Neuropathology and Applied Neurobiology (2015), 41, 686–689
doi: 10.1111/nan.12234
Scientific correspondence
Proximal weakness in a patient with MALT lymphoma: a case report and discussion of possible pathogenesis Necrotizing myopathy exhibits a specific histological pattern, characterized by significant and diffusely distributed myofiber necrosis, with muscle fiber regeneration, but frequently with sparse inflammatory infiltrates [1,2]. We describe a patient with acquired necrotizing myopathy associated with an extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue type (MALT lymphoma) of the left parotid gland, which had metastasized to the biopsied muscle. An 80-year-old woman presented with a several week history of subacute muscle weakness affecting her proximal muscles. It was more pronounced in the arms than in the legs, and accompanied by dysphagia during the following weeks. Creatine kinase (CK) levels were 1825 U/l (normal range < 167 U/l) and Creatine kinase-MB (CK-MB) was 190 U/l (normal range < 24 U/ l). Cardiac involvement was carefully excluded by a specialized examination, electrocardiography, echocardiography and normal levels of specific enzymes. She did not show any signs of skin involvement, especially no pruritus and no periungual erythema. Serology for autoantibodies including anti-SRP, anti-HMGCR, ANA, anti-SM, anti-dsDNA, anti-La, VDRL, c-ANCA, p-ANCA and rheumatoid factor was negative. Anti-Ro-52
antibodies were positive. Seven years earlier, she had been treated for an extranodal marginal zone lymphoma of MALT type of the parotid gland. Bone marrow biopsy revealed normocellular hematopoiesis with paratrabecular and interstitial lymphocellular aggregates at that time. In 2007, radiotherapy led to complete remission, and no chemotherapy was administered. To explain the present muscular signs, an idiopathic inflammatory myositis was suspected, and a biceps muscle biopsy was performed. At present, analysis of a muscle biopsy revealed scattered necrotic myofibres associated with lymphomonocytic infiltrates (Figure 1A). Alkaline phosphatase strongly stained the perimysial connective tissue (Figure 1B). CD45+, CD3+ and CD8+ T cells were observed in the endomysium (Figure 1C), and few CD20+ or CD79a+ non-proliferative (Mib-1; data not shown) B cells were detected (Figure 1D), but morphologically there was no obvious lymphoma infiltration detectable. However, molecular analysis according to the Biomed-2 protocol [3] revealed a monoclonal B cell population in the muscle, which was identical to the clone of the initial MALT lymphoma of the parotid gland and the bone marrow (Figure 1I). Major histocompatibility complex (MHC) class I showed sarcolemmal staining (Figure 1E). C5b9 membrane attack complex illustrated sarcolemmal deposits on some fibres (Figure 1F). Numerous CD68+ and non-specific esterase positive macrophages are detected in the endomysium (Figure 1G,H). For the
Figure 1. Biceps muscle biopsy: histopathological features of acquired necrotizing myopathy. (A) Scattered necrotic muscle fibres with associated macrophage infiltration and some dispersed lymphocytes (Gomori trichrome; scale bar = 100 μm). (B) Alkaline phosphatase strongly active in the endomysial and perimysial connective tissue (scale bar = 100 μm). (C) Numerous CD3+ T cells were observed in the endomysium (CD3, scale bar = 100 μm). (D) Scattered endomysial CD20+ B-lymphocytes (CD20, scale bar = 100 μm). (E) Sarcolemmal MHC class I upregulation on muscle fibres; the capillaries show a physiological MHC class I expression (MHC class I immunohistochemistry; scale bar = 100 μm); (F) Immunohistochemical analysis reveals C5b9 membrane attack complex deposits in some fibres and capillaries; necrotic fibres show accumulation of C5b9 in sarcoplasm (C5b9 immunohistochemistry; scale bar = 100 μm). (H) Numerous endomysial macrophages and myophagocytosis (CD68 immunohistochemistry; scale bar = 100 μm) and non-specific esterase positive macrophages (G). (I) Results of PCR amplification (BIOMED-2 protocol adapted for formalin-fixed tissue) with primer pairs IGH-B and IGH-C demonstrate products of identical size in all three biopsies/localizations, arguing for the presence of the same monoclonal B-cell population (fragment analysis – GeneScan (3130 Genetic Analizer, Life Technologies, Darmstadt, Germany) – of amplified rearranged immunoglobulin genes). IGH: immunoglobulin heavy chain; MALT, mucosa-associated lymphoid tissue; MHC: major histocompatibility complex; PCR, polymerase chain reaction.
686
© 2015 British Neuropathological Society
Scientific correspondence
© 2015 British Neuropathological Society
687
NAN 2015; 41: 686–689
688
Scientific correspondence
purpose of these investigations, the study was approved by the ethics committee and an informed consent was obtained. Although abdominal symptoms were not reported, a magnetic resonance imaging of the abdomen was performed to investigate further subclinical lesions and detected an asymptomatic nodule situated in the pararectal region. A needle biopsy was performed, and the morphological as well as the immunohistochemical features also revealed a non-Hodgkin lymphoma. The patient received chemotherapy with rituximab (375 mg/ m2) and bendamustine (70 mg/m2) associated with corticosteroids (methylprednisolone and prednisolone). After chemotherapy and corticosteroids, a significant improvement of the proximal weakness and myalgia as well as a relevant decrease of CK level (400 U/l) was observed. The spectrum of diseases associated with necrotizing myopathy is broad, and underlying causes may be difficult to dissect in daily routine [2]. These myopathies can be related to autoimmune mechanisms by the presence of specific autoantibodies such as anti-SRP and anti-HMGCR, or may be associated with specific connective tissue disorders [4]. Others are secondary to toxic agents [5], viral infections or reveal a paraneoplastic manifestation [2]. According to European Neuromuscular Centre criteria, the patient basically fulfilled the diagnostic criteria of necrotizing myopathy presenting with: (i) all required clinical criteria with the exception of rash; (ii) elevated serum CK; (iii) electromyography with increased insertional and spontaneous activity; and (iv) muscle biopsy with many necrotic muscle fibres as the predominant abnormal histological feature and sparse inflammatory cells [6]. The association between lymphoproliferative diseases and a primary autoimmune disorder has been documented for Sjögren syndrome [7–9], and B-cell activation has been discussed to be involved in pathogenesis. However, this association was not described for necrotizing myopathy. Primary non-Hodgkin lymphomas are uncommon in the salivary glands and account for only 2% of these tumours [10]. A careful search for autoantibodies associated with necrotizing myopathies was negative (especially for anti-SRP and anti-HMGCR autoantibodies), and we considered the possibility of a paraneoplastic manifestation. Paraneoplastic neurological disorders entail a group of heterogeneous neurological disorders that occur in patients with cancer and result from associated effects of © 2015 British Neuropathological Society
malignancy rather than from metastases or direct invasion by the tumour [11,12]. B-cell clonality analysis of the muscle tissue confirmed the presence of monoclonal cells. The clone was identical to the clone of the patient’s primary MALT lymphoma, implying a neoplastic infiltrate. Molecular analysis of bone marrow tissue also showed the identical clone of B-cells. The involvement of skeletal muscles by a non-Hodgkin marginal zone B-cell lymphoma is extremely rare and there is a single case reported, presenting as a mass in quadriceps muscle [13]. Taken together, we detected a mixed neoplastic and inflammatory infiltrate in the skeletal muscle of our patient. These intramuscular neoplastic lymphocytes indicated recurrence and metastatic spread of the MALT lymphoma prompting chemotherapy with rituximab and bendamustine. High histochemical alkaline phosphatase activity and complement deposition as well as presence of a significant lymphocytic infiltrate suggest an autoimmune aetiology of the necrotizing myopathy [2,14]. Whether and how these neoplastic cells in the biopsied muscle interact with the inflammatory lymphocytes on a functional level, or if they were coincidental bystanders, is a matter of speculation. Practically, paraneoplastic inflammatory myopathy associated with lymphoma in a patient’s history should always prompt analysis of clonality to exclude recurrence. To the best of our knowledge, this is the first report of neoplastic lymphoid cells from an extranodal marginal zone lymphoma of MALT type of salivary glands in muscle tissue associated with an acquired necrotizing myopathy. Further studies may elucidate the direct or indirect mechanisms linking neoplasia especially of hematopoietic origin with necrotizing myopathy.
Author contributions Dr Nunes: study concept and design, acquisition and interpretation of data, and drafting the manuscript. Dr Rinnenthal: study concept and design, and drafting the manuscript. Dr Allenbach: revising the manuscript for important intellectual content. Dr Lenze, Dr Hummel and Dr Jöhrens: acquisition and interpretation of data. Dr Walz: revising the manuscript for important intellectual content. Dr Goebel and Dr Heppner: revising the manuscript for important intellectual content. Dr Stenzel: study concept and design, acquisition and interpretation of data, and revising the manuscript for important intellectual content. NAN 2015; 41: 686–689
Scientific correspondence
Conflict of interest None declared. J. C. Nunes*,† J. L. Rinnenthal* Y. Allenbach* D. Lenze‡ M. Hummel‡ K. Jöhrens‡ R. Walz§ H. H. Goebel* F. L. Heppner* W. Stenzel* Departments of *Neuropathology and ‡Pathology, Charité-Universitätsmedizin, Berlin, Germany, and †Department of Pathology and §Internal Medicine, Universidade Federal de Santa Catarina, Florianópolis, Brazil
References 1 Allenbach Y, Benveniste O. Acquired necrotizing myopathies. Curr Opin Neurol 2013; 26: 554–60 2 Stenzel W, Goebel HH, Aronica E. Review: immunemediated necrotizing myopathies – a heterogeneous group of diseases with specific myopathological features. Neuropathol Appl Neurobiol 2012; 38: 632–46 3 Van Dongen JJ, Langerak AW, Brüggemann M, Evans PA, Hummel M, Lavender FL, Delabesse E, Davi F, Schuuring E, García-Sanz R, van Krieken JH, Droese J, González D, Bastard C, White HE, Spaargaren M, González M, Parreira A, Smith JL, Morgan GJ, Kneba M, Macintyre EA. Design and standardization of PCR primers and protocols for detection of clonal immunoglobulin and T-cell receptor gene recombinations in suspect lymphoproliferations: report of the BIOMED-2 concerted action BMH4-CT983936. Leukemia 2003; 17: 2257–317 4 Authier FJ, Kondo H, Ghnassia RT, Revuz J, Gherardi RK. Necrotizing myopathy with pipestem capillaries and minimal cellular infiltration: a case associated with
© 2015 British Neuropathological Society
5 6
7
8
9
10 11 12 13
14
689
cutaneous signs of dermatomyositis. Neurology 1996; 46: 1448–51 Pasnoor M, Barohn RJ, Dimachkie MM. Toxic myopathies. Neurol Clin 2014; 32: 647–70 Hoogendijk JE, Amato AA, Lecky BR, Choy EH, Lundberg IE, Rose MR, Vencowsky J, de Visser M, Hughes RA. 119th ENMC international workshop: trial design in adult idiopathic inflammatory myopathies, with the exception of inclusion body myositis, 10–12 October 2003, Naarden, The Netherlands. Neuromuscul Disord 2004; 14: 337–45 Nishishinya MB, Pereda CA, Munoz-Fernández S, PegoReigosa JM, Rúa-Figueroa I, Andreu JL, Fernández-Castro M, Rosas J, Loza Santamaría E. Identification of lymphoma predictors in patients with Sjögren’s syndrome: a systematic literature review und meta-analysis. Rheumatol Int 2015; 35: 17–26 Nocturne G, Mariette X. Sjögren syndrome-associated lymphomas: an update on pathogenesis and management. Br J Haematol 2015; 168: 317–27 Turner MD. Salivary gland disease in Sjögren’s syndrome: sialoadenitis to lymphoma. Oral Maxillofac Surg Clin North Am 2014; 26: 75–81 Gleeson MJ, Bennett MH, Cawson RA. Lymphomas of salivary glands. Cancer 1986; 58: 699–704 Sharp L, Vernino S. Paraneoplastic neuromuscular disorders. Muscle Nerve 2012; 46: 841–50 Baer AN. Paraneoplastic muscle disease. Rheum Dis Clin North Am 2011; 37: 185–200 Bozzola C, Boldorini R, Ramponi A, Monga G. Fine needle aspiration cytology in the diagnosis of non-Hodgkin’s lymphomas of the muscle: a report of 2 cases. Acta Cytol 2005; 49: 213–18 Levin MI, Mozaffar T, Al-Lozi MT, Pestronk A. Paraneoplastic necrotizing myopathy: clinical and pathologic features. Neurology 1998; 50: 764–7
Received 11 December 2014 Accepted after revision 18 February 2015 Published online Article Accepted on 12 March 2015
NAN 2015; 41: 686–689
doi: 10.1111/nan.12234
Scientific correspondence
Proximal weakness in a patient with MALT lymphoma: a case report and discussion of possible pathogenesis Necrotizing myopathy exhibits a specific histological pattern, characterized by significant and diffusely distributed myofiber necrosis, with muscle fiber regeneration, but frequently with sparse inflammatory infiltrates [1,2]. We describe a patient with acquired necrotizing myopathy associated with an extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue type (MALT lymphoma) of the left parotid gland, which had metastasized to the biopsied muscle. An 80-year-old woman presented with a several week history of subacute muscle weakness affecting her proximal muscles. It was more pronounced in the arms than in the legs, and accompanied by dysphagia during the following weeks. Creatine kinase (CK) levels were 1825 U/l (normal range < 167 U/l) and Creatine kinase-MB (CK-MB) was 190 U/l (normal range < 24 U/ l). Cardiac involvement was carefully excluded by a specialized examination, electrocardiography, echocardiography and normal levels of specific enzymes. She did not show any signs of skin involvement, especially no pruritus and no periungual erythema. Serology for autoantibodies including anti-SRP, anti-HMGCR, ANA, anti-SM, anti-dsDNA, anti-La, VDRL, c-ANCA, p-ANCA and rheumatoid factor was negative. Anti-Ro-52
antibodies were positive. Seven years earlier, she had been treated for an extranodal marginal zone lymphoma of MALT type of the parotid gland. Bone marrow biopsy revealed normocellular hematopoiesis with paratrabecular and interstitial lymphocellular aggregates at that time. In 2007, radiotherapy led to complete remission, and no chemotherapy was administered. To explain the present muscular signs, an idiopathic inflammatory myositis was suspected, and a biceps muscle biopsy was performed. At present, analysis of a muscle biopsy revealed scattered necrotic myofibres associated with lymphomonocytic infiltrates (Figure 1A). Alkaline phosphatase strongly stained the perimysial connective tissue (Figure 1B). CD45+, CD3+ and CD8+ T cells were observed in the endomysium (Figure 1C), and few CD20+ or CD79a+ non-proliferative (Mib-1; data not shown) B cells were detected (Figure 1D), but morphologically there was no obvious lymphoma infiltration detectable. However, molecular analysis according to the Biomed-2 protocol [3] revealed a monoclonal B cell population in the muscle, which was identical to the clone of the initial MALT lymphoma of the parotid gland and the bone marrow (Figure 1I). Major histocompatibility complex (MHC) class I showed sarcolemmal staining (Figure 1E). C5b9 membrane attack complex illustrated sarcolemmal deposits on some fibres (Figure 1F). Numerous CD68+ and non-specific esterase positive macrophages are detected in the endomysium (Figure 1G,H). For the
Figure 1. Biceps muscle biopsy: histopathological features of acquired necrotizing myopathy. (A) Scattered necrotic muscle fibres with associated macrophage infiltration and some dispersed lymphocytes (Gomori trichrome; scale bar = 100 μm). (B) Alkaline phosphatase strongly active in the endomysial and perimysial connective tissue (scale bar = 100 μm). (C) Numerous CD3+ T cells were observed in the endomysium (CD3, scale bar = 100 μm). (D) Scattered endomysial CD20+ B-lymphocytes (CD20, scale bar = 100 μm). (E) Sarcolemmal MHC class I upregulation on muscle fibres; the capillaries show a physiological MHC class I expression (MHC class I immunohistochemistry; scale bar = 100 μm); (F) Immunohistochemical analysis reveals C5b9 membrane attack complex deposits in some fibres and capillaries; necrotic fibres show accumulation of C5b9 in sarcoplasm (C5b9 immunohistochemistry; scale bar = 100 μm). (H) Numerous endomysial macrophages and myophagocytosis (CD68 immunohistochemistry; scale bar = 100 μm) and non-specific esterase positive macrophages (G). (I) Results of PCR amplification (BIOMED-2 protocol adapted for formalin-fixed tissue) with primer pairs IGH-B and IGH-C demonstrate products of identical size in all three biopsies/localizations, arguing for the presence of the same monoclonal B-cell population (fragment analysis – GeneScan (3130 Genetic Analizer, Life Technologies, Darmstadt, Germany) – of amplified rearranged immunoglobulin genes). IGH: immunoglobulin heavy chain; MALT, mucosa-associated lymphoid tissue; MHC: major histocompatibility complex; PCR, polymerase chain reaction.
686
© 2015 British Neuropathological Society
Scientific correspondence
© 2015 British Neuropathological Society
687
NAN 2015; 41: 686–689
688
Scientific correspondence
purpose of these investigations, the study was approved by the ethics committee and an informed consent was obtained. Although abdominal symptoms were not reported, a magnetic resonance imaging of the abdomen was performed to investigate further subclinical lesions and detected an asymptomatic nodule situated in the pararectal region. A needle biopsy was performed, and the morphological as well as the immunohistochemical features also revealed a non-Hodgkin lymphoma. The patient received chemotherapy with rituximab (375 mg/ m2) and bendamustine (70 mg/m2) associated with corticosteroids (methylprednisolone and prednisolone). After chemotherapy and corticosteroids, a significant improvement of the proximal weakness and myalgia as well as a relevant decrease of CK level (400 U/l) was observed. The spectrum of diseases associated with necrotizing myopathy is broad, and underlying causes may be difficult to dissect in daily routine [2]. These myopathies can be related to autoimmune mechanisms by the presence of specific autoantibodies such as anti-SRP and anti-HMGCR, or may be associated with specific connective tissue disorders [4]. Others are secondary to toxic agents [5], viral infections or reveal a paraneoplastic manifestation [2]. According to European Neuromuscular Centre criteria, the patient basically fulfilled the diagnostic criteria of necrotizing myopathy presenting with: (i) all required clinical criteria with the exception of rash; (ii) elevated serum CK; (iii) electromyography with increased insertional and spontaneous activity; and (iv) muscle biopsy with many necrotic muscle fibres as the predominant abnormal histological feature and sparse inflammatory cells [6]. The association between lymphoproliferative diseases and a primary autoimmune disorder has been documented for Sjögren syndrome [7–9], and B-cell activation has been discussed to be involved in pathogenesis. However, this association was not described for necrotizing myopathy. Primary non-Hodgkin lymphomas are uncommon in the salivary glands and account for only 2% of these tumours [10]. A careful search for autoantibodies associated with necrotizing myopathies was negative (especially for anti-SRP and anti-HMGCR autoantibodies), and we considered the possibility of a paraneoplastic manifestation. Paraneoplastic neurological disorders entail a group of heterogeneous neurological disorders that occur in patients with cancer and result from associated effects of © 2015 British Neuropathological Society
malignancy rather than from metastases or direct invasion by the tumour [11,12]. B-cell clonality analysis of the muscle tissue confirmed the presence of monoclonal cells. The clone was identical to the clone of the patient’s primary MALT lymphoma, implying a neoplastic infiltrate. Molecular analysis of bone marrow tissue also showed the identical clone of B-cells. The involvement of skeletal muscles by a non-Hodgkin marginal zone B-cell lymphoma is extremely rare and there is a single case reported, presenting as a mass in quadriceps muscle [13]. Taken together, we detected a mixed neoplastic and inflammatory infiltrate in the skeletal muscle of our patient. These intramuscular neoplastic lymphocytes indicated recurrence and metastatic spread of the MALT lymphoma prompting chemotherapy with rituximab and bendamustine. High histochemical alkaline phosphatase activity and complement deposition as well as presence of a significant lymphocytic infiltrate suggest an autoimmune aetiology of the necrotizing myopathy [2,14]. Whether and how these neoplastic cells in the biopsied muscle interact with the inflammatory lymphocytes on a functional level, or if they were coincidental bystanders, is a matter of speculation. Practically, paraneoplastic inflammatory myopathy associated with lymphoma in a patient’s history should always prompt analysis of clonality to exclude recurrence. To the best of our knowledge, this is the first report of neoplastic lymphoid cells from an extranodal marginal zone lymphoma of MALT type of salivary glands in muscle tissue associated with an acquired necrotizing myopathy. Further studies may elucidate the direct or indirect mechanisms linking neoplasia especially of hematopoietic origin with necrotizing myopathy.
Author contributions Dr Nunes: study concept and design, acquisition and interpretation of data, and drafting the manuscript. Dr Rinnenthal: study concept and design, and drafting the manuscript. Dr Allenbach: revising the manuscript for important intellectual content. Dr Lenze, Dr Hummel and Dr Jöhrens: acquisition and interpretation of data. Dr Walz: revising the manuscript for important intellectual content. Dr Goebel and Dr Heppner: revising the manuscript for important intellectual content. Dr Stenzel: study concept and design, acquisition and interpretation of data, and revising the manuscript for important intellectual content. NAN 2015; 41: 686–689
Scientific correspondence
Conflict of interest None declared. J. C. Nunes*,† J. L. Rinnenthal* Y. Allenbach* D. Lenze‡ M. Hummel‡ K. Jöhrens‡ R. Walz§ H. H. Goebel* F. L. Heppner* W. Stenzel* Departments of *Neuropathology and ‡Pathology, Charité-Universitätsmedizin, Berlin, Germany, and †Department of Pathology and §Internal Medicine, Universidade Federal de Santa Catarina, Florianópolis, Brazil
References 1 Allenbach Y, Benveniste O. Acquired necrotizing myopathies. Curr Opin Neurol 2013; 26: 554–60 2 Stenzel W, Goebel HH, Aronica E. Review: immunemediated necrotizing myopathies – a heterogeneous group of diseases with specific myopathological features. Neuropathol Appl Neurobiol 2012; 38: 632–46 3 Van Dongen JJ, Langerak AW, Brüggemann M, Evans PA, Hummel M, Lavender FL, Delabesse E, Davi F, Schuuring E, García-Sanz R, van Krieken JH, Droese J, González D, Bastard C, White HE, Spaargaren M, González M, Parreira A, Smith JL, Morgan GJ, Kneba M, Macintyre EA. Design and standardization of PCR primers and protocols for detection of clonal immunoglobulin and T-cell receptor gene recombinations in suspect lymphoproliferations: report of the BIOMED-2 concerted action BMH4-CT983936. Leukemia 2003; 17: 2257–317 4 Authier FJ, Kondo H, Ghnassia RT, Revuz J, Gherardi RK. Necrotizing myopathy with pipestem capillaries and minimal cellular infiltration: a case associated with
© 2015 British Neuropathological Society
5 6
7
8
9
10 11 12 13
14
689
cutaneous signs of dermatomyositis. Neurology 1996; 46: 1448–51 Pasnoor M, Barohn RJ, Dimachkie MM. Toxic myopathies. Neurol Clin 2014; 32: 647–70 Hoogendijk JE, Amato AA, Lecky BR, Choy EH, Lundberg IE, Rose MR, Vencowsky J, de Visser M, Hughes RA. 119th ENMC international workshop: trial design in adult idiopathic inflammatory myopathies, with the exception of inclusion body myositis, 10–12 October 2003, Naarden, The Netherlands. Neuromuscul Disord 2004; 14: 337–45 Nishishinya MB, Pereda CA, Munoz-Fernández S, PegoReigosa JM, Rúa-Figueroa I, Andreu JL, Fernández-Castro M, Rosas J, Loza Santamaría E. Identification of lymphoma predictors in patients with Sjögren’s syndrome: a systematic literature review und meta-analysis. Rheumatol Int 2015; 35: 17–26 Nocturne G, Mariette X. Sjögren syndrome-associated lymphomas: an update on pathogenesis and management. Br J Haematol 2015; 168: 317–27 Turner MD. Salivary gland disease in Sjögren’s syndrome: sialoadenitis to lymphoma. Oral Maxillofac Surg Clin North Am 2014; 26: 75–81 Gleeson MJ, Bennett MH, Cawson RA. Lymphomas of salivary glands. Cancer 1986; 58: 699–704 Sharp L, Vernino S. Paraneoplastic neuromuscular disorders. Muscle Nerve 2012; 46: 841–50 Baer AN. Paraneoplastic muscle disease. Rheum Dis Clin North Am 2011; 37: 185–200 Bozzola C, Boldorini R, Ramponi A, Monga G. Fine needle aspiration cytology in the diagnosis of non-Hodgkin’s lymphomas of the muscle: a report of 2 cases. Acta Cytol 2005; 49: 213–18 Levin MI, Mozaffar T, Al-Lozi MT, Pestronk A. Paraneoplastic necrotizing myopathy: clinical and pathologic features. Neurology 1998; 50: 764–7
Received 11 December 2014 Accepted after revision 18 February 2015 Published online Article Accepted on 12 March 2015
NAN 2015; 41: 686–689
