Clinical and laboratory features of hyponatremia-induced myopathy

Background The present study was undertaken to determine the clinical and laboratory features of hyponatremia-induced myopathy. Methods We collected 14 hyponatremic subjects (six men and eight women) with serum creatine kinase (CK) levels of more than 500 IU/ml during the 5-year period between 2001...
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Autor*in:	Sasaki, Masami [verfasserIn] Yuzawa, Miho [verfasserIn] Saito, Tomoyuki [verfasserIn] Ikoma, Aki [verfasserIn] Tamemoto, Hiroyuki [verfasserIn] Kawakami, Masanobu [verfasserIn] Ishikawa, San-e [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2007

Übergeordnetes Werk:	Enthalten in: Clinical and experimental nephrology - [Tokyo] : Springer, 1997, 11(2007), 4 vom: 01. Dez., Seite 283-286
Übergeordnetes Werk:	volume:11 ; year:2007 ; number:4 ; day:01 ; month:12 ; pages:283-286

Links:	Volltext

DOI / URN:	10.1007/s10157-007-0494-3

Katalog-ID:	SPR008962081

Internformat


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520			\|a Background The present study was undertaken to determine the clinical and laboratory features of hyponatremia-induced myopathy. Methods We collected 14 hyponatremic subjects (six men and eight women) with serum creatine kinase (CK) levels of more than 500 IU/ml during the 5-year period between 2001 and 2005. The mean ± SD patients’ age was 66.5 ± 16.7 years (range, 37 to 88 years). Results The causes of the hyponatremia were: syndrome of inappropriate secretion of antidiuretic hormone (SIADH; n = 4), mineralocorticoid-responsive hyponatremia of the elderly (MRHE; n = 2), hypopituitarism (n = 1), psychogenic polydipsia (n = 3), congestive heart failure (n = 3), and unknown cause (n = 1). The subjects were subgrouped into two groups: acute onset of myopathy and slowly progressive onset. The age at onset was 62.0 ± 5.7 years (mean ± SEM) in the subjects with acute onset, and 77.8 ± 1.5 years in those with slowly progressive onset (P = 0.02). At the onset, there was no difference in serum Na levels between the acute onset and the slowly progressive onset groups, but there was a significant difference in maximal serum CK levels between the groups (7072 ± 2317 vs 722 ± 104 IU/ml; P = 0.02). Maximal serum CK levels were widely distributed among the ages in the subjects with acute onset, whereas maximal serum CK levels were mildly elevated in the elderly subjects with slowly progressive onset. The elevated serum CK levels were normalized at a maximum of 14 days after the onset in all the subjects. Conclusions The present findings indicate that hyponatremia infrequently causes skeletal muscle disruption, and that there are two types of hyponatremia-induced myopathy, acute onset and slowly progressive onset.
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700	1		\|a Saito, Tomoyuki \|e verfasserin \|4 aut
700	1		\|a Ikoma, Aki \|e verfasserin \|4 aut
700	1		\|a Tamemoto, Hiroyuki \|e verfasserin \|4 aut
700	1		\|a Kawakami, Masanobu \|e verfasserin \|4 aut
700	1		\|a Ishikawa, San-e \|e verfasserin \|4 aut
773	0	8	\|i Enthalten in \|t Clinical and experimental nephrology \|d [Tokyo] : Springer, 1997 \|g 11(2007), 4 vom: 01. Dez., Seite 283-286 \|w (DE-627)306646900 \|w (DE-600)1499111-1 \|x 1437-7799 \|7 nnns
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912			\|a GBV_ILN_2057
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912			\|a GBV_ILN_2064
912			\|a GBV_ILN_2065
912			\|a GBV_ILN_2068
912			\|a GBV_ILN_2070
912			\|a GBV_ILN_2086
912			\|a GBV_ILN_2088
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author_variant	m s ms m y my t s ts a i ai h t ht m k mk s e i sei
matchkey_str	article:14377799:2007----::lnclnlbrtrfaueohpntei
hierarchy_sort_str	2007
bklnumber	44.88
publishDate	2007
allfields	10.1007/s10157-007-0494-3 doi (DE-627)SPR008962081 (SPR)s10157-007-0494-3-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.88 bkl Sasaki, Masami verfasserin aut Clinical and laboratory features of hyponatremia-induced myopathy 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The present study was undertaken to determine the clinical and laboratory features of hyponatremia-induced myopathy. Methods We collected 14 hyponatremic subjects (six men and eight women) with serum creatine kinase (CK) levels of more than 500 IU/ml during the 5-year period between 2001 and 2005. The mean ± SD patients’ age was 66.5 ± 16.7 years (range, 37 to 88 years). Results The causes of the hyponatremia were: syndrome of inappropriate secretion of antidiuretic hormone (SIADH; n = 4), mineralocorticoid-responsive hyponatremia of the elderly (MRHE; n = 2), hypopituitarism (n = 1), psychogenic polydipsia (n = 3), congestive heart failure (n = 3), and unknown cause (n = 1). The subjects were subgrouped into two groups: acute onset of myopathy and slowly progressive onset. The age at onset was 62.0 ± 5.7 years (mean ± SEM) in the subjects with acute onset, and 77.8 ± 1.5 years in those with slowly progressive onset (P = 0.02). At the onset, there was no difference in serum Na levels between the acute onset and the slowly progressive onset groups, but there was a significant difference in maximal serum CK levels between the groups (7072 ± 2317 vs 722 ± 104 IU/ml; P = 0.02). Maximal serum CK levels were widely distributed among the ages in the subjects with acute onset, whereas maximal serum CK levels were mildly elevated in the elderly subjects with slowly progressive onset. The elevated serum CK levels were normalized at a maximum of 14 days after the onset in all the subjects. Conclusions The present findings indicate that hyponatremia infrequently causes skeletal muscle disruption, and that there are two types of hyponatremia-induced myopathy, acute onset and slowly progressive onset. Yuzawa, Miho verfasserin aut Saito, Tomoyuki verfasserin aut Ikoma, Aki verfasserin aut Tamemoto, Hiroyuki verfasserin aut Kawakami, Masanobu verfasserin aut Ishikawa, San-e verfasserin aut Enthalten in Clinical and experimental nephrology [Tokyo] : Springer, 1997 11(2007), 4 vom: 01. Dez., Seite 283-286 (DE-627)306646900 (DE-600)1499111-1 1437-7799 nnns volume:11 year:2007 number:4 day:01 month:12 pages:283-286 https://dx.doi.org/10.1007/s10157-007-0494-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.88 ASE AR 11 2007 4 01 12 283-286
spelling	10.1007/s10157-007-0494-3 doi (DE-627)SPR008962081 (SPR)s10157-007-0494-3-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.88 bkl Sasaki, Masami verfasserin aut Clinical and laboratory features of hyponatremia-induced myopathy 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The present study was undertaken to determine the clinical and laboratory features of hyponatremia-induced myopathy. Methods We collected 14 hyponatremic subjects (six men and eight women) with serum creatine kinase (CK) levels of more than 500 IU/ml during the 5-year period between 2001 and 2005. The mean ± SD patients’ age was 66.5 ± 16.7 years (range, 37 to 88 years). Results The causes of the hyponatremia were: syndrome of inappropriate secretion of antidiuretic hormone (SIADH; n = 4), mineralocorticoid-responsive hyponatremia of the elderly (MRHE; n = 2), hypopituitarism (n = 1), psychogenic polydipsia (n = 3), congestive heart failure (n = 3), and unknown cause (n = 1). The subjects were subgrouped into two groups: acute onset of myopathy and slowly progressive onset. The age at onset was 62.0 ± 5.7 years (mean ± SEM) in the subjects with acute onset, and 77.8 ± 1.5 years in those with slowly progressive onset (P = 0.02). At the onset, there was no difference in serum Na levels between the acute onset and the slowly progressive onset groups, but there was a significant difference in maximal serum CK levels between the groups (7072 ± 2317 vs 722 ± 104 IU/ml; P = 0.02). Maximal serum CK levels were widely distributed among the ages in the subjects with acute onset, whereas maximal serum CK levels were mildly elevated in the elderly subjects with slowly progressive onset. The elevated serum CK levels were normalized at a maximum of 14 days after the onset in all the subjects. Conclusions The present findings indicate that hyponatremia infrequently causes skeletal muscle disruption, and that there are two types of hyponatremia-induced myopathy, acute onset and slowly progressive onset. Yuzawa, Miho verfasserin aut Saito, Tomoyuki verfasserin aut Ikoma, Aki verfasserin aut Tamemoto, Hiroyuki verfasserin aut Kawakami, Masanobu verfasserin aut Ishikawa, San-e verfasserin aut Enthalten in Clinical and experimental nephrology [Tokyo] : Springer, 1997 11(2007), 4 vom: 01. Dez., Seite 283-286 (DE-627)306646900 (DE-600)1499111-1 1437-7799 nnns volume:11 year:2007 number:4 day:01 month:12 pages:283-286 https://dx.doi.org/10.1007/s10157-007-0494-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.88 ASE AR 11 2007 4 01 12 283-286
allfields_unstemmed	10.1007/s10157-007-0494-3 doi (DE-627)SPR008962081 (SPR)s10157-007-0494-3-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.88 bkl Sasaki, Masami verfasserin aut Clinical and laboratory features of hyponatremia-induced myopathy 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The present study was undertaken to determine the clinical and laboratory features of hyponatremia-induced myopathy. Methods We collected 14 hyponatremic subjects (six men and eight women) with serum creatine kinase (CK) levels of more than 500 IU/ml during the 5-year period between 2001 and 2005. The mean ± SD patients’ age was 66.5 ± 16.7 years (range, 37 to 88 years). Results The causes of the hyponatremia were: syndrome of inappropriate secretion of antidiuretic hormone (SIADH; n = 4), mineralocorticoid-responsive hyponatremia of the elderly (MRHE; n = 2), hypopituitarism (n = 1), psychogenic polydipsia (n = 3), congestive heart failure (n = 3), and unknown cause (n = 1). The subjects were subgrouped into two groups: acute onset of myopathy and slowly progressive onset. The age at onset was 62.0 ± 5.7 years (mean ± SEM) in the subjects with acute onset, and 77.8 ± 1.5 years in those with slowly progressive onset (P = 0.02). At the onset, there was no difference in serum Na levels between the acute onset and the slowly progressive onset groups, but there was a significant difference in maximal serum CK levels between the groups (7072 ± 2317 vs 722 ± 104 IU/ml; P = 0.02). Maximal serum CK levels were widely distributed among the ages in the subjects with acute onset, whereas maximal serum CK levels were mildly elevated in the elderly subjects with slowly progressive onset. The elevated serum CK levels were normalized at a maximum of 14 days after the onset in all the subjects. Conclusions The present findings indicate that hyponatremia infrequently causes skeletal muscle disruption, and that there are two types of hyponatremia-induced myopathy, acute onset and slowly progressive onset. Yuzawa, Miho verfasserin aut Saito, Tomoyuki verfasserin aut Ikoma, Aki verfasserin aut Tamemoto, Hiroyuki verfasserin aut Kawakami, Masanobu verfasserin aut Ishikawa, San-e verfasserin aut Enthalten in Clinical and experimental nephrology [Tokyo] : Springer, 1997 11(2007), 4 vom: 01. Dez., Seite 283-286 (DE-627)306646900 (DE-600)1499111-1 1437-7799 nnns volume:11 year:2007 number:4 day:01 month:12 pages:283-286 https://dx.doi.org/10.1007/s10157-007-0494-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.88 ASE AR 11 2007 4 01 12 283-286
allfieldsGer	10.1007/s10157-007-0494-3 doi (DE-627)SPR008962081 (SPR)s10157-007-0494-3-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.88 bkl Sasaki, Masami verfasserin aut Clinical and laboratory features of hyponatremia-induced myopathy 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The present study was undertaken to determine the clinical and laboratory features of hyponatremia-induced myopathy. Methods We collected 14 hyponatremic subjects (six men and eight women) with serum creatine kinase (CK) levels of more than 500 IU/ml during the 5-year period between 2001 and 2005. The mean ± SD patients’ age was 66.5 ± 16.7 years (range, 37 to 88 years). Results The causes of the hyponatremia were: syndrome of inappropriate secretion of antidiuretic hormone (SIADH; n = 4), mineralocorticoid-responsive hyponatremia of the elderly (MRHE; n = 2), hypopituitarism (n = 1), psychogenic polydipsia (n = 3), congestive heart failure (n = 3), and unknown cause (n = 1). The subjects were subgrouped into two groups: acute onset of myopathy and slowly progressive onset. The age at onset was 62.0 ± 5.7 years (mean ± SEM) in the subjects with acute onset, and 77.8 ± 1.5 years in those with slowly progressive onset (P = 0.02). At the onset, there was no difference in serum Na levels between the acute onset and the slowly progressive onset groups, but there was a significant difference in maximal serum CK levels between the groups (7072 ± 2317 vs 722 ± 104 IU/ml; P = 0.02). Maximal serum CK levels were widely distributed among the ages in the subjects with acute onset, whereas maximal serum CK levels were mildly elevated in the elderly subjects with slowly progressive onset. The elevated serum CK levels were normalized at a maximum of 14 days after the onset in all the subjects. Conclusions The present findings indicate that hyponatremia infrequently causes skeletal muscle disruption, and that there are two types of hyponatremia-induced myopathy, acute onset and slowly progressive onset. Yuzawa, Miho verfasserin aut Saito, Tomoyuki verfasserin aut Ikoma, Aki verfasserin aut Tamemoto, Hiroyuki verfasserin aut Kawakami, Masanobu verfasserin aut Ishikawa, San-e verfasserin aut Enthalten in Clinical and experimental nephrology [Tokyo] : Springer, 1997 11(2007), 4 vom: 01. Dez., Seite 283-286 (DE-627)306646900 (DE-600)1499111-1 1437-7799 nnns volume:11 year:2007 number:4 day:01 month:12 pages:283-286 https://dx.doi.org/10.1007/s10157-007-0494-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.88 ASE AR 11 2007 4 01 12 283-286
allfieldsSound	10.1007/s10157-007-0494-3 doi (DE-627)SPR008962081 (SPR)s10157-007-0494-3-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.88 bkl Sasaki, Masami verfasserin aut Clinical and laboratory features of hyponatremia-induced myopathy 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The present study was undertaken to determine the clinical and laboratory features of hyponatremia-induced myopathy. Methods We collected 14 hyponatremic subjects (six men and eight women) with serum creatine kinase (CK) levels of more than 500 IU/ml during the 5-year period between 2001 and 2005. The mean ± SD patients’ age was 66.5 ± 16.7 years (range, 37 to 88 years). Results The causes of the hyponatremia were: syndrome of inappropriate secretion of antidiuretic hormone (SIADH; n = 4), mineralocorticoid-responsive hyponatremia of the elderly (MRHE; n = 2), hypopituitarism (n = 1), psychogenic polydipsia (n = 3), congestive heart failure (n = 3), and unknown cause (n = 1). The subjects were subgrouped into two groups: acute onset of myopathy and slowly progressive onset. The age at onset was 62.0 ± 5.7 years (mean ± SEM) in the subjects with acute onset, and 77.8 ± 1.5 years in those with slowly progressive onset (P = 0.02). At the onset, there was no difference in serum Na levels between the acute onset and the slowly progressive onset groups, but there was a significant difference in maximal serum CK levels between the groups (7072 ± 2317 vs 722 ± 104 IU/ml; P = 0.02). Maximal serum CK levels were widely distributed among the ages in the subjects with acute onset, whereas maximal serum CK levels were mildly elevated in the elderly subjects with slowly progressive onset. The elevated serum CK levels were normalized at a maximum of 14 days after the onset in all the subjects. Conclusions The present findings indicate that hyponatremia infrequently causes skeletal muscle disruption, and that there are two types of hyponatremia-induced myopathy, acute onset and slowly progressive onset. Yuzawa, Miho verfasserin aut Saito, Tomoyuki verfasserin aut Ikoma, Aki verfasserin aut Tamemoto, Hiroyuki verfasserin aut Kawakami, Masanobu verfasserin aut Ishikawa, San-e verfasserin aut Enthalten in Clinical and experimental nephrology [Tokyo] : Springer, 1997 11(2007), 4 vom: 01. Dez., Seite 283-286 (DE-627)306646900 (DE-600)1499111-1 1437-7799 nnns volume:11 year:2007 number:4 day:01 month:12 pages:283-286 https://dx.doi.org/10.1007/s10157-007-0494-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.88 ASE AR 11 2007 4 01 12 283-286
language	English
source	Enthalten in Clinical and experimental nephrology 11(2007), 4 vom: 01. Dez., Seite 283-286 volume:11 year:2007 number:4 day:01 month:12 pages:283-286
sourceStr	Enthalten in Clinical and experimental nephrology 11(2007), 4 vom: 01. Dez., Seite 283-286 volume:11 year:2007 number:4 day:01 month:12 pages:283-286
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container_title	Clinical and experimental nephrology
authorswithroles_txt_mv	Sasaki, Masami @@aut@@ Yuzawa, Miho @@aut@@ Saito, Tomoyuki @@aut@@ Ikoma, Aki @@aut@@ Tamemoto, Hiroyuki @@aut@@ Kawakami, Masanobu @@aut@@ Ishikawa, San-e @@aut@@
publishDateDaySort_date	2007-12-01T00:00:00Z
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id	SPR008962081
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Methods We collected 14 hyponatremic subjects (six men and eight women) with serum creatine kinase (CK) levels of more than 500 IU/ml during the 5-year period between 2001 and 2005. The mean ± SD patients’ age was 66.5 ± 16.7 years (range, 37 to 88 years). Results The causes of the hyponatremia were: syndrome of inappropriate secretion of antidiuretic hormone (SIADH; n = 4), mineralocorticoid-responsive hyponatremia of the elderly (MRHE; n = 2), hypopituitarism (n = 1), psychogenic polydipsia (n = 3), congestive heart failure (n = 3), and unknown cause (n = 1). The subjects were subgrouped into two groups: acute onset of myopathy and slowly progressive onset. The age at onset was 62.0 ± 5.7 years (mean ± SEM) in the subjects with acute onset, and 77.8 ± 1.5 years in those with slowly progressive onset (P = 0.02). 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author	Sasaki, Masami
spellingShingle	Sasaki, Masami ddc 610 bkl 44.88 Clinical and laboratory features of hyponatremia-induced myopathy
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topic_title	610 ASE 44.88 bkl Clinical and laboratory features of hyponatremia-induced myopathy
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title	Clinical and laboratory features of hyponatremia-induced myopathy
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title_full	Clinical and laboratory features of hyponatremia-induced myopathy
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author_browse	Sasaki, Masami Yuzawa, Miho Saito, Tomoyuki Ikoma, Aki Tamemoto, Hiroyuki Kawakami, Masanobu Ishikawa, San-e
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title_sort	clinical and laboratory features of hyponatremia-induced myopathy
title_auth	Clinical and laboratory features of hyponatremia-induced myopathy
abstract	Background The present study was undertaken to determine the clinical and laboratory features of hyponatremia-induced myopathy. Methods We collected 14 hyponatremic subjects (six men and eight women) with serum creatine kinase (CK) levels of more than 500 IU/ml during the 5-year period between 2001 and 2005. The mean ± SD patients’ age was 66.5 ± 16.7 years (range, 37 to 88 years). Results The causes of the hyponatremia were: syndrome of inappropriate secretion of antidiuretic hormone (SIADH; n = 4), mineralocorticoid-responsive hyponatremia of the elderly (MRHE; n = 2), hypopituitarism (n = 1), psychogenic polydipsia (n = 3), congestive heart failure (n = 3), and unknown cause (n = 1). The subjects were subgrouped into two groups: acute onset of myopathy and slowly progressive onset. The age at onset was 62.0 ± 5.7 years (mean ± SEM) in the subjects with acute onset, and 77.8 ± 1.5 years in those with slowly progressive onset (P = 0.02). At the onset, there was no difference in serum Na levels between the acute onset and the slowly progressive onset groups, but there was a significant difference in maximal serum CK levels between the groups (7072 ± 2317 vs 722 ± 104 IU/ml; P = 0.02). Maximal serum CK levels were widely distributed among the ages in the subjects with acute onset, whereas maximal serum CK levels were mildly elevated in the elderly subjects with slowly progressive onset. The elevated serum CK levels were normalized at a maximum of 14 days after the onset in all the subjects. Conclusions The present findings indicate that hyponatremia infrequently causes skeletal muscle disruption, and that there are two types of hyponatremia-induced myopathy, acute onset and slowly progressive onset.
abstractGer	Background The present study was undertaken to determine the clinical and laboratory features of hyponatremia-induced myopathy. Methods We collected 14 hyponatremic subjects (six men and eight women) with serum creatine kinase (CK) levels of more than 500 IU/ml during the 5-year period between 2001 and 2005. The mean ± SD patients’ age was 66.5 ± 16.7 years (range, 37 to 88 years). Results The causes of the hyponatremia were: syndrome of inappropriate secretion of antidiuretic hormone (SIADH; n = 4), mineralocorticoid-responsive hyponatremia of the elderly (MRHE; n = 2), hypopituitarism (n = 1), psychogenic polydipsia (n = 3), congestive heart failure (n = 3), and unknown cause (n = 1). The subjects were subgrouped into two groups: acute onset of myopathy and slowly progressive onset. The age at onset was 62.0 ± 5.7 years (mean ± SEM) in the subjects with acute onset, and 77.8 ± 1.5 years in those with slowly progressive onset (P = 0.02). At the onset, there was no difference in serum Na levels between the acute onset and the slowly progressive onset groups, but there was a significant difference in maximal serum CK levels between the groups (7072 ± 2317 vs 722 ± 104 IU/ml; P = 0.02). Maximal serum CK levels were widely distributed among the ages in the subjects with acute onset, whereas maximal serum CK levels were mildly elevated in the elderly subjects with slowly progressive onset. The elevated serum CK levels were normalized at a maximum of 14 days after the onset in all the subjects. Conclusions The present findings indicate that hyponatremia infrequently causes skeletal muscle disruption, and that there are two types of hyponatremia-induced myopathy, acute onset and slowly progressive onset.
abstract_unstemmed	Background The present study was undertaken to determine the clinical and laboratory features of hyponatremia-induced myopathy. Methods We collected 14 hyponatremic subjects (six men and eight women) with serum creatine kinase (CK) levels of more than 500 IU/ml during the 5-year period between 2001 and 2005. The mean ± SD patients’ age was 66.5 ± 16.7 years (range, 37 to 88 years). Results The causes of the hyponatremia were: syndrome of inappropriate secretion of antidiuretic hormone (SIADH; n = 4), mineralocorticoid-responsive hyponatremia of the elderly (MRHE; n = 2), hypopituitarism (n = 1), psychogenic polydipsia (n = 3), congestive heart failure (n = 3), and unknown cause (n = 1). The subjects were subgrouped into two groups: acute onset of myopathy and slowly progressive onset. The age at onset was 62.0 ± 5.7 years (mean ± SEM) in the subjects with acute onset, and 77.8 ± 1.5 years in those with slowly progressive onset (P = 0.02). At the onset, there was no difference in serum Na levels between the acute onset and the slowly progressive onset groups, but there was a significant difference in maximal serum CK levels between the groups (7072 ± 2317 vs 722 ± 104 IU/ml; P = 0.02). Maximal serum CK levels were widely distributed among the ages in the subjects with acute onset, whereas maximal serum CK levels were mildly elevated in the elderly subjects with slowly progressive onset. The elevated serum CK levels were normalized at a maximum of 14 days after the onset in all the subjects. Conclusions The present findings indicate that hyponatremia infrequently causes skeletal muscle disruption, and that there are two types of hyponatremia-induced myopathy, acute onset and slowly progressive onset.
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container_issue	4
title_short	Clinical and laboratory features of hyponatremia-induced myopathy
url	https://dx.doi.org/10.1007/s10157-007-0494-3
remote_bool	true
author2	Yuzawa, Miho Saito, Tomoyuki Ikoma, Aki Tamemoto, Hiroyuki Kawakami, Masanobu Ishikawa, San-e
author2Str	Yuzawa, Miho Saito, Tomoyuki Ikoma, Aki Tamemoto, Hiroyuki Kawakami, Masanobu Ishikawa, San-e
ppnlink	306646900
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isOA_txt	false
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doi_str	10.1007/s10157-007-0494-3
up_date	2024-07-04T00:04:09.286Z
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Clinical and laboratory features of hyponatremia-induced myopathy

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