of anecdote and impression with a limited amount of precise information. This is due mainly to a poor understanding of the disorder's causative factors and pathogenesis, and to its relative rarity. Our concept of polymyositis should be subject to continual revision as knowledge of it increases, and artificial classifications should be abandoned readily when no longer useful. The caveat aside, it can be agreed that polymyositis and dermatomyositis cover a wide spectrum of related disorders, characterized by inflammation and degeneration of varying amounts of skeletal muscle, with a clinical sine qua non of muscle weakness.1-3 In many patients with polymyositis and dermatomyositis, features of other rheumatic diseases will be noted, but in many others these features will not be present. Additional cases will occur in concert with malignancy, a relationship recently challenged but probably still valid. As suggested, there are various classifications of this disease, the most widespread being Pearson's classification2 which appears in the Primer on the Rheumatic Diseases.4 This will not be discussed here since it would not add much to our comprehension. If you remember that we are dealing with an inflammatory disease, that there is a loss of strength in all patients with the disease, that there may or may not be a skin rash, that there may be overlap with other related conditions and that there may be associated carcinoma, no further categorization is needed. It may well be that this clinical heterogeneity merely represents host variability to common or similar causative agents. One can imagine that tuberculosis, before its cause was discovered, may have been similarly puzzling to clinicians of old; the same organism may cause a wide range of syndromes, from positive findings on a skin test to miliary disease. This emphasizes how important it is to know the cause of any illness, since without this knowledge there can be no real understanding. Unlike ankylosing spondylitis, a disease of antiquity observable in mummies, but like rheumatoid arthritis, which has appeared relatively recently in man's evolution, this seems to be a "new" disease in the history of medicine. The first case of polymyositis was recognized by Wagner in 1863, and until about 1950 it was thought that in all cases skin lesions were present (that is, dermatomyositis). We now know that most patients do not have skin lesions (a report of 1887 THE WESTERN JOURNAL OF MEDICINE


DERMATOMYOSITIS TABLE 1.-Percentage of Clinical Signs and Symptoms in 200 Cases of Polymyositis""-4

Mutsculoskeletal Weakness Proximal muscles ............. Lower extremities ....... ............. Upper extremities ........ Distal muscles ............. ............. Neck flexors ............. .............. Dysphagia . ............................. .............. Facial muscles ............ ............. Extraocular muscles ........ .............. Pain or tenderness .......... ........ Arthritic or rheumatic features ......

95 76 27 62 47 6 2 48 24

Ski.n "Typical" dermatomyositis ....... "Atypical" features ........... Raynaud's phenomenon ........

............ 44 ............. ............

20 30

TABLE 2.-The First Symptom in 100 Cases"'

Muscular Weakness Legs ................................... 44 8 Arms ................................... Dysphagia ............................... 2 Skin rash .................................. 24 .............. 15 Joint or muscular pains ........ Constitutional ............................... 7

making this point was disregarded). The disorder was first referred to a pseudotrichinosis, which it most resembles phenotypically though not clinically. The advent of muscle biopsy has helped separate this entity from other myopathies, especially the dystrophies, although for accurate results impeccable technique and careful handling of the specimen are necessary. The first allusion to a kinship with malignancy was noted in 1916. While epidemiologic studies5 have shown no susceptible group geographically, they have at least shown that there are two peaks in age of incidence-one in early childhood, the second in the fourth and fifth decades. Five new cases per million population occur yearly, a rate similar to that of polycythemia vera. There is no familial pattern or associated histocompatability antigen. In both incidence peaks there is a 2:1 female predominance, in both pure and overlap cases. The picture can vary from the explosive onset of profound weakness, heliotrope rash, and systemic complaints on the one hand, for example, to the gradual development of slight pelvic girdle weakness over several years on the other. Table 1 shows the range of signs and symptoms gleaned collectively from several series. 318

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124 * 4

First let us consider the strictly muscular syndromes. It would appear that a good rule of thumb is "no weakness, no diagnosis." In most cases, onset of weakness is subacute and symmetrical, the proximal muscles of the lower extremities usually causing early complaints such as difliculty in climbing stairs or boarding a bus. Upper extremity problems may be noted, for instance, when a patient attempts to comb the hair. The frequency of affliction of neck flexors is important to remember in the physical examination. Weakness of the facial and extraocular groups is very unusual, and therefore so is diplopia. Dysphagia, however, via dysfunction of the striated pharyngeal musculature is not, as we have heard. Dysphagia and resultant aspiration tend to be prominent in more acutely developing cases, and are more often linked with poor prognosis. Fortunately, respiratory paralysis is hardly ever encountered except in the most aggressive forms of the disease. The presence of pain and tenderness is not essential for diagnosis. Atrophy and contractures are likely to occur, largely when treatment has been delayed or is ineffective. Some precipitating factors apparently exist. Older papers comment on the role of the menopause, but this is doubtless an artifact given the peak age incidence and sex predilection for women. Infections, trauma and systemic stress are said to bring it on, but this is in no way distinctive for polymyositis. We have now discussed

the range of muscle symptomatology, but the first symptom is likewise of note (Table 2). This is of a muscular nature in 69 percent of patients, but dermatologic in 24 percent. The remaining 7 percent often provide diagnostic dilemmas; I have personally seen polymyositis manifest as a fever of unknown origin (FUO), and Barwick and Walton' have documented similar atypical presentations. Raynaud's phenomenon occurs in 30 percent of cases in some point in the course. Careful analysis of this symptom in polymyositis discloses that it correlates best with the presence of an overlap syndrome, in the main when elements of scleroderma are encountered as well as those of myositis. The same is true of arthritis, that is, it is unusual in pure polymyositis or dermatomyositis, but fairly frequent when hints of another rheumatic condition are detectable. Concerning overlap, criteria should be considered individually for the diagnosis of each condition when more than one is suspected.6 Confounding the issue is the


lack of universally accepted criteria for this type for polymyositis-such as already exist, for example, in the disorders of rheumatoid arthritis and lupus erythematosus. The typical rash of dermatomyositis is seen in 40 percent of cases. It is a dusky eruption in the malar and periorbital distribution; in the latter area it is referred to as the heliotrope. This may extend onto the upper thorax in a V-shaped pattern. Noteworthy when present are hyperemic patches which may be slightly raised and scaly and found on the elbows, knuckles and malleoli. These are called Gottron's papules. The rash can be precipitated or exacerbated by exposure to sun. As has been pointed out, such a rash is the initial manifestation of dermatomyositis in most patients. In rare cases, this dermatologic feature alone may be present for several years without the evolution of muscle weakness. Less specific than these findings are the subcuticular telangiectasias which are visible grossly on occasion, but which are more striking when viewed through a drop of oil with an ophthalmoscope at +20 to +40 diopters. Similar abnormalities of the capillary loops occur in rheumatoid arthritis, systemic lupus erythematosus and progressive systemic sclerosis, and it is said that astute diagnosticians can even distinguish among these diseases by certain subtle differences at capillarioscopy. The cuticle of the nail, whether or not there are telangiectasias, may be reddened, roughened, irregular and hyperkeratotic, even in the absence of overzealous manicuring. These nail changes are instructive to look for, and are clearly useful to clinicians.7'8 In summary, (1) the weakness is proximal, usually starting in the legs; (2) the rash when present is very distinctive; (3) there is dysphagia in the more severe cases; (4) Raynaud's phenomenon and arthritis are more likely to occur when aspects of other rheumatic diseases are concomitantly present. What then of inflammatory myopathy associated with a malignancy? It is taught in the textbooks that when dermatomyositis is found in a male over the age of 40, there is a 50 percent likelihood of an associated tumor being present. The basis for this deduction comes from a few small studies done in about 1940 in which the diagnosis of polymyositis was only speculative, there being no biopsy technique or enzyme studies available. Any one of a number of neuromuscular complications of carcinoma or other conditions

have been present in these selected series. Welldocumented instances of polymyositis associated with a tumor are infrequent in the literature. Nonetheless, most authorities do agree that the instances of such association are more numerous than would be accounted for by chance alone.9 Where well studied, the myositis has tended to precede the tumor, often by years, and a rash (that is, dermatomyositis) was found more often than in spontaneous cases. The opinion still exists that tumor-associated myositis pursues a more virulent course than polymyositis and is steroidresistant, though ample proof of these observations is wanting. Cure of cancer has resulted in remission of the associated dermatomyositis. In cases of dermatomyositis an extensive search for hidden malignancy is unwarranted and likely to be unrevealing unless there are findings on clinical examination that point to a specific organ system. In patients with dermatomyositis and cancer who die, death results from the muscle disease in about half the cases and is the direct effect of the tumor in the remainder. Despite the putative autoimmune basis of all of the rheumatic diseases, it is only polymyositis that has been linked with a higher incidence of many different types of tumors. As to other organs, interstitial pneumonitis and cardiac muscle infiltration are observed in a small percent of nonoverlap polymyositis.10,11 What other diseases can produce proximal weakness with suggestive findings on laboratory tests? Muscular dystrophies, when confined to the girdle muscles, may appear in adults like polymyositis, but the family history is positive and findings on muscle biopsy do not show inflammation to be present. Myasthenia gravis, potentially proximal, affects muscles used the most (like the external ocular muscles), responds to edrophonium, has normal serum enzymes and shows electromyogram (EMG) fatiguing. Almost any endocrine disorder (too much or too little hormone) can cause this pattern of weakness. The major entity meriting serious consideration is thyrotoxic myopathy. This may be exceedingly cryptic and indistinguishable from polymyositis, especially in older patients where no other findings of thyrotoxicosis may be found. You need only to think of it for diagnosis. Steroid myopathy is easy to dismiss when it is primary, but not when a patient is being treated with these agents exogenously for a disease which itself can cause weakness. This thorny problem THE WESTERN JOURNAL OF MEDICINE



was encountered in today's patient. The electromyography tracing is not altered in steroid myopathy in contrast to other myopathies, but this may already be abnormal from the disease under treatment. One may be forced to decrease dosage temporarily and observe for response. Fluorinated compounds like triamcinolone are perhaps more culpable. No precise correlation between duration and dose of steroids and occurrence of myopathy is observed. As another cause of proximal muscle weakness, rhabdomyolysis can be seen as an acute event secondary to binge drinking or to muscle compression of any cause, but here weakness is less prominent than are the very high levels of muscle enzymes in the serum. The polymyopathy of hypokalemic periodic paralysis is most striking in adolescence, but may reappear in middle age as indolent weakness. Findings on biopsy are distinctive, showing vacuolization and hydrops of the myocytes. The absence of visible fasciculations excludes lower motor neuron disease, itself typified by distal loss of strength rather than proximal. Long tract signs can be in evidence. In any patient with weakness of all four extremities, no matter how obvious the cause may seem, cervical spine films should be made in the first evaluation to exclude remediable lesions such as osteoarthritic spur. As for infectious (or pseudoinfectious) causes, sarcoidosis is the only process which gives a true proximal weakness, and granulomata are found on biopsy studies. These are a few important differential considerations, and many others may be found in the literature.12 Given clinical features that suggest polymyositis, what is the best way to use laboratory tests in confirming this suspicion? A systematic approach to this problem was presented in a paper by Vignos and Goldwyn,13 who looked at the utility of tests commonly used in diagnosis and management of fairly well-documented cases. The four most valuable are determination of serum levels of muscle enzymes, urinary creatine measurement, muscle biopsy and electromyography (the first two being most useful in following therapy). Antinuclear antibodies are consistently negative despite superficial resemblance of the heliotrope to lupus erythematosus (LE). Creatine, the anhydride of which is creatinine, is synthesized in the liver, is stored in muscle and is normally present in small amounts in the urine. In any organic disease of muscle, urinary excretion of creatine rises and in this series all patients 320

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had greater than a "6 percent creatinuria" expressed as the concentration of urinary creatine over the sum of concentration of urinary creatine plus creatinine. Besides use in initial diagnosis, this was the first aberration to appear during relapse under therapy, occurring before the rise in serum enzymes. Of the serum enzymes, creatine phosphokinase (CPK) is the most sensitive, elevated in more than 80 percent of cases. Levels of CPK may be normal now and then in biopsy-proven cases, especially early in untreated patients and late in the course of the disease when widespread fibrosis and atrophy have supervened. The measurement of transaminase and aldolase is popular in some hospitals, but these enzymes have the disadvantage of being found in other tissues. Naturally, studies of muscle enzymes are convenient to obtain too, and findings can be used in assessing therapeutic endeavors. Just as the creatine levels in urine rise during exacerbations, these serum enzyme levels rise before weakness occurs and fall before strength returns in responsive cases. Bear in mind that these changes in enzyme levels occur later than urinary creatine change. For biopsy, pick a muscle that is weak, and one in which an electromyography needle has not been used because it is important to know that inflammation is not iatrogenic. There are two types of skeletal muscle fibers which are hard to tell apart by light microscopy but are different physiologically. The first type, which mediates most routine muscle contractions, operates aerobically and at slow speeds, generates little force, but is indefatigable. The second type of fiber produces greater force, but for short periods and often anaerobically. The typical biopsy findings show fiber degeneration and attempts at regeneration indicated by basophilia and varying fiber size and round cell infiltrates. Nuclei are large and central. Cell infiltration is said to be less prominent if there is an associated malignancy. For me an electromyogram is exceeded in complexity only by an electroencephalogram (EEG)-in patterns, terminology and interpretation. It promises to remain safely within the diagnostic domain of the neurologists. You will read of the myopathic triad of fibrillatory potentials, polyphasic bursts on voluntary contraction and pseudomyotonia. A few words of explanation might help. In muscle disease the electrical pattern is an active one since many units are required to do the same amount of work that nor-


mally would be done by a few. The contraction of abnormal fibers gives electromyographic deflections whichi are smaller and shorter, somewhat "'moth-eaten" in appearance. The normal fiber potential on voluntary contraction is bigger and shorter, and has less than four phases. Diseased potentials typically have more than four and thus are polyphasic, in addition to being more numerous. Fibrillation, however, and pseudomyotonia are types of involuntary activity that can be noted with nonspecific nerve or muscle injury. Normal muscle records no activity during resting. Since dermatomyositis is a patchy disease, both biopsy and electromyography are subject to sampling error and on occasion give normal finding. In difficult cases the paraspinous muscle group of the back may be the only area abnormal electromyographically.3 In summary, a reasonable approach to the investigation of a patient with muscle weakness might be (1) measure urinary creatine and the serum level of muscle enzymes because an abnormality will indicate myopathy, albeit nonspecifically; (2) then proceed to biopsy and electromyography, picking an abnormal site based upon areas of weakness; (3) should findings on the latter two studies be normal or nondiagnostic, then the appropriate search for other causes of myopathy can be carried out. When all else fails, observation and repeat testing should give the right answer. Now I would like to turn to a speculation or two upon the causative factors and pathogenesis of the perplexing disorder. The association with malignancy adds further interest. Does the tumor make a substance that is toxic to muscle? Does the immune mechanism attempting to eradicate the neoplasm cross-react with muscle? Does the same agent (a hidden virus?) cause both or either independently? It remains uncertain. Viruslike particles of various structural types have been detected in the myocytes of patients with polymyositis by electron microscopy. Circulating antibodies to muscle may be found after any muscle injury, but a recent report describes immunoglobulin and complement deposits in vessel walls of patients with polymyositis.14 Such deposits are observed mainly in children in whom this disorder behaves like a vasculitis, a feature more compatible with circulating immune complexes. Two patients with agammaglobulinemia have been described as having polymyositis suggesting that gamma globulin is not required in all cases.

Typical dermatomyositis has occurred in a patient with C2 deficiency,15 indicating that the classic pathway of complement activation is not always required either. Such immune deficiencies might render the patient more susceptible to other immunological injury, for various rheumatic diseases have occurred among persons with various deficiencies of the complement system. Cell mediated immunity may have a role in polymyositis in adults. Lymphocytes from patients with active myositis cause cytotoxic changes when layered upon autologous or chick muscle cells in culture.16 These cytotoxic changes were interpreted as secondary to T-cell production of lymphotoxin, a lymphokine recognized as a participant in delayed hypersensitivity. Such damage at the membrane or subcellular level might account for diffuse clinical weakness when only patchy changes are seen on pathological specimens. The soluble mediator of injury (lymphotoxin) was postulated to diffuse through the tissues and to injure sarcolemma of remote fibers, without a cellular response that would need only to be present at the site of the instigating antigen. The antigen could be part of the muscle but need not be, as it as easily might be a fellow traveler located in that tissue. All this remains speculative. In short, there are many tantalizing suggestions as to the immunological or viral (or both) causative factors in this disease.'7-19 Some proven viral diseases, such as influenza B, may cause muscle pain and swelling with notably elevated levels of serum enzymes, but without weakness. Other myolytic states may show very high levels of enzymes with preservations of strength. These observations lend further credence to the notion that weakness in polymyositis is due less to the actual amount of necrosis than it is to some physiologic derangement. How should polymyositis be treated? Winkelmann reviewed statistics from the presteroid era from the Mayo Clinic experience,20 and contrasted them with those from patients given corticoids. Polymyositis undergoes spontaneous remission in many patients and there exists no proof that steroid therapy increases this rate of remission. This author did conclude that steroids hasten remission, and therefore avert contractions and atrophy, surely a benefit. It is not clear that the groups are well defined in this retrospective study, but the conclusions have not been refuted. Death from polymyositis occurs most frequently in the first two years. The outlook is THE WESTERN JOURNAL OF MEDICINE



worse when aspiration occurs,21 and this observation is applicable to today's patient. Empirically, therapy with steroids is begun at about 60 mg of prednisone per day, without reduction in dosage until levels of serum enzymes are normal and urinary creatine reduced by half. One also follows muscle strength. Therapy should not be thought a failure until a four month trial has been administered. In the face of a poor response, or development of intolerable complications of corticoids, immunosuppressive agents have been used. Methotrexate has been most widely used,22 but a variety of other agents have been tried. As in today's patient, methotrexate is given in relatively small doses by vein. In this way the drug bypasses the portal circulation, perhaps -reducing hepatotoxicity. You cannot help but be concerned about giving immunosuppressive drugs of this type for a condition that is usually benign. My own experience in the immunosuppressive treatment of polymyositis has been quite favorable in the short-term. The long-term effects are still uncertain. I cannot disagree with the use of such therapy for the patient being discussed today because of the severity of the illness. REFERENCES 1. Barwick DD, Walton JN: Polymyositis. Am J Med 35:646660, Nov 1963 2. Pearson CM: Polymyositis. Ann Rev Med 17:63-82, 1966


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3. Bohan A, Peter JB: Polymyositis and dermatomyositis. N J Med 292: 344-349, 403-407, Feb 1975 4. Rodman GP, McEwen C, Wallace SL (Eds): Primer on the rheumatic diseases-Section 10: Polymyositis and dermatomyositis. JAMA 224 (Suppl): 717-719, Apr 30, 1973 5. Medsger TA, Dawson WN, Masi AT: Epidemiology of polymyositis. Am J Med 48:715-723, Jun 1970 6. Tuffanelli DL, Winkelmann RK: Scleroderma and its relationship to dermatomyositis, lupus erythematosus, rheumatoid arthritis, and Sjogren's. Am J Med Sci 43:133-146, Feb 1962 7. Bohan A, Peter JB: Authors' reply to letters regarding reference number 3. N Engl J Med 292:1352, Jun 1975 8. Samitz MH: CuticuLlar changes in dermatomyositis. Arch Derm 110: 866-867, Dec 1974 9. Williams RC: Dermatomyositis and malignancy-A literature review. Ann Intern Med 50:1174-1181, May 1959 10. Schaumburg HH, Nielsen SL, Yurchak PM: Heart block in polymyositis. N Engl J Med 284:480-481, Mar 1971 11. Frazier AR, Miller RD: The lung in polymyositis. Chest 65:403-407, Apr 1974 12. McArdle B: Metabolic myopathies. Am J Med 35:661-672, Nov 1963 13. Vignos PJ, Goldwyn J: Evaluation of laboratory tests in diagnosis and management of polymyositis. Am J Med Sci 263: 291-308, Apr 1972 14. Witaker JN, Engel WK: Vascular deposits of immunoglobulin and complement in inflammatory myopathy. N Engl J Med 286:333-338, Feb 1972 15. Leddy JP, Griggs RC, Klemperer MR: Hereditary C2 deficiency and dermatomyositis. Am J Med 58:83-91, Jan 1975 16. Dawkins RL, Mastaglia FL: Cell-mediated cytotoxicity to muscle in polymyositis. N Engl J Med 288:434-438, Mar 1973 17. Dawkins RL, Zilko PJ: Polymyositis and myasthenia gravis immunodeficiency disease of skeletal muscle. Lancet 1:200-202, Jan 1975 18. Dantzig P1: Kaposi sarcoma and polymyositis. Arch Derm


110:605-607, Oct 1974 19. Kagen LJ, Kimball AC, Christian CL: Serologic evidence of toxoplasmosis among patients with polymyositis. Am J Med 56: 186-192, Feb 1974 20. Winkelmann RK: Course of dermatomyositis and polymyo-

sitis-Comparison of treated and untreated groups. Mayo Clin Proc 43:545-556, Aug 1968 21. Medsger TA, Masi AT: Factors affecting survivorship in polymyositis. Arthr Rheum 14:249-258, Mar-Apr 1971 22. Metzger AL: Polymositis and dermatomyositis combined methotrexate and corticosteroid therapy. Ann Intern Med 81: 182-189, Aug 1974


Refer to: Dermatomyositis-Medical Staff Conference, University of California, San Francisco. West J Med 124:316-322, Apr 1976 Medical Staff Conferenc...
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