HomeLarge Type Edition
HOME ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Services
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
PubMed
Right arrow PubMed Citation
The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 57:M378-M384 (2002)
© 2002 The Gerontological Society of America

Muscle Diseases in Elders

A 10-Year Retrospective Study

Montserrat Lagunoa, Òscar Miróa, Milagrosa Pereaa, Marta Picóna, Álvaro Urbano-Márqueza and Josep M. Graua

a Muscle Research Unit, Department of Internal Medicine, "August Pi i Sunyer" Biomedical Research Institute (IDIBAPS), Hospital Clínic, University of Barcelona, Catalonia, Spain

Josep M. Grau, Muscle Research Unit, Department of Internal Medicine, Hospital Clínic, Villarroel 170, 08036 Barcelona, Catalonia, Spain E-mail: jmgrau{at}clinic.ub.es.


    Abstract
 Top
 Abstract
 Methods
 Results
 Discussion
 References
 
Background. Muscle complaints are frequent among older adults, but histological data in this setting are scarce. Our objective was to detect the major categories of muscle diseases in the elderly population based on histological study.

Methods. We reviewed all muscle biopsies performed in our hospital on patients older than the age of 65 during a 10-year period (1988–1997). As a control group, we included the next patient younger than 65 who underwent muscle biopsy after each elderly patient. We recorded demographic, clinical, and histological data of the patients, as well as the final diagnosis. Concordance between pre- and postbiopsy diagnosis was also analyzed.

Results. We included 239 muscle biopsies corresponding to elderly patients and 239 to controls. Compared with the control group, elderly patients more frequently exhibited type II fiber atrophy and were diagnosed with a specific myopathy. The latter was achieved in 86 cases (36%), idiopathic inflammatory myopathies and vasculitis being the most frequent diagnoses. Interestingly, in about one quarter of the elderly patients in whom a definite diagnosis of muscle disease was achieved, this diagnosis had not been clinically suspected prior to muscle biopsy. Overall, in 60 out of 239 elderly patients (25%), a specific therapeutic regimen could be instituted on the basis of the muscle biopsy results.

Conclusions. Muscle diseases are not rare in elderly patients. Therefore, muscle biopsy constitutes a safe and useful tool for diagnosis because, if not performed, some potentially treatable diseases may be undiagnosed or misdiagnosed.

DESPITE muscular symptoms being a relatively frequent complaint leading to the seeking of medical advice, primary muscle diseases are unusual (1). This is especially true in the elderly population, in whom weakness, exercise intolerance, or musculoskeletal pain are usually referred. Because such symptoms are due to a wide variety of medical conditions, they have a very low specificity in detecting muscle disorders. In addition, most muscle disorders are currently diagnosed at birth or during childhood (e.g., muscular dystrophies, congenital or metabolic myopathies) or develop at middle age (e.g., idiopathic inflammatory myopathies), thereby reinforcing the idea that the incidence of primary muscle diseases in elders is low. Aging itself seems to lead to mild isokinetic strength reduction with a lower percentage of type I fiber and capillary-to-fiber ratio, in contrast with the accepted concept of selective type II atrophy (2). Perhaps for these reasons, there are only a few studies analyzing the diagnosis of muscle disease in aged patients (3)(4). In one of these, muscular neurogenic abnormalities and type II fiber atrophy were more frequently seen in aged patients compared with a younger group, and, interestingly, prominent myopathic features were found on histological examination in nearly half of patients older than 65 (3). Accordingly, the authors suggested that muscle disorders should not be underestimated in elderly patients, and muscle biopsy should be recommended for selected cases. In view of these results, the aim of the present study was to review our series in order to ascertain the main muscle disorders affecting elderly patients and to test the adequacy of muscle biopsy in performing the diagnosis.


    Methods
 Top
 Abstract
 Methods
 Results
 Discussion
 References
 
The present study was carried out in an urban, tertiary care, 850-bed, university teaching hospital that provides health care to a population of about 500,000 people. From January 1988 to December 1997 (10 years), our Muscle Research Unit performed 1258 skeletal muscle biopsies on individuals older than 14 years of age for diagnostic purposes. Muscle biopsies are routinely performed by experienced clinicians of our Muscle Research Unit through an open surgical procedure of deltoid, quadriceps, or gastrocnemius muscles. It is a relatively simple procedure, it is feasible to perform on an outpatient basis, and it includes careful selection of biopsy site, local anesthesia, atraumatic dissection, and immediate processing of muscle samples. Time spent for the overall procedure is about 30 to 45 minutes, and special instrumentation is not required. In some patients, when a systemic vasculitis is clinically suspected, a concurrent nerve biopsy (sural nerve) is performed at the same time as the muscle biopsy.

Muscle fragments are frozen and processed for conventional stainings and reacted with histoenzymatic reagents on 6-µ-thick cryostat sections, as reported elsewhere (5)(6). The remainder of the muscle sample is fixed in glutaraldehyde and is stored for further ultrastructural or biochemical studies, which are only performed in cases with reasonable clinical or histological suspicion of a congenital or metabolic muscle disease (7)(8)(9).

We retrospectively reviewed the diagnosis of muscle biopsies performed on all patients older than the age of 65 during the aforementioned 10-year period after excluding patients biopsied in the setting of investigative protocols. As a control group, we included for each elderly patient the next patient younger than 65 years who underwent muscle biopsy after each elderly patient, whatever the cause leading to muscle biopsy. All charts corresponding to such patients were reexamined, and demographic and clinical data were recorded in all cases. The reason leading to muscle biopsy was also registered, and histological findings were analyzed in detail. Based on widely accepted criteria (10)(11), we categorized the final diagnosis according to the most prominent histological features, such as (a) consistent with myopathy (random variation in fiber size with small rounded fibers, necrosis, phagocytosis, regenerating muscle fibers, inflammation, increase in internal nuclei, ragged-red fibers, increase in connective tissue, or characteristic changes of certain specific myopathies); (b) predominant neurogenic changes (angulated atrophic fibers of both histochemical types, fiber-type grouping, group atrophy, pyknotic nuclear clumps, and target fibers); (c) type II fiber atrophy (if the predominant, when not isolated, finding was exclusively atrophy of type II fibers); or (d) normal skeletal muscle or nonspecific mild abnormalities (minimal, focal round-cell inflammation without muscle fiber abnormalities, occasional internalization of myonuclei, variation in muscle fiber size, or angulation of fibers if each of these abnormalities was mild and not associated with other myopathic or neurogenic changes) (3). To detect those myopathies potentially less suspected in elderly patients, we compared pre- and postbiopsy diagnoses in order to know the degree of concordance between clinically suspected myopathy and the final pathological diagnosis.

Results are presented as mean ± SD and percentages. Comparisons among qualitative variables were performed using the Fisher's exact test and are expressed as odds ratio with a 95% confidence interval (CI). The differences are considered statistically significant if such interval excluded the value 1 or if the p value was less than .05.


    Results
 Top
 Abstract
 Methods
 Results
 Discussion
 References
 
Two hundred thirty-nine out of 1258 (19%) muscle biopsies belonged to patients older than 65. Muscle biopsy was performed in the work-up of weakness in 178 (74%) cases and by the study of raised elevated serum creatine kinase (CK) in otherwise asymptomatic patients in the remaining 61 (26%) cases. In 44 patients, a concurrent nerve biopsy was performed. Patients included in the elderly group had a mean age of 72.1 ± 5.0 years, and 111 (46%) were men, whereas the mean age in the patients included in the control (younger) group was 40 ± 16 years, and 120 (50%) were men. For both groups together, the muscles selected for biopsy were the deltoid in 253 (53%) cases, the quadriceps in 143 (30%) cases, and the gastrocnemius in 82 (17%) cases. Neither elderly nor young individuals presented major surgical complications related to biopsy; 15 (3%) patients developed a queloid scar, 11 (2%) subcutaneous hematoma, and 5 (1%) superficial wound infection. A summary of the main final diagnoses for patients and controls is presented in Table 1 .


View this table:
[in this window]
[in a new window]
 
Table 1. Main Diagnostic Groups

 
With respect to the control group, elderly people were more frequently diagnosed as having a myopathy (p = .013) or type II fiber atrophy (p < .001), and they less frequently showed normal or nearly normal muscle biopsy (p < .001). In elderly patients, muscle biopsy allowed or contributed to establishing the diagnosis of a muscle disease in 86 cases (36%): 74/178 patients with weakness and 12/61 with raised CK values. When analyzing the type of myopathy in such patients, we observed that the most frequent diagnosis was idiopathic inflammatory myopathy (38 cases, 44%), with nearly a quarter of these patients being affected by an inclusion body myositis. There were 23 cases of dermatomyositis (DM) and 6 cases of polymyositis (PM). In 6 out of 23 DM cases (26%), but in no one PM case, a coexisting neoplastic condition could be diagnosed in the work-up (three breast, two ovarian, one lung). The remaining diagnoses are summarized in Table 2 . In Fig. 1, examples of muscle biopsies corresponding to elderly people are represented. As can be seen in Table 2 , elderly patients were more frequently affected by vasculitic syndromes (p = .023) while the frequency of the remaining diagnostic categories did not differ between the two groups. On analyzing the whole group, 60 (25%) elderly patients had a potentially treatable muscle disease (i.e., inflammatory myopathy excluding inclusion body myositis, vasculitis, and toxic, infectious, and endocrine myopathy). It is noteworthy that such a percentage was significantly higher than the corresponding figure for younger patients, in whom only 33 (14%) were affected by treatable muscle disorders (odds ratio for elderly with respect to young people 2.09; 95% CI from 1.31 to 3.35; p = .003).


View this table:
[in this window]
[in a new window]
 
Table 2. Muscle Diseases Found in Patients in Whom a Final Diagnosis Was Achieved

 











View larger version (1434K):
[in this window]
[in a new window]
 
Figure 1. A, Dermatomyositis (hematoxylin-eosin x 140). Marked variability in fiber size with perifascicular atrophy and dense perivascular inflammatory response. B, Inclusion body myositis (hematoxylin-eosin x 550). Atrophic rounded fibers with endomysial fibrosis and typical lined vacuoles with basophilic granular inclusions. C, Classical polyarteritis nodosa type vasculitis (hematoxylin-eosin x 300). Severe inflammatory infiltrate through the wall in a medium-size muscle artery. Grouped angular fibers suggestive of denervation atrophy are also present. D, Mitochondrial myopathy (Gomori's trichrome x 440). In this staining, numerous ragged-red fibers are present. E, Adult-onset acid maltase deficiency [periodic acid-Schiff (PAS) x 300]. Vacuolar myopathy where strongly PAS-positive material is present. F, Oculopharyngeal dystrophy (Gomori's trichrome x 550). Variability in fiber size with the presence of some angulated fibers and the characteristic rimmed vacuole in the center of the small fiber. G, Chloroquine myopathy (Gomori's trichrome x 300). Extensive vacuolar myopathy (autophagic vacuoles). H, Hypothyroid myopathy (periodic acid-Schiff x 550). Fiber atrophy with discrete PAS-positive subsarcolemmal aggregates. I, Acute quadriplegic myopathy with loss of thick (myosin) filaments (electron micrograph x 15,000). J, Nemaline myopathy (electron micrograph x 10,000). Numerous rod bodies are present.

 
On the basis of prebiopsy suspicion of the clinician who referred the patients for muscle biopsy, in 23 out of 86 (27%) elderly patients, we considered that the final clinicopathological diagnosis was not suspected prior to performing muscle biopsy. There were some unexpected diagnoses: mitochondrial myopathy in four patients, an adult-onset acid maltase deficiency in one case, and two adult nemaline myopathies. In fact, when the specific diagnoses of elderly patients were analyzed according to whether they were or were not previously suspected (Table 3 ), congenital and metabolic myopathies had a higher likelihood of being unsuspected, although these differences did not reach statistical significance. Interestingly, among idiopathic inflammatory myopathies, inclusion body myositis (IBM) was significantly less suspected than dermatomyositis-polymyositis (odds ratio for IBM 10.8; 95% CI from 1.8 to 64.1; p = .010).


View this table:
[in this window]
[in a new window]
 
Table 3. Muscle Diseases in Elderly Patients in Whom a Final Diagnosis Was Achieved

 

    Discussion
 Top
 Abstract
 Methods
 Results
 Discussion
 References
 
We analyzed the major categories of muscle diseases and evaluated the utility of muscle biopsy in establishing the diagnosis in elders. In accordance with some previously reported results (3), elderly people showed a greater proportion of nonspecific type II fiber atrophy and a lower percentage of normal muscle biopsies than the control group. Our data also demonstrate that skeletal muscle biopsy is a safe and useful procedure in this subset of patients, that it allows the establishment of the diagnosis of myopathy in more than a third of the patients (some unsuspected), and that histological results help to implement appropriate treatment. The usefulness of muscle biopsy is proven by its contribution in establishing the correct diagnosis of myopathy in 36% of our cases, a percentage quite near the 42% reported by Lacomis and colleagues (3). These results indicate that, in this population, the frequency of muscle disorders is high enough to be routinely considered by the attending physicians. Indeed, we found that muscle biopsy was even more helpful in the diagnosis of myopathy in older than in younger individuals. With respect to its safety, the number of complications observed in our series was low and irrelevant. During the past decades, needle muscle biopsy has been increasingly used with respect to open surgical biopsy because it is less costly and time consuming, as well as less traumatic (12)(13)(14)(15)(16). Nonetheless, surgical biopsy is still preferred by our group and others (17) because it provides large samples to perform a more complete set of studies, allows for adequate hemostasis, and minimizes the contraction artefact if muscle specimens are properly handled. Potential disadvantages include postoperative complications, scar formation, and reluctance of some patients to be submitted to the procedure (15).

A wide variety of muscle diseases were diagnosed in the older adults. Some particular aspects in this population subset deserve additional comments. First, among idiopathic inflammatory myopathies, it is important to distinguish IBM from the rest, because this myopathy is steroid resistant. It is often observed in patients older than 50 years of age (18), it has a slow clinical course, and, from a histological point of view, it can be initially misdiagnosed as polymyositis. For these reasons, in elderly patients diagnosed with polymyositis showing a poor response to steroids, IBM should be suspected in order to avoid ineffective, and otherwise hazardous, therapies (19)(20).

Vasculitis constituted the second main group of muscular diagnoses in aged individuals, with most of the cases being consistent with polyarteritis nodosa type vasculitis (PAN). Actually, vasculitis was more frequently diagnosed in older than in younger people. A complete typical picture of PAN was rarely seen in elderly patients, and several only complained of nonspecific clinical symptoms such as malaise, low-grade fever, weight loss, weakness, muscular pain, and asthenia, which were accompanied by mild anemia and increased erythrocyte sedimentation rate. In fact, cases solely affecting the calf muscles without other organ involvement have been reported (21). Our present observations are in agreement with Puisieux and colleagues (22), who reported an increased frequency of weight loss and a decreased frequency of cutaneous signs (purpura and nodes) in such a population. The importance of achieving the correct diagnosis promptly and starting the appropriate therapy is reinforced because PAN vasculitis has a higher mortality rate among the elderly population (22), and specific treatment usually allows a good outcome (23).

Although commonly diagnosed at birth or childhood, nine patients in our series fulfilled the criteria for metabolic myopathies. It is remarkable that one woman was diagnosed with adult-onset acid maltase deficiency at the age of 72 years. This is a rare cause of muscle disease in adult patients. In fact, until 1995, only 38 cases had been reported (24). It shows a wide clinical variability with signs and symptoms usually including progressive limb weakness and/or restrictive lung disease, mild elevation in serum CK, a reduction in the forced vital capacity, and abnormal spontaneous activity in resting muscles during needle electromyography (24)(25).

On the other hand, although none of our cases could be classified as having a particular mitochondrial myopathy, all showed closely related findings to those reported by Johnston and colleagues in nine older patients (older than 69 years old) (26). This particular form of late-onset mitochondrial myopathy is clinically characterized by insidious mild proximal muscle weakness, associated, in some cases, with easy fatigability. Patients demonstrated an increased percentage of ragged red fibers (27), negative cytochrome c oxidase fibers, and hyperreactive succinate dehydrogenase fibers on histological study. Because multiple mtDNA deletions and altered muscle energy status have been demonstrated, it is possible that such patients could represent an exaggerated form of what is observed in the normal aging process (26)(28)(29).

Although in most cases of muscular drug toxicity only histological data of nonspecific myopathy are present (30)(31)(32), some specific patterns have been defined for some cases, such as colchicine (33), chloroquine (34), or corticosteroid/neuromuscular blockers (35), as observed in our series. Toxic myopathy is expected to be more prevalent in older individuals, because they receive a higher number of drugs for chronic diseases. In addition, drug toxicity may be increased in this population because of the presence of liver and/or renal dysfunction. However, whereas severe symptoms of proximal weakness and raised muscle enzymes in a young patient taking a single medication may lead to a straightforward diagnosis, the tendency for elderly patients (often with multisystem diseases and on multiple medications) to have several potential causes for weakness makes the diagnosis of toxic myopathy less evident (31). Furthermore, we have reported that toxic myopathies often follow a clinical paucisymptomatic form, and, in nearly 50% of the cases, there is no increase in serum muscle enzymes (32). In this scenario, muscle biopsy gave positive or negative useful information in 60% of the cases, by ruling out other possible causes of myopathy.

The remaining cases were diagnosed with a dystrophic, infectious, congenital, or endocrine myopathy. Overall, these entities actually represent few cases (36)(37), but in some, their diagnosis implies important therapeutic decisions as in infectious or endocrine myopathy. However, while infectious myopathy is easily suspected, endocrine myopathies can be easily overlooked. This is the case with thyroid hypofunction that could be paucisymptomatic in the elderly population and could be expressed only as hypothyroid myopathy, which is characterized by muscle weakness, myalgia, cramps, increase in muscle volume, and slow contraction and relaxation of the muscular fiber, as observed in one of our cases. In this case, histologic findings (type II fiber atrophy, abnormalities in the oxidative pattern of muscle cells, and glycogen deposition) were highly suggestive of this entity (37)(38).


    Acknowledgments
 
This study was supported in part by grants from the Spanish Ministry of Health (FIS 99/0231) and Comissionat per a Universitats i Recerca (1999SGR 00279). Dr. M. Laguno was funded by Hospital Clínic (Premi Fi de Residència 1999–2000).

Received October 1, 2001

Accepted January 3, 2002


    References
 Top
 Abstract
 Methods
 Results
 Discussion
 References
 

  1. Griggs RC, Karpati G, 1999. Muscle pain, fatigue and mitochondriopathies. N Engl J Med 341:1077-1078.
  2. Frontera WR, Hughes VA, Fielding RA, Fiatarone MA, Evans WJ, Roubenoff R, 2000. Aging of skeletal muscle: a 12-yr longitudinal study. J Appl Physiol 88:1321-1326. [Abstract/Free Full Text]
  3. Lacomis D, Chad DA, Smith TW, 1993. Myopathy in the elderly: evaluation of the histopathologic spectrum and the accuracy of clinical diagnosis. Neurology. 43:825-828. [Abstract/Free Full Text]
  4. Pautas E, Cherin P, Piette JC, et al. 2000. Features of polymiositis and dermatomyositis in the elderly: a case control study. Clin Exp Rheumatol. 18:241-244. [Medline]
  5. Grau JM, Masanés F, Pedrol E, Casademont J, Fernández-Solá J, Urbano-Márquez A, 1993. Human immunodeficiency virus type 1 infection and myopathy: clinical relevance of zidovudine therapy. Ann Neurol. 34:206-211. [Medline]
  6. Miró O, Pedrol E, Casademont J, et al. 1996. Muscle involvement in rheumatoid arthritis: clinicopathological study of 21 symptomatic cases. Semin Arthritis Rheum. 25:421-428. [Medline]
  7. Miró O, Cebrián M, Cardellach F, Grau JM, 1998. Deficit de carnitina palmitoil transferasa como causa de rabdomiólisis de esfuerzo. Med Clin (Barc). 111:436-437. [Medline]
  8. Miró O, Laguno M, Masanés F, Perea M, Urbano-Márquez A, Grau JM, 2000. Congenital and metabolic myopathies of childhood or adult onset. Semin Arthritis Rheum. 29:335-347. [Medline]
  9. Miró O, Salmerón JM, Masanés F, et al. 1999. Acute quadriplegic myopathy with myosin-deficient muscle fibres after liver transplantation: defining the clinical picture and delimiting the risk factors. Transplantation. 67:1144-1151. [Medline]
  10. Banker BQ, Engel AG, 1986. Basic reactions in muscle. Engel AG, Banker BQ, , ed.Myology 845-907. McGraw-Hill, New York, NY.
  11. Dubowitz D, Brooke MH. Muscle Biopsy. A Modern Approach. London: WB Saunders; 1973.
  12. Young A, Wiles CM, Edwards RHT, 1978. University College Hospital muscle-biopsy needle. Lancet. 2:1285[Medline]
  13. Pamphlett R, Harper C, Tan N, Kakulas BA, 1985. Needle muscle biopsy: will it make open biopsy obsolete?. Aust N Z J Med. 15:199-202. [Medline]
  14. Magistris MR, Kohler A, Pizzolato G, et al. 1998. Needle muscle biopsy in the investigation of neuromuscular disorders. Muscle Nerve. 21:194-200. [Medline]
  15. O'Rourke K, Blaivas M, Ike RW, 1994. Utility of needle muscle biopsy in a university rheumatology practice. J Rheumatol. 21:413-424. [Medline]
  16. Coggan AR, 1995. Muscle biopsy as a tool in the study of aging. J Gerontol Biol Sci Med Sci. 50A: (Special Issue I) 30-34.
  17. Berman AT, Garbarino JL, Rosenberg H, Heiman-Patterson T, Bosacco SJ, Weiss AA, 1985. Muscle biopsy: proper surgical technique. Clin Orthop. 198:240-243.
  18. Maat-Schieman ML, Macfarlane JD, Bots GT, Wintzen AR, 1992. Inclusion body myositis: its relative frequency in elderly people. Clin Neurol Neurosurg. 94:118-120.
  19. Askanas V, Engel WK, 1998. Sporadic inclusion-body myositis and hereditary inclusion-body myopathies: diseases of oxidative stress and aging?. Arch Neurol. 55:915-920. [Free Full Text]
  20. Miró O, Laguno M, Alonso JR, et al. 1999. Evolución de las miopatías inflamatorias idiopáticas: complicaciones, supervivencia y factores pronóstico. Med Clin (Barc). 112:521-526. [Medline]
  21. García F, Pedrol E, Casademont J, et al. 1992. Polyarteritis nodosa confined to calf muscles. J Rheumatol. 19:303-305. [Medline]
  22. Puisieux F, Woesteland H, Hachulla E, Hatron PY, Dewailly P, Devulder B, 1997. Symptomatologie clinique et pronostic de la periarterite noueuse du sujet agé. Etude retrospective de 25 periarterites noueuses de l'adulte jeune et de 22 periarterites noueuses du sujet agé. Rev Med Interne. 18:195-200. [Medline]
  23. Haugeberg G, Bie R, Benvold A, Larsen AS, Johnsen V, 1998. Primary vasculitis in a Norwegian community hospital: a retrospective study. Clin Rheumatol. 17: (5) 364-368. [Medline]
  24. Felice KJ, Alessi AG, Grunnet ML, 1995. Clinical variability in adult-onset acid maltase deficiency: report of affected sibs and review of the literature. Medicine. 74:131-135. [Medline]
  25. Wokke JH, Ausems MG, van den Boogaard MJ, et al. 1995. Genotype-phenotype correlation in adult-onset acid maltase deficiency. Ann Neurol. 38: (3) 450-454. [Medline]
  26. Johnston W, Karpati G, Carpenter S, Arnold D, Shoubridge EA, 1995. Late-onset mitochondrial myopathy. Ann Neurol. 37:16-23. [Medline]
  27. Rifai Z, Welle S, Kamp C, Thornton CA, 1995. Ragged red fibers in normal aging and inflammatory myopathy. Ann Neurol. 37:24-29. [Medline]
  28. Fernandez-Solà J, Casademont J, Grau JM, et al. 1992. Adult-onset mitochondrial myopathy. Postgrad Med J. 68:212-215. [Abstract/Free Full Text]
  29. Mendell JR, 1995. Mitochondrial myopathy in the elderly: exaggerated aging in the pathogenesis of disease. Ann Neurol. 37:3-4. [Medline]
  30. Kuncl RW, George EB, 1993. Toxic neuropathies and myopathies. Curr Opin Neurol. 6: (5) 695-704. [Medline]
  31. Pascuzzi RM, 1998. Drugs and toxins associated with myopathies. Curr Opin Rheumatol. 10:511-520. [Medline]
  32. Fernandez-Solà J, Pedrol E, Masanés F, Casademont J, Grau JM, Urbano-Márquez A, 1993. Miopatías tóxicas: estudio clínico, etiológico e histológico de 74 casos. Med Clin (Barc). 100:721-724. [Medline]
  33. Fernandez-Solà J, Pedrol E, Campistol JM, Masanés F, Grau JM, Urbano-Márquez A, 1993. Miopatía y polineuropatía por colquicina. Rev Clin Esp. 193:182-184. [Medline]
  34. Avina-Zubieta JA, Johnson ES, Suárez-Almazor ME, Russell AS, 1995. Incidence of myopathy in patients treated with antimalarials. A report of three cases and a review of the literature. Br J Rheumatol. 34:166-170. [Abstract/Free Full Text]
  35. Miró O, Grau JM, Nadal P, Picado C, Plaza V, Urbano-Márquez A, 1994. Miopatía aguda en relación a la administración de glucocorticoides y bloqueadores neuromusculares. Med Clin (Barc). 103:458-460. [Medline]
  36. Gyure KA, Prayson RA, Estes ML, 1997. Adult-onset nemalyne myopathy: a case report and review of the literature. Arch Pathol Lab Med. 121:1210-1213. [Medline]
  37. Monforte R, Fernandez-Solà J, Casademont J, Vernet M, Grau JM, Urbano-Márquez A, 1990. Miopatía hipotioridea. Estudio clínico e histológico de 19 pacientes. Med Clin (Barc). 95:126-129. [Medline]
  38. Bahillo MT, Burgos-Bretones J, Gaztambide S, Vázquez JA, Rivera-Pomar JM, 1984. Correlación clinicopatologica de la afección muscular en pacientes hipotiroideos, antes y después del tratamiento. Med Clin (Barc). 83:697-701. [Medline]



This article has been cited by other articles:


Home page
Rheumatology (Oxford)Home page
C. M. Cardy and T. Potter
The predictive value of creatine kinase, EMG and MRI in diagnosing muscle disease
Rheumatology, October 1, 2007; 46(10): 1617 - 1618.
[Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Services
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
PubMed
Right arrow PubMed Citation


HOME ARCHIVE SEARCH TABLE OF CONTENTS