Researchers Database

nagashima takao

    InternalMedicineRheumatology&ClinicalImmunology Associate Professor
Last Updated :2021/12/08

Researcher Information

J-Global ID

Research Interests

  • MRL-lpr   全身性エリテマトーデス   lpr   スタチン   フルバスタチン   アポトーシス   lprマウス   Fluvastatin   

Research Areas

  • Life sciences / Infectious disease
  • Life sciences / Allergies and connective tissue disease

Academic & Professional Experience

  • 2004  Jichi Medical University助手

Published Papers

  • Jun Nakamura, Takao Nagashima, Katsuya Nagatani, Taku Yoshio, Masahiro Iwamoto, Seiji Minota
    INTERNATIONAL JOURNAL OF RHEUMATIC DISEASES 19 (5) 470 - 475 1756-1841 2016/05 [Refereed][Not invited]
    Objective: To examine the incidence of hepatitis B virus (HBV) reactivation in patients with rheumatoid arthritis (RA) receiving biological disease-modifying antirheumatic drugs (DMARDs). Methods: We retrospectively reviewed RA patients treated with biological DMARDs at our institution from July 2010 to December 2012. Patients with antibodies for hepatitis B core antigen and/or hepatitis B surface antigen were regarded as having prior HBV infection. Clinical data on these patients, including HBV-DNA levels, were retrieved from the medical records. Results: During the study period, 251 patients were administered various biological DMARDs. Six patients with a history of HBV vaccination and one patient with positive HBV surface antigen were excluded from the study. Fifty-seven of the remaining 244 patients (23.4%) had prior HBV infection. These patients were followed for a median of 18 months (range: 2-27 months) and HBV-DNA was examined a median of seven times (range: 227). HBV-DNA was detected in three patients (5.3%), comprising two receiving tocilizumab and one receiving etanercept. However, HBV-DNA levels were below the quantitation limit (<2.1 log copies mL(-1)) in all three patients. HBV-DNA became negative again within several months in all three patients, while biological DMARDs were continued and liver function tests remained normal throughout. Conclusion: HBV-DNA reactivation occurred in 5.3% of RA patients with prior HBV infection during treatment with biological DMARDs, but there were no associated clinical manifestations. Accordingly, it seems that biological DMARDs can be used safely in patients with RA.
  • Takao Nagashima, Seiji Minota
    RHEUMATOLOGY INTERNATIONAL 34 (7) 1025 - 1026 0172-8172 2014/07 [Refereed][Not invited]
  • Takamasa Murosaki, Takao Nagashima, Kyoko Honne, Yoko Aoki, Seiji Minota
    INTERNATIONAL JOURNAL OF RHEUMATIC DISEASES 17 (4) 476 - 478 1756-1841 2014/05 [Refereed][Not invited]
  • Takao Nagashima, Kazuko Matsumoto, Takamasa Murosaki, Mari Okada, Masahiro Iwamoto, Shinji Makino, Seiji Minota
    Rheumatology International 33 (7) 1915 - 1916 0172-8172 2013/07 [Refereed][Not invited]
  • Kyoko Honne, Takao Nagashima, Sachiko Onishi, Katsuya Nagatani, Masahiro Iwamoto, Seiji Minota
    Journal of Clinical Rheumatology 19 (2) 104 - 105 1076-1608 2013/03 [Refereed][Not invited]
  • Akihito Maruyama, Takao Nagashima, Yasuyuki Kamata, Katsuya Nagatani, Takamasa Murosaki, Taku Yoshio, Seiji Minota
    Rheumatology International 33 (1) 267 - 268 0172-8172 2013/01 [Refereed][Not invited]
  • Akihito Maruyama, Takao Nagashima, Kohei Ikenoya, Yoko Aoki, Yasushi Matsuyama, Masahiro Iwamoto, Seiji Minota
    INTERNAL MEDICINE 52 (16) 1833 - 1837 0918-2918 2013 [Refereed][Not invited]
    We herein report the findings of 2 cases of normotensive scleroderma renal crisis (SRC) that developed soon after the commencement of a glucocorticoid therapy. We also review 8 cases of normotensive SRC reported in Japan, including our cases. The common characteristics of these 8 cases are as follows: the recent onset of systemic sclerosis, the presence of diffuse skin sclerosis, the presence of myositis and/or serositis, a high titer of antinuclear antibody and positivity for anti-Scl-70 antibody. In 7 of the 8 patients, thrombotic microangiopathy developed within one month of starting the glucocorticoid treatment. We should be careful with the use of glucocorticoids in systemic sclerosis patients exhibiting these features in order to avoid cases of normotensive SRC.
  • Jun Nakamura, Takao Nagashima, Yoichiro Akiyama, Seiji Minota
    Internal Medicine 52 (24) 2837  0918-2918 2013 [Refereed][Not invited]
  • Takao Nagashima, Hitoaki Okazaki, Yasuyuki Kamata, Seiji Minota
    MODERN RHEUMATOLOGY 4 22 (4) 638 - 639 1439-7595 2012/08 [Refereed][Not invited]
  • Takao Nagashima, Akihito Maruyama, Yasuyuki Kamata, Seiji Minota
    RHEUMATOLOGY INTERNATIONAL 32 (7) 2231 - 2232 0172-8172 2012/07 [Refereed][Not invited]
  • Takao Nagashima, Akihito Maruyama, Shino Takatori, Meri Saito, Jun-ichi Osuga, Seiji Minota
    RHEUMATOLOGY INTERNATIONAL 32 (6) 1851 - 1852 0172-8172 2012/06 [Refereed][Not invited]
  • Yasushi Matsuyama, Hitoaki Okazaki, Motoaki Hoshino, Sachiko Onishi, Yasuyuki Kamata, Katsuya Nagatani, Takao Nagashima, Masahiro Iwamoto, Taku Yoshio, Hiromi Ohto-Ozaki, Hiroyuki Tamemoto, Mayumi Komine, Hitoshi Sekiya, Shin-ichi Tominaga, Seiji Minota
    RHEUMATOLOGY INTERNATIONAL 5 32 (5) 1397 - 1401 0172-8172 2012/05 [Refereed][Not invited]
    Although TNF inhibitors have dramatically improved the outcome of patients with rheumatoid arthritis, 30-40% of patients do not respond well to them and treatment needs to be changed. In an effort to discriminate good and poor responders, we focused on the change in serum and synovial fluid levels of interleukin (IL-) 33 before and after treatment with TNF inhibitors. They were also measured in synovial fluids from 17 TNF inhibitor-na < ve patients, and fibroblast-like synoviocytes (FLS) in-culture from 6 patients and correlated with various pro-inflammatory cytokines. Serum levels of IL-33 at 6 months after treatment decreased significantly in responders, while they did not change in non-responders. Synovial fluid levels of IL-33 in 6 patients under treatment with TNF inhibitors stayed high in 3 who were refractory and slightly elevated in 2 moderate responders, while they were undetectable in one patient under remission. Among inflammatory cytokines measured in 17 synovial fluids from TNF inhibitor-na < ve patients, levels of IL-33 showed a significant positive correlation only to those of IL-1 beta. IL-1 beta increased IL-33 expression markedly in FLS in vitro, compared to TNF-alpha. IL-1 beta might be inducing RA inflammation through producing pro-inflammatory IL-33 in TNF inhibitor-hypo-responders. Sustained elevation of serum and/or synovial levels of IL-33 may account for a poor response to TNF inhibitors, although how TNF inhibitors affect the level of IL-33 remains to be elucidated.
  • Masahiro Iwamoto, Takeshi Kamimura, Takao Nagashima, Yasuyuki Kamata, Yoko Aoki, Sachiko Onishi, Seiji Minota
    RHEUMATOLOGY INTERNATIONAL 32 (3) 801 - 804 0172-8172 2012/03 [Refereed][Not invited]
    Prospective observational study was performed to elucidate the incidence and characteristics of healthcare-associated infections in a university hospital for rheumatology care. In this study, a total of 1,226 patients were prospectively enrolled between March 2004 and February 2006 and between April 2008 and December 2008. Healthcare-associated infection was defined as an infection developing after the third day of admission to the rheumatology ward. We detected the following 54 healthcare-associated infections in 49 patients: respiratory tract infection, 14 cases; Clostridium difficile infection, 2 cases; urinary tract infection, 4 cases; bloodstream infection, 9 cases; skin infection, 2 cases; reactivation of latent cytomegalovirus infection, 6 cases; herpes zoster infection, 5 cases; Candida infection, 7 cases; others, 4 cases. The incidence rate of respiratory tract infection was the highest. Methicillin-resistant Staphylococcus aureus was the causative bacterium in 21% of respiratory tract infections cases. Bloodstream infection due to the insertion of a catheter and opportunistic infection by a latent virus were also occurred commonly. Respiratory tract infection, bloodstream infection and opportunistic infection by a latent virus were the most common causes of healthcare-associated infection in rheumatology. It is important to pay more attention to healthcare-associated infection.
  • Kazuko Matsumoto, Takao Nagashima, Masahiro Iwamoto, Seiji Minota
    INTERNATIONAL JOURNAL OF RHEUMATIC DISEASES 15 (1) e2 - e3 1756-1841 2012/02 [Refereed][Not invited]
  • Nagashima T, Iwamoto M, Matsumoto K, Minota S
    Internal medicine (Tokyo, Japan) 4 51 449; author reply 451  0918-2918 2012 [Refereed][Not invited]
  • Takamasa Murosaki, Takao Nagashima, Kazuko Matsumoto, Seiji Minota
    INTERNAL MEDICINE 51 (11) 1451 - 1451 0918-2918 2012 [Refereed][Not invited]
  • Takamasa Murosaki, Takao Nagashima, Yoko Aoki, Yukiko Imai, Masahiro Iwamoto, Seiji Minota
    INTERNAL MEDICINE 51 (22) 3181 - 3183 0918-2918 2012 [Refereed][Not invited]
    A 59-year-old woman with a 10-year history of rheumatoid arthritis (RA) presented with chronic ulcers on both feet while undergoing treatment with etanercept. Rheumatoid vasculitis (RV) was diagnosed, and the patient was treated with immunosuppressant drugs and skin grafting. Although anti-tumor necrosis factor (TNF) agents are known to induce vasculitis, vasculitis can also be caused by active RA. Accordingly, the cause of vasculitis in RA patients receiving anti-TNF therapy must be evaluated carefully.
  • Takao Nagashima, Masahiro Iwamoto, Seiji Minota
    CLINICAL RHEUMATOLOGY 30 (6) 875 - 876 0770-3198 2011/06 [Refereed][Not invited]
  • Takao Nagashima, Masahiro Iwamoto, Seiji Minota
    RHEUMATOLOGY INTERNATIONAL 31 (5) 705 - 706 0172-8172 2011/05 [Refereed][Not invited]
  • Takao Nagashima, Seiji Minota
    RHEUMATOLOGY 50 (5) 994 - 996 1462-0324 2011/05 [Refereed][Not invited]
  • Nagashima T, Minota S
    The Journal of rheumatology 3 38 574; author reply 575  0315-162X 2011/03 [Refereed][Not invited]
  • Yasushi Matsuyama, Takao Nagashima, Kyoko Honne, Yasuyuki Kamata, Masahiro Iwamoto, Hitoaki Okazaki, Kazuya Sato, Keiya Ozawa, Seiji Minota
    INTERNAL MEDICINE 6 50 (6) 639 - 642 0918-2918 2011 [Refereed][Not invited]
    A 63-year-old woman receiving tumor necrosis factor (TNF) inhibitors for rheumatoid arthritis (RA) was found to have smoldering IgA-kappa type multiple myeloma (MM). Retrospective examination of stored serum samples revealed a steady increase of serum IgA levels after the start of TNF inhibitor therapy. The patient's articular symptoms showed marked exacerbation when TNF inhibitors were discontinued because of fear of worsening the MM. Tocilizumab improved RA symptoms dramatically and stabilized serum IgA levels for 13 months after a transient steep rise. This case suggests that tocilizumab can be used safely in patients with inflammatory disorders with coexisting MM.
  • Sachiko Onishi, Taku Yoshio, Takao Nagashima, Seiji Minota
    MODERN RHEUMATOLOGY 5 20 (5) 528 - 530 1439-7595 2010/10 [Refereed][Not invited]
  • Kyoko Honne, Akihito Maruyama, Sachiko Onishi, Takao Nagashima, Seiji Minota
    JOURNAL OF RHEUMATOLOGY 37 (10) 2194 - 2196 0315-162X 2010/10 [Refereed][Not invited]
  • Takao Nagashima, Toshimi Imai, Kazuko Matsumoto, Sachiko Onishi, Shino Takatori, Masahiro Iwamoto, Seiji Minota
    RHEUMATOLOGY INTERNATIONAL 30 (11) 1549 - 1550 0172-8172 2010/09 [Refereed][Not invited]
  • Takao Nagashima, Seiji Minota
    CLINICAL RHEUMATOLOGY 29 (7) 819 - 820 0770-3198 2010/07 [Refereed][Not invited]
  • Takao Nagashima, Seiji Minota
    JOURNAL OF RHEUMATOLOGY 37 (5) 1066 - 1066 0315-162X 2010/05 [Refereed][Not invited]
  • Takao Nagashima, Seiji Minota
    CLINICAL RHEUMATOLOGY 29 (4) 449 - 450 0770-3198 2010/04 [Refereed][Not invited]
  • Yasushi Matsuyama, Hitoaki Okazaki, Hiroyuki Tamemoto, Hirotaka Kimura, Yasuyuki Kamata, Katsuya Nagatani, Takao Nagashima, Morisada Hayakawa, Masahiro Iwamoto, Taku Yoshio, Shin-Ichi Tominaga, Seiji Minota
    JOURNAL OF RHEUMATOLOGY 37 (1) 18 - 25 0315-162X 2010/01 [Refereed][Not invited]
    Objective. To determine levels of interleukin 33 (IL-33) in serum and synovial fluid (SF) and their clinical associations in patients with rheumatoid arthritis (RA). To evaluate the ability of activated peripheral blood mononuclear cells (PBMC) and fibroblast-like synoviocytes (FLS) from RA patients to release IL-33. Methods. Sera were obtained from 59 patients with RA, 10 patients with infectious diseases, and 42 healthy volunteers. SF samples were obtained from 15 patients with RA and 13 with osteoarthritis. IL-33 levels were measured using a sandwich ELISA after removal of rheumatoid factor with protein A-Sepharose beads. FLS were stimulated with IL-1 beta and tumor necrosis factor, and treated with or without chemical damage. PBMC were stimulated with anti-CD3/CD28 antibodies. The levels of IL-33 were measured in the culture supernatants and cell lysates by ELISA or immunoblotting. Results. Serum IL-33 levels were significantly higher in RA patients, especially in the high disease activity group compared to the moderate or low activity group. IL-33 levels in SF were elevated in all 15 RA patients measured. IL-33 levels were higher in SF samples than in sera in 7 RA patients measured simultaneously. The 30-kDa IL-33 precursor was detected in the culture supernatants of damaged FLS but was not detected in those of activated PBMC and non-damaged FLS. Conclusion. IL-33 levels were elevated in sera and SF samples from patients with RA, and correlated with disease activity. IL-33 was produced mainly in inflamed joints; IL-33/ST2L signaling might play an important role in joint inflammation of human RA. (First Release Nov 15 2009; J Rheumatol 2010;37;18-25; doi:10.3899/jrheum.090492)
  • Yoko Aoki, Masahiro Iwamoto, Yasuyuki Kamata, Takao Nagashima, Taku Yoshio, Hitoaki Okazaki, Seiji Minota
    RHEUMATOLOGY INTERNATIONAL 29 (11) 1327 - 1330 0172-8172 2009/09 [Refereed][Not invited]
    The objective of this study is to investigate the clinical markers of life-threatening Pneumocystis pneumonia (PCP) in patients with collagen vascular diseases (CVD). The patients who contracted Pneumocystis jeroveccii were retrospectively selected from our medical charts and conditions related to the patients' death were reviewed. The findings indicated that lower levels of serum albumin and cholinesterase, increased alveolar-arterial oxygen gradient, intratracheal intubation, and necessity to treat in the intensive care unit were significantly related to deaths associated with PCP in CVD. A special attention should be paid to decreased serum albumin and cholinesterase as ominous predictors in PCP occurred in patients with CVD.
  • Takao Nagashima, Hidetomo Sato, Seiji Minota
    JOURNAL OF RHEUMATOLOGY 36 (9) 2133 - 2134 0315-162X 2009/09 [Refereed][Not invited]
  • Takao Nagashima, Sachiko Onishi, Yasuyuki Kamata, Seiji Minota
    RHEUMATOLOGY INTERNATIONAL 29 (10) 1261 - 1262 0172-8172 2009/08 [Refereed][Not invited]
  • Takao Nagashima, Motoaki Hoshino, Shin Shimoji, Noritsugu Morino, Takeshi Kamimura, Hitoaki Okazaki, Seiji Minota
    RHEUMATOLOGY INTERNATIONAL 7 29 (7) 817 - 820 0172-8172 2009/05 [Refereed][Not invited]
    Protein-losing gastroenteropathy (PLGE) is a rare manifestation of primary Sjogren's syndrome (SS). We report a case of a 41-year-old Japanese man, who is the first male patient, with PLGE associated with primary SS. Although serum anti-SSA and SSB antibodies were detected, he had no subjective sicca symptoms. He had multiple annular erythema: a characteristic skin manifestation of Asian SS patients. A diagnosis of PLGE was made from results of Tc-99m-labelled albumin scintigraphy and a faecal alpha-1-antitrypsin clearance test. Intravenous administration of high-dose glucocorticoid was not effective, but pulse methylprednisolone therapy alleviated disease manifestations. As all cases of PLGE associated with primary SS have been reported from East Asia, this complication could be essentially limited to Asian patients.
  • Ken Futaki, Mayumi Komine, Satomi Hosoda, Miho Hirashima, Hideto Yokokura, Tomoko Yamada, Satoru Murata, Yasushi Matsuyama, Takao Nagashima, Hiroyuki Nara, Seiji Minota, Mamitaro Ohtsuki
    EUROPEAN JOURNAL OF DERMATOLOGY 19 (3) 266 - 267 1167-1122 2009/05 [Refereed][Not invited]
  • Kazuko Matsumoto, Takao Nagashima, Shino Takatori, Yuta Kawahara, Masaki Yagi, Masahiro Iwamoto, Hitoaki Okazaki, Seiji Minota
    CLINICAL RHEUMATOLOGY 28 (4) 485 - 487 0770-3198 2009/04 [Refereed][Not invited]
    We report a 29-year-old Japanese woman with disseminated intravascular coagulation (DIC) and adult onset Still's disease (AOSD). Her disease was refractory to high-dose glucocorticoids, two courses of steroid pulse therapy, and addition of cyclosporine (3.5 mg/kg/day). The serum interleukin-6 level was markedly elevated. Therefore, we administered an anti-interleukin-6 receptor antibody (tocilizumab, 8 mg/kg fortnightly), which dramatically improved her symptoms and the levels of acute-phase proteins. In addition, rapid tapering of the glucocorticoid dose was possible. Four months later, she was maintained on tocilizumab infusion once a month with low-dose steroid therapy. Cyclosporine is one of the first-line immunosuppressants for AOSD, especially when associated with DIC, hepatic failure, or hemophagocytic syndrome. In patients with cyclosporine-resistant AOSD, tocilizumab may be another useful option.
  • Takao Nagashima, Yoko Aoki, Sachiko Onishi, Masahiro Iwamoto, Hitoaki Okazaki, Seiji Minota
    CLINICAL RHEUMATOLOGY 27 (11) 1451 - 1453 0770-3198 2008/11 [Refereed][Not invited]
    We report two Japanese women with severe hepatic dysfunction and adult onset Still's disease. A 51-year-old woman had been diagnosed with adult onset Still's disease 3 years earlier. She relapsed while on maintenance therapy with prednisolone and methotrexate. After induction of remission with methylprednisolone pulse therapy, indomethacin, and methotrexate, severe hepatic failure occurred. This patient lacked the typical symptoms of adult onset Still's disease. The second patient was a 32-year-old woman with typical adult onset Still's disease. Remission was induced by high-dose prednisolone and methylprednisolone pulse therapy plus cyclosporine. After she stopped cyclosporine, severe liver dysfunction occurred. In both patients, liver dysfunction occurred during high-dose steroid therapy, and oral cyclosporine (3 mg/kg per day) dramatically improved their liver function. When steroid-resistant severe hepatic failure occurs in patients with adult onset Still's disease, cyclosporine may be the immunosuppressant of choice.
  • Takao Nagashima, Kazuko Matsumoto, Reiko Yamamoto, Masahiro Iwamoto, Seiji Minota
    RHEUMATOLOGY INTERNATIONAL 28 (10) 1065 - 1066 0172-8172 2008/08 [Refereed][Not invited]
  • Takao Nagashima, Hikaru Okubo-Fornbacher, Yoko Aoki, Yasuyuki Kamata, Hirotaka Kimura, Takeshi Kamimura, Hiroyuki Nara, Masahiro Iwamoto, Taku Yoshio, Hitoaki Okazaki, Seiji Minota
    JOURNAL OF RHEUMATOLOGY 35 (5) 936 - 938 0315-162X 2008/05 [Refereed][Not invited]
  • Takao Nagashima, Masahiro Iwamoto, Seiji Minota
    Modern Rheumatology 16 (5) 330 - 331 1439-7595 2006/10 [Refereed][Not invited]
  • Yoko Aoki, Takao Nagashima, Takeshi Kamimura, Masahiro Iwamoto, Seiji Minota
    JOURNAL OF RHEUMATOLOGY 33 (8) 1705 - 1706 0315-162X 2006/08 [Refereed][Not invited]
  • Nagashima T, Kamimura T, Nara H, Iwamoto M, Okazaki H, Minota S
    Circulation 1 114 e10 - 1 0009-7322 2006/07 [Refereed][Not invited]
  • T Nagashima, H Okazaki, K Yudoh, H Matsuno, S Minota
    ARTHRITIS AND RHEUMATISM 54 (2) 579 - 586 0004-3591 2006/02 [Refereed][Not invited]
    Objective. To determine whether statins induce apoptosis in rheumatoid arthritis (RA) synoviocytes. Methods. The effects of lipophilic and hydrophilic statins (fluvastatin and pravastatin, respectively) on the apoptosis of cultured RA synoviocytes were examined in vitro. Apoptosis was analyzed by flow cytometry after staining with JC-1. (to measure the mitochondrial transmembrane potential), active caspase 3, annexin V, and propidium iodide. Add-back experiments were conducted to determine which downstream products of the mevalonate pathway could suppress apoptosis. Modulation of various signaling pathways induced by statins, including protein prenylation, was also investigated. Results. Fluvastatin, but not pravastatin, induced apoptosis in RA synoviocytes in a concentration-dependent (1-1.0 mu M) and time-dependent (48-96 hours) manner. Another lipophilic statin, pitavastatin, displayed almost the same effects as fluvastatin. In sharp contrast lipophilic statins did not significantly increase apoptosis in synoviocytes from patients with ostcoarthropathy. Apoptosis induced by fluvastatin was mitochondrial- and caspase 3-dependent and was abrogated by mevalonate and geranylgeranyl pyrophosphate, but not by farnesyl pyrophosphate. In addition, the geranylgeranyl transferase inhibitor GGTI-298 mim-icked the effect of fluvastatin on RA synoviocytes. Treatment of RA synoviocytes with the RhoA kinase inhibitor Y-27632 caused apoptosis. Fluvastatin decreased the amount of RhoA protein in the membrane fraction, but increased the amount in the cytosolic fraction. Conclusion. Fluvastatin induced apoptosis in RA synoviocytes through a mitochondrial- and caspase 3-dependent pathway and by the blockage of mevalonate pathways, particularly through the inhibition of protein geranylgeranylation and RhoA/RhoA kinase pathways. These findings suggest that lipophilic statins have potential as novel therapeutic agents for RA.
  • T Nagashima, J Masuyama, H Okubo, S Minota
    JOURNAL OF RHEUMATOLOGY 32 (6) 1168 - 1169 0315-162X 2005/06 [Refereed][Not invited]
  • Okazaki H, Nagashima T, Minota S
    Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology 6 27 357 - 360 0911-4300 2004/12 [Refereed][Not invited]
  • Daisuke Hirata, Takao Nagashima, Shin Saito, Hitoaki Okazaki, Shogo Kano, Seiji Minota
    Modern Rheumatology 12 (2) 186 - 189 1439-7595 2002 [Refereed][Not invited]
    We report a case of hypocalcemic myopathy confounded by polymyositis due to an elevated level of serum creatine kinase (CK). A 30-year-old man was referred to our hospital for the treatment of provisionally diagnosed polymyositis. His presentation with tetany, hyporeflexia, and general fatigue, in addition to muscle weakness on admission, prompted us to scrutinize a blood sample in search of secondary myopathy. Blood chemistry revealed an elevated level of serum CK, marked hypocalcemia, hyperphosphatemia, and a low serum level of intact parathyroid hormone. The Ellsworth Howard test confirmed the diagnosis of hypoparathyroidism. Supplementation with calcium and 1α-hydroxyvitamin D3 improved his muscle weakness rapidly, and his serum CK level returned to the normal range. Hypoparathyroidism should be included in differential diagnoses of elevated serum CK.
  • Nagashima T, Hirata D, Yamamoto H, Okazaki H, Minota S
    American journal of kidney diseases : the official journal of the National Kidney Foundation 5 37 E38  0272-6386 2001/05 [Refereed][Not invited]


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