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Journal articles on the topic 'Sarcoid myopathy'

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Author: Grafiati

Published: 10 March 2023

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1

Kumamoto, Toshihide, Makoto Takemaru, and Takahiro Himeno. "Chronic Sarcoid Myopathy." Japanese Journal of Sarcoidosis and Other Granulomatous Disorders 32, no. 1 (2012): 33–37. http://dx.doi.org/10.7878/jjsogd.32.33.

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2

Vahdani, Kaveh, and Geoffrey E. Rose. "Sarcoid Orbital Myopathy." Ophthalmic Plastic and Reconstructive Surgery 36, no. 1 (2020): 61–66. http://dx.doi.org/10.1097/iop.0000000000001462.

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3

Berger, Christian, Clemens Sommer, and Hans-M. Meinck. "Isolated sarcoid myopathy." Muscle & Nerve 26, no. 4 (September 30, 2002): 553–56. http://dx.doi.org/10.1002/mus.10220.

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4

Uwatoko, Hisashi, Ichiro Yabe, Shinichi Shirai, Ikuko Takahashi, Masaaki Matsushima, Takahiro Kano, and Hidenao Sasaki. "Pseudodystonia in sarcoid myopathy." Neurology and Clinical Neuroscience 5, no. 1 (September 7, 2016): 34–35. http://dx.doi.org/10.1111/ncn3.12093.

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5

Levine, Charles D., Jeffrey J. Miller, Galen Stanislaus, Ronald H. Wachsberg, and Marc Simmons. "Sarcoid myopathy: Imaging findings." Journal of Clinical Ultrasound 25, no. 9 (November 1997): 515–17. http://dx.doi.org/10.1002/(sici)1097-0096(199711/12)25:9<515::aid-jcu11>3.0.co;2-3.

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6

Tews, D. S., and D. E. Pongratz. "Immunohistological analysis of sarcoid myopathy." Journal of Neurology, Neurosurgery & Psychiatry 59, no. 3 (September 1, 1995): 322–25. http://dx.doi.org/10.1136/jnnp.59.3.322.

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7

Ellatif, Mostafa, Parthdev Bhasin, Carlo Urigo, and Ajay Sahu. "Symptomatic nodular myopathy: an atypical presentation of sarcoidosis." BMJ Case Reports 14, no. 5 (May 2021): e241206. http://dx.doi.org/10.1136/bcr-2020-241206.

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Symptomatic myopathy is a very rare extrapulmonary manifestation of sarcoidosis that may not be readily recognised in the absence of a known history of sarcoid. Nodular myopathy is the most uncommon subtype of musclar sarcoidosis and, when encountered, establishing the diagnosis can be challenging. We present a case of symptomatic nodular myopathy as a first presentation of sarcoidosis in a young man who required a multidisciplinary approach to diagnose. The patient presented to our radiology department following a short period of flu-like illness and multiple soft tissue lesions. Biopsy of the lesions demonstrated noncaseating granulomata, and a diagnosis of sarcoidosis was established after important differential diagnoses were excluded. We present a literature review of sarcoid-related myopathy and the multimodality imaging characteristics of the different subtypes.

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8

Dewberry, Robert G., Lawrence H. Phillips, Bernard F. Schneider, and William F. Cale. "Sarcoid myopathy presenting with diaphragm weakness." Muscle & Nerve 16, no. 8 (August 1993): 832–35. http://dx.doi.org/10.1002/mus.880160805.

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9

Dierks, Alexander, Malte Kircher, Stefan J. Schmid, Daniela Kramer, Andreas K. Buck, and Constantin Lapa. "Tiger man sign in sarcoid myopathy." European Journal of Nuclear Medicine and Molecular Imaging 46, no. 4 (January 12, 2019): 1039–40. http://dx.doi.org/10.1007/s00259-019-4264-8.

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10

Akbar, Shalla, Sandhya Dasaraju, and Osama Elkadi. "A Case of Immune-Mediated Necrotizing Myopathy With Associated Skeletal Muscle Involvement by Sarcoid Granulomata: A Rare Association." American Journal of Clinical Pathology 152, Supplement_1 (September 11, 2019): S69. http://dx.doi.org/10.1093/ajcp/aqz113.078.

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Abstract Skeletal muscle involvement by noncaseating granulomata occurs in a variety of conditions, including sarcoidosis, infections, and rarely in association with primary inflammatory myopathies such as inclusion body myositis (IBM) and dermatomyositis (DM). Sarcoid myopathy is typically asymptomatic; however, a picture of acute myositis with proximal muscle weakness has been described. Immune-mediated necrotizing myopathy (IMNM) is a subgroup of inflammatory myopathies typically presenting with proximal muscle weakness and markedly elevated muscle enzymes, mostly occurring in the setting of statin treatment. IMNM is associated with positive autoantibodies, but a subset of cases is antibody negative. Here we describe a case of myopathy occurring in association with sarcoidosis with combined features of granulomatous and necrotizing myopathy. The patient was a 54-year-old African American male with medical history significant for statin use 3 years ago, which was discontinued due to myalgia and elevated muscle enzymes and biopsy-proven sarcoidosis diagnosed on a pulmonary lymph node biopsy. He presented with progressive worsening of bilateral proximal weakness involving the upper and lower extremities. Electromyogram showed features of active myopathy with no evidence of peripheral neuropathy. Myositis panel was negative for the following antibodies: anti-Jo1, Mi-2, anti-Ku, PL-7, PL-12, OJ, EJ, and SRP. However, there was elevation of aldolase, CRP, and CK-MB. Biopsy of thigh and deltoid muscle showed necrotic muscle fibers, myophagocytosis with associated minimal inflammation, and multiple well-formed nonnecrotizing granulomas with multinucleated giant cells. Myopathic features include increased internalized nuclei, round atrophic fibers, and scattered split fibers. Specific features of IBM or DM were not present. Conclusion Myopathies developing or worsening after discontinuation of statin are rare. The association of necrotizing myopathy with sarcoidosis is not well described in the literature. Additional studies are warranted to elucidate this association.

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11

Isobe, Takashi, Madoka Mori-Yoshimura, Yasushi Oya, Yuko Saito, Miho Murata, Ichizo Nishino, and Yuji Takahashi. "A case of chronic sarcoid myopathy with Basedow’s disease and Sjogren’s syndrome: A case series of sarcoid myopathy." Rinsho Shinkeigaku 57, no. 5 (2017): 220–24. http://dx.doi.org/10.5692/clinicalneurol.cn-001012.

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12

O'Dowd, Sean, Tudor Munteanu, Daniel Hardiman, Yvonne Langan, Francesca Brett, and Janice Redmond. "OCKHAM'S RAZOR OR HICKAM'S DICTUM? THE DIAGNOSTIC JOURNEY OF A PATIENT WITH PROXIMAL MYOPATHY." Journal of Neurology, Neurosurgery & Psychiatry 86, no. 11 (October 14, 2015): e4.53-e4. http://dx.doi.org/10.1136/jnnp-2015-312379.146.

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A 39-year old Congolese native presented with a ten-year history of myalgia and progressive muscle weakness. He had a known tissue diagnosis of pulmonary, mediastinal and hepatic sarcoidosis, as well as latent tuberculosis. Family history was unavailable. Examination revealed deformity of the distal joints; shoulder girdle and proximal lower limb atrophy; proximal muscle weakness and a waddling gait. CK was 2560 IU/l (normal <290). Plain films of the hands revealed cystic bony change. EMG demonstrated features consistent with a necrotising myopathy. MRI of proximal muscle groups revealed abnormal high signal consistent with myositis. Biopsy of quadriceps was abnormal but failed to demonstrate features consistent with inflammation. A second biopsy targeted the deltoid- again no convincing evidence of inflammation was present; no granulomata were detected; the possibility of an underlying inherited myopathy was queried. The patient continued to experience progressive muscle symptoms. A third muscle biopsy of the contralateral deltoid was ultimately diagnostic, demonstrating a number of non-caseating granulomata.Symptomatic sarcoid myopathy is rare, although the literature suggests high rates of asymptomatic muscle involvement. Securing an accurate diagnosis in this case was essential in order to guide appropriate use of immunosuppression. The clinical features and management of sarcoid myopathy are reviewed.

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13

Miyazaki, Masayuki, Madoka Mori-Yoshimura, Toshiyuki Yamamoto, Yasushi Oya, Yuko Saito, Ichizo Nishino, and Yuji Takahashi. "Chronic sarcoid myopathy mimicking sporadic inclusion body myositis." Clinical Neurology and Neurosurgery 182 (July 2019): 84–86. http://dx.doi.org/10.1016/j.clineuro.2019.05.001.

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14

Takemaru, Makoto, Toshio Okazaki, Kenichiro Nakamura, Noriyuki Kimura, Hideo Horinouchi, Hidetsugu Ueyama, and Toshihide Kumamoto. "A Case of Chronic Sarcoid Myopathy with Lobulated Fibers." Japanese Journal of Sarcoidosis and Other Granulomatous Disorders 31, no. 1 (2011): 49–55. http://dx.doi.org/10.7878/jjsogd.31.49.

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15

Kurashima, Kazuyoshi, Hiroshi Shimizu, Haruhiko Ogawa, Takio Ohka, Kouji Nobata, Kyousuke Ueno, Shigeho Rikimaru, Masaki Fujimura, and Tamotsu Matsuda. "MR and CT in the Evaluation of Sarcoid Myopathy." Journal of Computer Assisted Tomography 15, no. 6 (November 1991): 1004–7. http://dx.doi.org/10.1097/00004728-199111000-00019.

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16

HERSHCOVICI, TIBERIU, SERGEI MEKHMANDOROV, YITZHAK BEIGEL, and RUTH HARDOFF. "The Value of Ga-67 Scintigraphy in Sarcoid Myopathy." Clinical Nuclear Medicine 26, no. 6 (June 2001): 540–41. http://dx.doi.org/10.1097/00003072-200106000-00013.

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17

Itagane, Masaki, and Mitsuyo Kinjo. "Unusual organ involvement in sarcoidosis: sarcoid myopathy and peritoneal sarcoidosis." BMJ Case Reports 14, no. 7 (July 2021): e244134. http://dx.doi.org/10.1136/bcr-2021-244134.

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Myopathy and peritoneal involvement are rare complications of sarcoidosis, and the latter can mimic malignancy with peritoneal dissemination. In this case, a patient with a history of polyarthritis and positive rheumatoid factor presented with proximal muscle weakness and abdominal pain. Biopsies of muscle and peritoneum revealed non-caseating granuloma suggesting sarcoidosis. Ocular and pulmonary involvement later developed and confirmed the diagnosis of sarcoidosis.

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18

Kobak, Şenol, Murat Yalçin, Fidan Sever, and Guray Oncel. "Sarcoidosis Presenting as Löfgren’s Syndrome with Myopathy." Case Reports in Rheumatology 2013 (2013): 1–3. http://dx.doi.org/10.1155/2013/125251.

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A 34-year-old female patient, who had proximal muscle weakness for 8 months, presented with erythema nodosum lesions on the pretibial region in addition to pain, swelling, and movement restriction in both ankles for the last one month. Thoracic CT demonstrated hilar and mediastinal lymphadenopathy. She underwent mediastinoscopic lymph node biopsy; biopsy result was consistent with noncaseating granuloma. Serum angiotensin converting enzyme level and muscle enzymes have been elevated. Muscular MRI and EMG findings were consistent with myositis. Muscle biopsy was done, and myopathy was found. The patient was diagnosed with sarcoidosis, Löfgren's syndrome, and sarcoid myopathy. The patient displayed remarkable clinical and radiological regression after 6-month corticosteroid and MTX therapy.

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19

Hyodo, Masamitsu. "A Case of Cricopharyngeal Sarcoid Myopathy Presenting with Swallowing Disorder." Practica Oto-Rhino-Laryngologica 112, no. 11 (2019): 712–13. http://dx.doi.org/10.5631/jibirin.112.712.

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20

Tatsuno, Kentarou, Seika Nakamura, Tomoko Asayama, and Satoshi Nakano. "A patient with chronic sarcoid myopathy without other organ involvement." Rinsho Shinkeigaku 54, no. 4 (2014): 313–16. http://dx.doi.org/10.5692/clinicalneurol.54.313.

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21

GRANIERI, JANICE, JEFFREY J. WISNIESKI, RICHARD C. GRAHAM, HOWARD SMITH, PREMA GOGATE, and JOHN N. AUCOTT. "Sarcoid Myopathy in a Patient With Human Immunodeficiency Virus Infection." Southern Medical Journal 88, no. 5 (May 1995): 591–95. http://dx.doi.org/10.1097/00007611-199505000-00018.

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22

Ito, Yasuo, Toshimasa Yamamoto, Aya Ohkuma, Yoshikazu Mizoi, Naotoshi Tamura, and Nobuo Araki. "A case of elderly-onset sarcoid myopathy with features resembling polymyositis." Nippon Ronen Igakkai Zasshi. Japanese Journal of Geriatrics 46, no. 1 (2009): 85–89. http://dx.doi.org/10.3143/geriatrics.46.85.

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23

Sanmaneechai, Oranee, Andrea Swenson, Alicia K. Gerke, Steven A. Moore, and Michael E. Shy. "Inclusion body myositis and sarcoid myopathy: Coincidental occurrence or associated diseases." Neuromuscular Disorders 25, no. 4 (April 2015): 297–300. http://dx.doi.org/10.1016/j.nmd.2014.12.005.

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24

Karasoy, H., M. Eroglu, F. Gokcay, M. Argin, O. Ekmekci, and A. Yuceyar. "A case of chronic sarcoid myopathy with IBM like distal muscle involvement." Neuromuscular Disorders 25 (October 2015): S248. http://dx.doi.org/10.1016/j.nmd.2015.06.231.

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25

Suehiro, S., S. Shiokawa, S. Taniguchi, Y. Sakai, H. Goda, M. Shiratsuchi, T. Sugimura, et al. "Gallium-67 scintigraphy in the diagnosis and management of chronic sarcoid myopathy." Clinical Rheumatology 22, no. 2 (May 1, 2003): 146–48. http://dx.doi.org/10.1007/s10067-002-0686-x.

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26

Kono, M., M. Kono, and S. Jodo. "A case of refractory acute sarcoid myopathy successfully treated with intravenous immunoglobulin." Scandinavian Journal of Rheumatology 47, no. 2 (January 29, 2018): 168–69. http://dx.doi.org/10.1080/03009742.2017.1393559.

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27

Peris, P., J. Font, J. M. Grau, M. J. Martínez de Osaba, X. Filella, and J. Muñoz-Gómez. "Calcitriol-Mediated Hypercalcaemia and Increased Interleukins in a Patient with Sarcoid Myopathy." Clinical Rheumatology 18, no. 6 (December 2, 1999): 488–91. http://dx.doi.org/10.1007/s100670050144.

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28

Kumamoto, Toshihide, Keiko Yukishige, Tomoko Ito, Shin-ichiro Nagao, Toshio Mori, Hidetsugu Ueyama, Hiroshi Tsumura, and Tomiyasu Tsuda. "Cellular distribution of proteolytic enzymes in the skeletal muscle of sarcoid myopathy." Acta Neuropathologica 104, no. 1 (March 14, 2002): 38–44. http://dx.doi.org/10.1007/s00401-002-0517-9.

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29

Nishiyama, Kazutoshi, Kazumasa Yokoyama, Hiroshi Kuroda, Yoko Takiyama, and Noriyuki Kimura. "Revision of Guideline for Diagnosis and Treatment of Neuro-sarcoidosis and Sarcoid Myopathy." Japanese Journal of Sarcoidosis and Other Granulomatous Disorders 36, no. 1_2 (2016): 13–16. http://dx.doi.org/10.7878/jjsogd.36.1_2_13.

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30

Reichmann, Heinz, Berthold Schalke, Peter Seibel, Markus Naumann, and Klaus Toyka. "Sarcoid myopathy and mitochondrial respiratory chain defects: clinicopathological, biochemical and molecular biological analyses." Neuromuscular Disorders 5, no. 4 (July 1995): 277–83. http://dx.doi.org/10.1016/0960-8966(94)00060-m.

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31

Androdias, G., D. Maillet, R. Marignier, L. Pinede, C. Confavreux, C. Broussolle, S. Vukusic, and P. Seve. "Mycophenolate mofetil may be effective in CNS sarcoidosis but not in sarcoid myopathy." Neurology 76, no. 13 (March 28, 2011): 1168–72. http://dx.doi.org/10.1212/wnl.0b013e318212aafb.

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32

Nishimura, Ayako, Ryotaro Ikeguchi, Masaki Kobayashi, Megumi Takeuchi, Yuko Shimizu, Hideto Saigusa, and Kazuo Kitagawa. "Chronic sarcoid myopathy manifesting only as dysphagia and dysarthria in an 84-year-old woman." Clinical Neurology and Neurosurgery 173 (October 2018): 58–60. http://dx.doi.org/10.1016/j.clineuro.2018.07.018.

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33

KATO, Masataka, Osamu HASHIMOTO, Masahiko MURASE, Midori UMEDA, Masahiro YAMATO, Toshikatsu TERAKURA, Tetsu TAKAT, and Yasutoshi MUTO. "A case of adjuvant disease of man associated with myopathy showing sarcoid-like lesion due to mammoplasty." Nihon Naika Gakkai Zasshi 76, no. 3 (1987): 445–50. http://dx.doi.org/10.2169/naika.76.445.

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34

Ogane, Kunihiro, Takashi Kato, Ichiro Mizushima, Mitsuhiro Kawano, and Masakazu Yamagishi. "A case of sarcoidosis developing as sarcoid myopathy concomitant with systemic sclerosis and review of the literature." Modern Rheumatology 22, no. 1 (February 2012): 142–46. http://dx.doi.org/10.3109/s10165-011-0482-z.

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35

Schubert, W., M. Friedenberger, R. Haars, M. Bode, L. Philipsen, T. Nattkemper, and H. Ritter. "Automatic Recognition of Muscle-Invasive T-Lymphocytes Expressing Dipeptidyl-Peptidase IV (CD26) and Analysis of the Associated Cell Surface Phenotypes." Journal of Theoretical Medicine 4, no. 1 (2002): 67–74. http://dx.doi.org/10.1080/10273660290015189.

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A neural cell detection system (NCDS) for the automatic quantitation of fluorescent lymphocytes in tissue sections was used to analyze CD26 expression in muscle-invasive T-cells. CD26 is a cell surface dipeptidyl-peptidase IV (DPP IV) involved in co-stimulatory activation of T-cells and also in adhesive events. The NCDS system acquires visual knowledge from a set of training cell image patches selected by a user. The trained system evaluates an image in 2 min calculating (i) the number, (ii) the positions and (iii) the phenotypes of the fluorescent cells. In the present study we have used the NCDS to identity DPP IV (CD26) expressing invasive lymphocytes in sarcoid myopathy and to analyze the associated cell surface phenotypes. We find highly unusual phenotypes characterized by differential combination of seven cell surface receptors usually involved in co-stimulatory events in T-lymphocytes. The data support a differential adhesive rather than a co-stimulatory role of CD26 in muscle-invasive cells. The adaptability of the NCDS algorithm to diverse types of cells should enable us to approach any invasion process, including invasion of malignant cells.

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36

Pina, Sérgio, Teresa Salero, Mariana Figueiras, Rui Osório, and Sofia Amálio. "Case Report: Isolated hepatosplenic sarcoidosis treatment improving glycaemic control in a type 1 diabetic patient." F1000Research 9 (January 27, 2020): 50. http://dx.doi.org/10.12688/f1000research.21798.1.

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Sarcoidosis is a multi-systemic disease characterized by non-caseating granulomas in various organs. The aetiology is still unknown. Although the liver is the third most commonly affected organ, hepatosplenic sarcoidosis without lung involvement is very uncommon. There is a high frequency of certain autoimmune illnesses observed in sarcoidosis, but association with type 1 diabetes is infrequent. We present the case of a 31-year-old woman, with type 1 diabetes mellitus diagnosed 22 years before with a glycated haemoglobin (HbA1c) above 14%, diabetic nephropathy, retinopathy and neuropathy, hypercholesterolemia and beta thalassemia. She was medicated with an angiotensin-converting enzyme inhibitor, a dihydropyridine calcium antagonist and insulin. The patient presented with a 4-month history of tiredness, abdominal pain, weight lost and hepatosplenomegaly. Abdominal ultrasound revealed hepatomegaly with regular contours, diffuse heterogeneous texture, containing numerous nodules with slight enlargement of the spleen. Serum angiotensin converting enzyme (ACE) was 67 IU/L and a sedimentation rate of 120 mm/h. Computer tomography (CT) scan confirmed hepatosplenomegaly and suggested infiltration in both organs. Liver biopsies were compatible with sarcoidosis. After ruling other organ involvement, a diagnosis of isolated hepatosplenic sarcoidosis was provided and prednisolone (40mg/day) was started. After a few months the patient developed a corticoid-induced myopathy confirmed with electromyography. Prednisolone was reduced to 20mg/day and azathioprine (50mg/day) treatment initiated. After a 7-month treatment, chest-abdomen-pelvis CT scan showed a marked reduction of the nodularity and hepatosplenomegaly and after 1 year the patient was completely asymptomatic (HbA1c, 7.5%; ACE, 24IU/L). At 18-month follow-up there was no evidence of recurrence (HbA1c, 7%), with optimum glycaemic control with total daily insulin dose lowered to half. This is an uncommon case in which the treatment of hepatosplenic sarcoidosis with regression of sarcoid tissue can help explain the improvement of glycaemic control in this patient.

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37

Anger, M., F. Lambert, D. Chemla, P. Desche, E. Scalbert, A. M. Lompre, and Y. Lecarpentier. "Sarcoplasmic reticulum Ca2+ pumps in heart and diaphragm of cardiomyopathic hamster: effects of perindopril." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 5 (May 1, 1995): H1947—H1953. http://dx.doi.org/10.1152/ajpheart.1995.268.5.h1947.

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The polymyopathy of the Syrian hamster is associated with alterations of cellular calcium regulation and contractile performance of cardiac and skeletal muscles and, in particular, the diaphragm. Angiotensin-converting enzyme (ACE) inhibitors have been shown to preserve contractile performance. Therefore we analyzed the expression of the genes coding for the sarco(endo)plasmic reticulum Ca(2+)-adenosinetriphosphatase (SERCA) in heart and diaphragm of the cardiomyopathic Syrian hamster (CSH) from the dilated strain Bio 53-58, and we tested the influence of ACE inhibition on accumulation of the different SERCA mRNAs. In the diaphragm of healthy hamsters, two SERCA mRNA isoforms were present: SERCA 1 and SERCA 2. At 6 mo of age, the myopathic process resulted in decreased levels of SERCA 1, whereas the level of SERCA 2 was unchanged. The ACE inhibitor perindopril (1 mg.kg-1.day-1), administered by force feeding from 1 to 6 mo of age, had no effect on the SERCA 1 mRNA level. In heart, the myopathy was associated with a depressed level of SERCA 2 mRNA in 9- but not in 6-mo-old animals. Perindopril treatment from 6 to 9 mo reversed cardiac hypertrophy and the relative decrease in SERCA 2 mRNA level. Preventive treatment with perindopril from 1 to 9 mo tended to prevent (not significantly) the development of cardiac hypertrophy and reduction in SERCA gene expression. In conclusion, the myopathic process affects SERCA gene expression in the diaphragm and subsequently in the heart. Perindopril treatment can prevent SERCA mRNA loss in heart but not in diaphragm.

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38

Takada, Leonel T. "The Genetics of Monogenic Frontotemporal Dementia." Dementia & Neuropsychologia 9, no. 3 (September 2015): 219–29. http://dx.doi.org/10.1590/1980-57642015dn93000003.

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ABSTRACT Around 10-15% of patients diagnosed with frontotemporal dementia (FTD) have a positive family history for FTD with an autosomal dominant pattern of inheritance. Since the identification of mutations in MAPT(microtubuleassociated protein tau gene) in 1998, over 10 other genes have been associated with FTD spectrum disorders, discussed in this review. Along with MAPT, mutations in GRN(progranulin) and C9orf72(chromosome 9 open reading frame 72) are the most commonly identified in FTD cohorts. The association of FTD and motor neuron disease (MND) can be caused by mutations in C9orf72and other genes, such as TARDBP(TAR DNA-binding protein), FUS(fused in sarcoma), UBQLN2(ubiquilin 2). Multisystem proteinopathy is a complex phenotype that includes FTD, Paget disease of the bone, inclusion body myopathy and MND, and can be due to mutations in VCP(valosing containing protein) and other recently identified genes.

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39

Oldfield, Christopher J., Teri L. Moffatt, Vernon W. Dolinsky, and Todd A. Duhamel. "Sirtuin 3 overexpression preserves maximal sarco(endo)plasmic reticulum calcium ATPase activity in the skeletal muscle of mice subjected to high fat – high sucrose feeding." Canadian Journal of Physiology and Pharmacology 100, no. 4 (April 2022): 361–70. http://dx.doi.org/10.1139/cjpp-2021-0587.

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Sarco(endo)plasmic reticulum calcium (Ca2+) ATPase (SERCA) transports Ca2+ in muscle. Impaired SERCA activity may contribute to diabetic myopathy. Sirtuin (SIRT) 3 regulates muscle metabolism and function; however, it is unknown if SIRT3 regulates muscle SERCA activity or acetylation. We determined if SIRT3 overexpression enhances SERCA activity in mouse gastrocnemius muscle and if SIRT3 overexpression preserves gastrocnemius SERCA activity in a model of type 2 diabetes, induced by high fat – high sucrose (HFHS) feeding. We also determined if the acetylation status of SERCA proteins in mouse gastrocnemius is altered by SIRT3 overexpression or HFHS feeding. Wild-type (WT) and SIRT3 transgenic (SIRT3TG) mice, overexpressing SIRT3 in skeletal muscle, were fed a standard or HFHS diet for 4 months. SIRT3TG and WT mice developed obesity and glucose intolerance after 4 months of HFHS feeding. SERCA Vmax was higher in gastrocnemius of SIRT3TG mice compared with WT mice. HFHS-fed mice had lower SERCA1a protein levels and lower SERCA Vmax in their gastrocnemius than control-fed mice. The decrease in SERCA Vmax in gastrocnemius muscle due to HFHS feeding was attenuated by SIRT3 overexpression in HFHS-fed SIRT3TG mice. SERCA1a and SERCA2a acetylation in mouse gastrocnemius was not altered by genotype or diet. These findings suggest SIRT3 overexpression improves SERCA function in mouse skeletal muscle.

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40

Akyürek, Eylem Emek, Francesca Busato, Leonardo Murgiano, Elisa Bianchini, Marcello Carotti, Dorianna Sandonà, Cord Drögemüller, Arcangelo Gentile, and Roberta Sacchetto. "Differential Analysis of Gly211Val and Gly286Val Mutations Affecting Sarco(endo)plasmic Reticulum Ca2+-ATPase (SERCA1) in Congenital Pseudomyotonia Romagnola Cattle." International Journal of Molecular Sciences 23, no. 20 (October 15, 2022): 12364. http://dx.doi.org/10.3390/ijms232012364.

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Congenital pseudomyotonia in cattle (PMT) is a rare skeletal muscle disorder, clinically characterized by stiffness and by delayed muscle relaxation after exercise. Muscle relaxation impairment is due to defective content of the Sarco(endo)plasmic Reticulum Ca2+ ATPase isoform 1 (SERCA1) protein, caused by missense mutations in the ATP2A1 gene. PMT represents the only mammalian model of human Brody myopathy. In the Romagnola breed, two missense variants occurring in the same allele were described, leading to Gly211Val and Gly286Val (G211V/G286V) substitutions. In this study, we analyzed the consequences of G211V and G286V mutations. Results support that the reduced amount of SERCA1 is a consequence of the G211V mutation, the G286V mutation almost being benign and the ubiquitin–proteasome system (UPS) being involved. After blocking the proteasome using a proteasome inhibitor, we found that the G211V mutant accumulates in cells at levels comparable to those of WT SERCA1. Our conclusion is that G211/286V mutations presumably originate in a folding-defective SERCA1 protein, recognized and diverted to degradation by UPS, although still catalytically functional, and that the main role is played by G211V mutation. Rescue of mutated SERCA1 to the sarcoplasmic reticulum membrane can re-establish resting cytosolic Ca2+ concentration and prevent the appearance of pathological signs, paving the way for a possible therapeutic approach against Brody disease.

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Zullo, Alberto, Giuseppa Perrotta, Rossana D'Angelo, Lucia Ruggiero, Elvira Gravino, Luigi Del Vecchio, Lucio Santoro, Francesco Salvatore, and Antonella Carsana. "RYR1 Sequence Variants in Myopathies: Expression and Functional Studies in Two Families." BioMed Research International 2019 (April 21, 2019): 1–13. http://dx.doi.org/10.1155/2019/7638946.

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The skeletal muscle ryanodine receptor (RyR1), i.e., the Ca2+ channel of the sarco/endoplasmic reticulum (S/ER), and the voltage-dependent calcium channel Cav1.1 are the principal channels involved in excitation-contraction coupling in skeletal muscle. RYR1 gene variants are linked to distinct skeletal muscle disorders, including malignant hyperthermia susceptibility and central core disease (CCD), mainly with autosomal dominant inheritance, and autosomal recessive myopathies with a broad phenotypic and histopathological spectrum. The age at onset of RYR1-related myopathies varies from infancy to adulthood. We report the identification of four RYR1 variants in two Italian families: one with myopathy and variants c.4003C>T (p.R1335C) and c.7035C>A (p.S2345R), and another with CCD and variants c.9293G>T (p.S3098I) and c.14771_14772insTAGACAGGGTGTTGCTCTGTTGCCCTTCTT (p.F4924_V4925insRQGVALLPFF). We demonstrate that, in patient-specific lymphoblastoid cells, the c.4003C>T (p.R1335C) variant is not expressed and the in-frame 30-nucleotide insertion variant is expressed at a low level. Moreover, Ca2+ release in response to the RyR1 agonist 4-chloro-m-cresol and to thapsigargin showed that the c.7035C>A (p.S2345R) variant causes depletion of S/ER Ca2+ stores and that the compound heterozygosity for variant c.9293G>T (p.S3098I) and the 30-nucleotide insertion increases RyR1-dependent Ca2+ release without affecting ER Ca2+ stores. In conclusion, we detected and functionally characterized disease-causing variants of the RyR1 channel in patient-specific lymphoblastoid cells.

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Levy, Robert M., Dale E. Bredesen, and Mark L. Rosenblum. "Neurological manifestations of the acquired immunodeficiency syndrome (AIDS): Experience at UCSF and review of the literature." Journal of Neurosurgery 107, no. 6 (December 2007): 1253–73. http://dx.doi.org/10.3171/jns-07/12/1253.

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✓In this review of the acquired immunodeficiency syndrome (AIDS), the authors have evaluated a total of 352 homosexual patients with AIDS or generalized lymphadenopathy managed at the University of California, San Francisco (UCSF), between 1979 and 1984. Of an initial unselecled group of 318 patients, 124 (39%) were neurologically symptomatic, and one-third already had their neurological complaints at the time of presentation. An additional 210 AIDS patients with neurological symptoms have been reported in the literature. Thus, a total of 366 neurologically symptomatic patients with AIDS or lymphadenopathy are reviewed. Central nervous system (CNS) complications, encountered in 315 patients, included the following viral syndromes: subacute encephalitis (54), atypical aseptic meningitis (21), herpes simplex encephalitis (nine), progressive multifocal leukoencephalopathy (six), viral myelitis (three), and varicella-zoster encephalitis (one). Non-viral infections were caused by Toxoplasma gondii (103), Cryptococcus neoformans (41), Candida albicans (six), Mycobacteria (six), Treponema pallidum (two), coccidioidomycosis (one), Mycobacterium tuberculosis (one), Aspergillus fumigatus (one), and Escherichia coli (one). Neoplasms included primary CNS lymphoma (15), systemic lymphoma with CNS involvement (12), and metastatic Kaposi's sarcoma (three). Cerebrovascular complications were seen in four patients with hemorrhage and five with infarction. Five patients in the UCSF series had multiple intracranial pathologies, including two cases of simultaneous Toxoplasma gondii infections and primary CNS lymphoma, two cases of coexistent Toxoplasma gondii and viral infections, and one case of combined Toxoplasma gondii and atypical mycobacterial infection. Cranial or peripheral nerve complications, seen in 51 patients, included cranial nerve syndromes secondary to chronic inflammatory polyneuropathy (five), lymphoma (five), and Bell's palsy (five). Peripheral nerve syndromes included chronic inflammatory polyneuropathy (12), distal symmetrical neuropathy (13), herpes zoster radiculitis (six), persistent myalgias (two), myopathy (two), and polymyositis (one). In light of the protean behavior of AIDS and the problems related to the clinical, radiological, and serological diagnosis of the unusual and varied associated nervous system diseases, patients with AIDS and neurological complaints require a rigorous and detailed evaluation. The authors' experience suggests that biopsy of all CNS space-occupying lesions should be performed for tissue diagnosis prior to the institution of other therapies.

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Levy, Robert M., Dale E. Bredesen, and Mark L. Rosenblum. "Neurological manifestations of the acquired immunodeficiency syndrome (AIDS): Experience at UCSF and review of the literature." Journal of Neurosurgery 62, no. 4 (April 1985): 475–95. http://dx.doi.org/10.3171/jns.1985.62.4.0475.

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✓ In this review of the acquired immunodeficiency syndrome (AIDS), the authors have evaluated a total of 352 homosexual patients with AIDS or generalized lymphadenopathy managed at the University of California, San Francisco (UCSF), between 1979 and 1984. Of an initial unselected group of 318 patients, 124 (39%) were neurologically symptomatic, and one-third already had their neurological complaints at the time of presentation. An additional 210 AIDS patients with neurological symptoms have been reported in the literature. Thus, a total of 366 neurologically symptomatic patients with AIDS or lymphadenopathy are reviewed. Central nervous system (CNS) complications, encountered in 315 patients, included the following viral syndromes: subacute encephalitis (54), atypical aseptic meningitis (21), herpes simplex encephalitis (nine), progressive multifocal leukoencephalopathy (six), viral myelitis (three), and varicella-zoster encephalitis (one). Non-viral infections were caused by Toxoplasma gondii (103), Cryptococcus neoformans (41), Candida albicans (six), Mycobacteria (six), Treponema pallidum (two), coccidioidomycosis (one), Mycobacterium tuberculosis (one), Aspergillus fumigatus (one), and Escherichia coli (one). Neoplasms included primary CNS lymphoma (15), systemic lymphoma with CNS involvement (12), and metastatic Kaposi's sarcoma (three). Cerebrovascular complications were seen in four patients with hemorrhage and five with infarction. Five patients in the UCSF series had multiple intracranial pathologies, including two cases of simultaneous Toxoplasma gondii infections and primary CNS lymphoma, two cases of coexistent Toxoplasma gondii and viral infections, and one case of combined Toxoplasma gondii and atypical mycobacterial infection. Cranial or peripheral nerve complications, seen in 51 patients, included cranial nerve syndromes secondary to chronic inflammatory polyneuropathy (five), lymphoma (five), and Bell's palsy (five). Peripheral nerve syndromes included chronic inflammatory polyneuropathy (12), distal symmetrical neuropathy (13), herpes zoster radiculitis (six), persistent myalgias (two), myopathy (two), and polymyositis (one). In light of the protean behavior of AIDS and the problems related to the clinical, radiological, and serological diagnosis of the unusual and varied associated nervous system diseases, patients with AIDS and neurological complaints require a rigorous and detailed evaluation. The authors' experience suggests that biopsy of all CNS space-occupying lesions should be performed for tissue diagnosis prior to the institution of other therapies.

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Ali, Saadia Sasha, Mark Russell, James Galloway, and Ioana Onac. "EP23 Symptomatic sarcoid myopathy: a rare extra-pulmonary manifestation of sarcoidosis." Rheumatology Advances in Practice 4, Supplement_1 (October 1, 2020). http://dx.doi.org/10.1093/rap/rkaa052.022.

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Abstract Case report - Introduction Sarcoidosis is a multisystem disorder of unknown aetiology that is characterised pathologically by the presence of non-caseating granulomata. The disease is known for its multitude of presentations and can affect almost any organ system. Symptomatic skeletal muscle involvement in sarcoidosis is infrequent and occurs in < 3% of all sarcoidosis patients. We present the case of a 47-year-old male with multisystem sarcoidosis involving his lungs, eyes, and liver, who presented to our tertiary sarcoid centre with proximal muscle weakness. This case is significant as it highlights the diagnostic challenges that can arise when muscle weakness occurs on a background of sarcoidosis. Case report - Case description A 47-year-old gentleman presented to Rheumatology with a ten-year history of progressive lower extremity muscle weakness. He was known to have multisystem sarcoidosis affecting his lungs (diffuse interstitial lung disease), eyes (anterior uveitis) and liver (liver fibrosis). His sarcoidosis was initially diagnosed ten years beforehand, from confirmatory histology obtained via Endobronchial Ultrasound sampling. He was previously a keen runner; however, he had observed a gradual decline in his ability to run. Over a period of two years his mobility further deteriorated, and he required two sticks to walk. Physical examination revealed a waddling gait with wasting to his quadriceps bilaterally. He had reduced power of 2/5 on hip flexion on the Medical Research Council (MRC) muscle grading scale. There was no bulbar involvement and facial and upper extremity strength was normal. His past medical history was also remarkable for anxiety and depression. There was no family history of muscle disease. Serology revealed a Creatine Kinase (CK) of 773 IU/L (32-294 IU/L). He had an equivocal signal recognition particle (SRP) antibody result, which was later repeated and found to be negative. His EMG showed myopathic changes in his distal and proximal lower limb muscles with profuse spontaneous activity, indicating an active myopathic process. MRI of his lower limbs showed symmetrical fatty infiltration in the distal semimembranosus and short head of biceps femoris muscles with no clear oedema. A muscle biopsy showed diffuse MHC Class 1 upregulation with nemaline rods. Treatment with pulsed IV methylprednisolone was started, in addition to Mycophenolate Mofetil (MMF) as steroid therapy was not sufficient to suppress his disease. He had a reduction in his CK to 205 IU/L and no activity in his skeletal muscle on FDG-PET CT. His power improved to 3/5 on MRC grading. Case report - Discussion Three distinct patterns of muscle involvement in sarcoidosis are recognised: chronic myopathy, nodular myopathy, and acute myopathy. Symptomatic muscle disease in sarcoidosis is rare and it is important to consider other potential aetiologies of a progressive myopathy, even in a patient with established multisystem sarcoidosis. This case is interesting as there was diagnostic difficulty in ascertaining the diagnosis, which potentially included a corticosteroid-induced myopathy, SRP necrotising myopathy, or even a nemaline myopathy. Corticosteroid myopathy has a similar distribution to a sarcoid myopathy. However, the patient’s clinical phenotype, elevated muscle enzymes, EMG findings, and histological data favoured an inflammatory myositis. SRP necrotising myopathy is characterised by rapidly progressive proximal muscle weakness with necrotic muscle fibres, scant inflammation, and a significant elevation in muscle enzymes, which were not seen in this patient. The patient’s weakness was more insidious in onset, with diffuse inflammation on muscle biopsy. Nemaline rods were seen on biopsy, however these were only present in one area, which is atypical of a nemaline myopathy. Furthermore, the presence of many loculated fibres on biopsy and upregulation of MHC class 1 was more in keeping with a diagnosis of an inflammatory myopathy secondary to sarcoidosis, even in the absence of non-caseating granulomas on muscle biopsy. There are no randomised controlled trials of treatments in sarcoid myopathy. While methotrexate is most used in steroid-recalcitrant myositis, the patient’s liver fibrosis preluded this therapy, thus MMF was trialled instead. Co-existing inflammatory muscle disease with sarcoidosis has been documented infrequently in the literature. They both have overlapping symptoms with contrasting treatment strategies. In this patient, the muscle biopsy pointed to an idiopathic inflammatory myopathy (IIM) without granulomatous infiltration, it is intriguing to consider whether treatment of an IIM with intravenous immunoglobulin or rituximab would have resulted in better clinical outcomes. Case report - Key learning points Key points: Even though symptomatic muscle involvement in sarcoidosis is uncommon, a sarcoid myopathy should be suspected in symptomatic patients with known or suspected pulmonary or extrapulmonary sarcoidosis. In patients without known sarcoidosis but with unexplained muscle symptoms, particularly in the setting of a multisystem illness, sarcoid myopathy should be considered in the differential diagnosis.MRI and muscle biopsy are useful in distinguishing a sarcoid myopathy from a corticosteroid-induced myopathy as illustrated in this case.Fluorine 18 fluorodeoxyglucose (FDG) PET/CT is sensitive for assessment of the inflammatory activity of sarcoidosis in any organ. In this patient, FDG-PET was useful in evaluating active sarcoid lesions and evaluating the therapeutic effects of Mycophenolate Mofetil on his sarcoid myopathy. Although there is limited data to guide treatment in a sarcoid myopathy, Mycophenolate Mofetil can be used as an alternative to Methotrexate.

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Bhowmick, Jayeeta, Pramila Dharmshaktu, and Subhro Chakraborty. "Isolated sarcoid myopathy: an unusual presentation." Rheumatology Reports 6, no. 1 (August 20, 2014). http://dx.doi.org/10.4081/rr.2014.5024.

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Kuzume, Ayumi, Toshiki Terao, Daisuke Miura, Kengo Takeuchi, and Kosei Matsue. "Tiger man sign in sarcoid myopathy." Rheumatology, December 25, 2020. http://dx.doi.org/10.1093/rheumatology/keaa833.

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Fonseca, João Ferreira, Flávio Costa, Manuel Teixeira Veríssimo, and Armando Carvalho. "Old tiger man: a case of sarcoid myopathy." BMJ Case Reports, August 7, 2017, bcr—2017–220177. http://dx.doi.org/10.1136/bcr-2017-220177.

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Rampes, Sanketh, Vishit Patel, Deepak Nagra, Jennifer Hannah, and James Galloway. "EP21 Tumour necrosis factor inhibitor for the treatment of refractory extra-pulmonary disease including sarcoid arthritis and myositis." Rheumatology Advances in Practice 4, Supplement_1 (October 1, 2020). http://dx.doi.org/10.1093/rap/rkaa052.020.

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Abstract Case report - Introduction Sarcoid myositis is a rare extrapulmonary manifestation of sarcoid, histologically characterised by non-caseating granuloma in the perimysial connective tissue. Muscle involvement is often asymptomatic but can cause weakness, myalgia, or muscle nodules. The first line treatment for sarcoid myositis is steroids. This case report details a case of sarcoid myositis and multi-system disease refractory to both steroids and mycophenolate mofetil. The use of infliximab, a Tumour Necrosis Factor α inhibitor (TNFi) resulted in drastic clinical and radiological resolution of sarcoid myositis. The patient is still on the TNFi and his sarcoid remains relatively well controlled. Case report - Case description A 33-year old Afro-Caribbean gentleman with a 10-year history of sarcoid (biopsy confirmed, affecting lymph nodes, lung) presented in May 2017 with joint pain, weakness, difficulty walking and cognitive impairment. At the time of the original diagnosis of sarcoid, he had concurrently been diagnosed with schizophrenia and steroids had been avoided. His only medication was olanzapine 5mg. Due to declining cognitive function, his psychiatrists arranged an MRI brain which showed extensive leptomeningeal disease. Lumbar puncture excluded infection and neurosarcoid was diagnosed. Prednisolone resulted in partial improvement in cognition, however joint symptoms and weakness persisted. On rheumatologic assessment there was an asymmetric inflammatory arthropathy, with small joint synovitis as well as large volume joint effusions of elbows and knees. Radiologic investigations showed characteristic lattice bony destruction, consistent with osseous sarcoid. His gait was waddling, and muscle strength was reduced symmetrically in the proximal groups. His creatinine kinase was 865, myositis specific antibody screen was negative although U1RNP was equivocal. Serum ACE was 102, CRP 17, ESR 25. CT-PET demonstrated FDG avidity in lymph nodes, lung parenchyma, bones, muscles, and testes. The muscle involvement was typical of nodular sarcoid and did not correlate with his weakness. The disease failed to respond adequately to either methotrexate or mycophenolate. He started Infliximab (5mg/kg). There was remarkable resolution of symptoms, including improvement in cognition. Follow up CT-PET confirmed response. Three years on he remains well, and no longer takes olanzapine. Case report - Discussion Muscle involvement occurs in 50-80% of sarcoidosis patients. Symptomatic myositis is rare (0.5-2.5%). There are three types of sarcoid myositis: nodular form, chronic myopathy, and acute myositis. Nodular involvement, as seen in our patient, usually occurs in young adults who experience palpable, painless nodules which may occur in any muscle. Nodules are not usually associated with weakness or limitation of movement. EMG and CK are usually normal. Chronic myopathy is rarely observed. It is characterised by a slowly progressive, symmetrical proximal myopathy with myopathic EMG changes but normal muscle enzymes, usually in women aged 50-60. Acute myositis typically affects younger patients (<40 years old) with diffuse muscle swelling, pain and proximal weakness which may progress to hypertrophy and contractures. Fatigue, fever, joint symptoms, and erythema nodosum are frequently seen. Inclusion Body Myositis is another granulomatous myopathy and should be considered as a differential, particularly in cases of treatment failure. The patient has had several episodes of psychosis and confusion which were previously diagnosed as schizophrenia and corticosteroid induced psychosis, meaning the team used steroids cautiously. MRI brain imaging revealed the presence of extensive neurosarcoidosis, and the neurocognitive improvement with treatment of a TNF inhibitor, suggested that the underlying pathology was sarcoidosis. Steroids could therefore be utilised appropriately for ongoing management. This case illustrates the difficulty of teasing out the underlying aetiology of neurocognitive dysfunction in patients with extensive sarcoidosis. TNFα released by alveolar macrophages is implicated in the induction and maintenance of sarcoid granulomas. Limited data from small randomised controlled trials and increasing data from non-randomised studies have led to consensus-based recommendations for TNFi use in pulmonary, ocular, cutaneous, neurological, and multi-system sarcoidosis. To our knowledge, this case is the first documented example of rapid clinical and radiological resolution of sarcoid myositis with an anti-TNF agent. Case report - Key learning points There are three important points to take away from this case. First, this case highlights the importance of a PET scan in demonstrating multi-system involvement in sarcoidosis. The PET scan was key in highlighting the extent of disease including sarcoid myositis. MRI scans of the brain were also important in highlighting the extent of neurosarcoidosis. Second, the patient presented with psychosis in 2013. This was thought to be corticosteroid-induced at the time. However, since treatment with the TNF inhibitor the patient experienced a significant neurocognitive improvement. The drastic improvement undermines the diagnosis of primary psychosis and suggests that the psychosis may have been due to neurosarcoidosis. In the context of patients with multi-organ sarcoidosis, psychosis secondary to neurosarcoid should be considered as a differential, even in the context of an earlier diagnosis of schizophrenia pre-dating the diagnosis of sarcoid. Third, the drastic resolution of sarcoid myositis and arthritis with a TNF inhibitor suggests that TNF inhibitors should be considered as treatment for cases of sarcoid myositis or sarcoid arthritis refractory to steroids. Whilst TNF inhibitors are currently unlicensed for this use in the UK, there is a growing body of evidence for their effectiveness in treating refractory extra-pulmonary sarcoidosis.

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Marotta, Dario A., and Hassan Kesserwani. "Association Between Treatment-Resistant Sarcoid Myopathy and Inclusion Body Myositis." Cureus, January 14, 2020. http://dx.doi.org/10.7759/cureus.6656.

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"0252 Cellular distribution of proteolytic enzymes in the skeletal muscle of sarcoid myopathy." Journal of the Neurological Sciences 238 (January 2005): S164. http://dx.doi.org/10.1016/s0022-510x(05)80623-9.

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