- Email: [email protected]
Relationship between Sudden Sensorineural Hearing Loss and Vascular Risk Factors
Journal of Otology 2009
Vol. 4
No. 1
·55·
Original Article Relationship between Sudden Sensorineural Hearing Loss and Vascular Risk Factors ZHU Wen-yan1, DAI Yan-hong1, SHE Wandong1, WANG Lu2, Gao Xia1
1
Department of Otolaryngology-Head and Neck Surgery, Drum Tower Clinical Medical School, 2
Nanjing Medical University, Nanjing 210008, China Department of Medical English, School of Foreign Language, Nanfang Medical University, Guangzhou 510510, China
Abstract Objective To explore the relationship between sudden sensorineural hearing loss（SSNHL）and vascular risk factors（including serum lipids and uric acid）. Method This is a retrospective analysis of 100 cases of SSNHL seen at the Drum Tower Hospital, Nanjing Medical University, between Jan. 2007 and Apr. 2008。Patient history, blood test results and imaging scans were analyzed. Levels of triglyceride（TG）, cholesterols（CHO）, high density lipoprotein-cholesterol（HDL-CH）, low density lipoprotein-cholesterol（LDL-CH）, apolipoprotein AI（ApoAI）, apolipoprotein B（ApoB）and uric acid（UA）from these patients were compared with a control group of 56 patients treated for vocal cord polyps or nasal septum deviation during the same period. Patients with hypertension, diabetes, heart, brain, liver or kidney disorders are excluded from the present investigation. Results HDL-CH level was higher and UA level lower in the study group than the control group（P < 0.05）. HDL-CH and UA showed no significant differences among different age-groups（P > 0.05）. There were no significant differences in the levels of TG, CHO, LDL-CH, ApoAI and ApoB（P > 0.05）. Conclusion These data indicate that metabolic disturbances of serum lipids and/or uric acid may be potential risk factors for SSNHL Key words Sudden Sensorineural Hearing Loss; Lipid; Uric Acid; Age Introduction Sudden sensorineural hearing loss（SSNHL） has been defined as sensorineural hearing loss of 20 dB over at least 3 contiguous audiometric frequencies, occurring within 3 days ［1］. Approximately15, 000 new cases of SSNHL occur annually worldwide, accounting for 1% of all cases of sensorineural hearing loss［2,3］. Being a typi⁃ cal acute（mostly unilateral）inner ear disorder with un⁃ known etiology, SSNHL is assumed to be a multi-factori⁃ al disorder with different underlying etiologies. At pres⁃ ent, SSNHL remains one of the refractory diseases to otologist. Efforts by many experts to find its causes have Corresponding Author: SHE Wan-dong, Department of Otolaryn⁃ gology-Head and Neck Surgery, the Affiliated Drum Tower Hospi⁃ tal, Nanjing Medical University, Nanjing 210008, China. Email: [email protected]
failed to yield results. Etiologies can be identified in about 10-15% of all cases, including microcirculatory disturbance, infection, autoimmune disorders, but the majority of cases are idiopathic. Microcirculation distur⁃ bance in the cochlea as the cause of SSNHL has always been a research hotspot. The deep position of the co⁃ chlea within the temporal bone makes it difficult to di⁃ rectly study cochlear microcirculation disturbance or embolism in SSNHL patients. But there seem to be simi⁃ larities between cochlear microcirculation disturbance and cardio- or cerebrovascular embolism. In recent years, many studies have been directed to evaluating the role of various cardiovascular risk factors and blood vessel embolism in SSNHL［3-7］. High serumcholesterol, anticardiolipin antibodies, plasminogen acti⁃ vator inhibitor, blood plasma viscosity, increased fibrino⁃ gen, and decreased red blood cell filtration rate have
· 56 · been suggested to be associated with SSNHL, although not without controversies［5，6］. Uric acid, as purine metab⁃ olites, can stimulate proliferation of vascular smooth muscle cell and generation of local thronboxane after en⁃ tering the cell［8］, with possible effects on the process of cochlear microvascular embolization. The present study is aimed at studying the relationship between SSNHL and vascular risk factors through retrospective case anal⁃ ysis. 1
Material and Methods
1.1 Subjects 1.1.1 SSNHL Group Subjects were 100 patients seen at the Department of Otolaryngology-Head and Neck surgery, the Affiliat⁃ ed Drum Tower Hospital of Nanjing Medical University between Jan. 2007 and Apri.2008 with a diagnosis of SSNHL. There were 50 males and 50 females in this group with a mean age of 42.23 years（ranging from 15 to 69 years）. Diagnosis of SSNHL was made based upon the criteria established at Jinan Conference［1］. All cases were unilateral, of which 50 were on right ears and 50 on left. All patients underwent complete audiometric evaluation. Evaluation also included detailed history, physical examination, imaging studies and blood tests. Collected history covered time interval between onset of hearing loss and hospital admission, associated symp⁃ toms, emotional disturbances and demographic informa⁃ tion including occupation. Body weight was also taken. 1.1.2 Control Group he control group included 56 patients treated for na⁃ sal septum deviation or vocal cord polyps during the same period of time as the SSNHL patients. There were 30 males and 26 females with a mean age of 33 years （ranging from 17 to 60 years）. All individuals in this group had normal hearing Exclusion criteria included diseases such as hyperten⁃ sion, diabetes mellitus, cardiac or cerebral diseases, liv⁃ er and kidney diseases, and neoplasm. 1.2 Methods 1.2.1 Blood test indices Fasting venous blood specimens were sent to the labo⁃ ratory for testing. Levels of triglyceride（TG）, cholesterol （CHO）, high density lipoprotein-cholesterol （HDL-CH）, low density lipoprotein-cholesterol
Journal of Otology 2009 Vol. 4 No. 1
（LDL-CH）, apolipoprotein AI（ApoAI）, apolipoprotein B （ApoB） and uric acid（UA） were tested. Patients were divided into four age groups（≤20, 21-40, 41-60, and >60）. 1.2.2 Statistical Analysis Covariance analysis was conducted using the SPSS10.0 software. Statistical significance was accepted when p < 0.05. 2 Results 2.1 Subject population Of the 100 patients, 56% had office jobs, 35% were manual laborers and 9% were in non-specified profes⁃ sions. Events at the onset of SSNHL included fatigue （71.43%）, mood changes（84%）, and life style changes （16%）such as smoking and drinking. Associated symp⁃ toms included vertigo（51%）, tinnitus（96%）, nausea （34%）, and vomiting（24%）. The average Body Mass in⁃ dexes（BMI）was 22.10 ± 2.38 kg/m2 in the control group and 22.30 ± 2.27 kg/m2 in study patients, respectively （t = 0.62）. 2.2 Serum Lipid and Uric Acid Table 1 shows results of the tested parameters. Be⁃ cause age distribution was different between SSNHL pa⁃ tients and the control group（t = 0.000）, age factor was not included in the disease-control comparison analy⁃ sis. Covariance analysis was used to mitigate the influ⁃ ence of age factor. When compared between the two groups, the differences of HDC-CH and UA levels reached statistical significance （p=0.0010 and p= 0.0008, respectively）, and those of the rest indexes did not. The combined 156 cases were divided into 4 age groups（see methods） and one-factor analysis of vari⁃ ance was used to test influence of age on the indexes. The comparison among the age groups showed no statis⁃ tically significant differences with HDL-CH, LDC-CH, ApoAI, ApoB and UA（p > 0.05）, indicating no age ef⁃ fects on lipid or UA metabolism. 3 Discussion The pathogenesis of SSNHL remains unknown, and is generally believed to be related with virus infection and vascular embolism. There are numerous factors affecting cochlea microcirculation and many studies have focused
Journal of Otology 2009
Vol. 4 Table 1
Item（unit）
TG（mmol/L）
CHO（mmol/L）
HDC-CH（mmol/L）
LDC-CH （mmol/L） ApoAI（g/L）
ApoB（g/L）
UA（umol/L）
No. 1
·57·
Comparison between the SSNHL and control groups（x ± s） SSNHL Group
Control Group
Fvalue
4.41 ± 0.98
4.11 ± 1.00
0.23
1.13 ± 0.80 1.12 ± 0.31 2.34 ± 0.73 1.35 ± 0.32 0.76 ± 0.26
332.02 ± 74.96
on the mechanism of its disturbance recently. However, the studies have been inconclusive. As one of the risk factors for atherosclerosis, hypercholesterolemia contrib⁃ utes to heart/brain/aorta occlusion. Similar effects on the cochlear ischemia-reperfusion injury from hypercholes⁃ terolemia have been suspected. Marcucci and his col⁃ leagues［4］ concluded that hypercholesterolemia was an independent risk factor for SSNHL through his study on the relationship between SSNHL and risk factors for car⁃ diovascular and thrombosis. LU Yuan-yuan's research ［7］ showed that Total CHO, TG, and lipoprotein A in SSNHL group were higher than the control group. Gabriella Cadoni and his colleagues ［9］ were not able to confirm the association between congenital and acquired thrombus risk factors and SSNHL. Like⁃ wise, Claudia Rudack and his colleagues ［10］ found no correlation between HDL，CHO，LDL and CHO and SSNHL. Our study shows that total CHO was not differ⁃ ent between the SSNHL and control groups, but the HDL-CH level in SSNHL group was lower than the con⁃ trol group. HDL-CH is a type of CHO carried by HDL and indirectly reflects HDL levels. It is well known that HDL drives CHO to counter transport, eliminates extra cholesterol from blood and organs and eventually slows the process of atherosclerosis［11］. HDL can also reverse endothelial dysfunction, inhibit LDL oxidation, stimu⁃ late endothelial cell proliferation and prostacyclin gener⁃ ation（a vasodilative and anti-thrombosis agent）, reduce platelet aggregation ［12］, and much more. Lowered HDL levels diminish these benefits and increase the risk for thrombosis. Improved therapeutic results have been re⁃ ported when blood lipoid adjustment is included in the SSNHL treatment protocol, probably from decreased co⁃
1.39 ± 0.90
Pvalue
3.49
0.0638
1.30 ± 0.29
11.22
0.0010
1.19 ± 0.26
0.48
2.18 ± 0.66 0.76 ± 0.36
284.73 ± 91.15
0.26 0.00 7.24
0.6320 0.6094 0.4907 0.9901 0.0080
chear ischemia-reperfusion injury［13］ and blood viscosity . The higher blood UA level in the SSNHL group than the control group seen in this study suggests a possible relationship between UA and SSNHL. Increased blood UA level may lead to UA deposits in vascular intima, re⁃ sulting in local damage and inflammation, aggravated ar⁃ teriosclerosis and accelerated formation of thrombosis ［16］ . However, some researchers insist that UA is the most important antioxidant in blood that can prevent cells from tyrosine residue nitration and prevent extra⁃ cellular superoxide dismutase from degradation［17］, thus exerting protective effects in heart and cerebral vascular conditions. More than 80% of our patients experienced signifi⁃ cant mood swings at the onset of SSNHL, similar to re⁃ ports by Jae-Ho Ban and Yuan-yuan Lu［6，18］. Job pres⁃ sure, emotional and physical stress can lead to anxiety, overexcitation in the nervous system and excessive re⁃ lease of catecholamine, which in turn may result in in⁃ ner ear vasospasm, increased platelet aggregation and a tendency to thrombosis. In conclusion, our study indicates a relationship be⁃ tween the occurrence of SSNHL and a number of vascu⁃ lar risk factors including blood lipids and uric acid me⁃ tabolism disorder. Further studies are needed to investi⁃ gate pathopoiesis of HDL-C and UA in SSNHL. ［14，15］
Acknowlegment This study was supported by a grant from Nanjing Medi⁃ cal Development Foundation（NO: YKK05098）
References
· 58 · 1 Society for Otorhinolaryngology-Head and Neck Surgery of Chinese Medical Association. Diagnosis criteria and treatment guideline for Sudden Sensorineural Hearing Loss. Chinese J of Otorhinolaryngology-Head and Neck Surgery. 2006, 41:325. 2 Olzowy B, Osterkorn D, Suckfull M. The incidence of senso⁃ neurinal sudden hearing loss is greater than previously presumed. MMW Fortschr Med. 2005, 147: 37-38. 3 Cadoni G，Scipione S, Agostino S,et al. Coenzyme Q 10 and cardiovascular risk factor in idiopathic sudden sensorineural hear⁃ ing loss patients [J]. Otol Neurotol. 2007, 28: 878-883. 4 Marcucci R, Sodi A, Giambene B, et al. Cardiovascular and thrombophilic risk factors for idiopathic sudden sensorineural hearing loss［J］. Thromb Haemost, 2005, 3: 929-934. 5 Markus Suckfüll, Christoph Wimmer, Oliver Reichel, et al. Hyperfibrinogenemia as a Risk Factor for Sudden Hearing Loss [J]. Otology & Neurotology. 2002, 23: 309-311. 6 Cadoni G, Agostino S, Scipione S, et al. Low serum foliate lev⁃ els: a risk factor for sudden sensorineural hearing loss? [J]. Acta Otolaryngol. 2004, 124: 608-611. 7 Lu YY, Tong BS, Yang JM, et al. Relationship between dis⁃ turbed microcirculation and sudden deafness.Chinese Journal of Otology［J］. 2007, 5: 45-48. 8 Johnson RJ, Kang DH, Feig D, et al. Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal dis⁃ ease?［J］. Hypertension. 2003, 41: 1183-1190. 9 Cadoni G, Scipione S, Rocca B, et al. Lack of association be⁃ tween inherited thrombophilic risk factors and idiopathic sudden sensorineural hearing loss in Italian patients［J］. Ann Otol Rhinol Laryngol. 2006, 115: 195-200.
Journal of Otology 2009 Vol. 4 No. 1 10 Rudack C, Langer C, Stoll W, et al. Vascular risk factors in sudden hearing loss［J］. Thromb Haemost. 2006, 95: 454-461. 11 Toth PP. Reverse cholesterol transport high-density lipopro⁃ tein′ s magnificent mile［J］. Current Arteriosclerosis Reports. 2003, 5: 386-393. 12 Nofer J, Kehrel B, Fobker M, et al. HDL and arteriosclerosis: beyond reverse cholesterol transport［J］. Atherosclerosis. 2002, 161: 1-16. 13 Hatano M, Uramoto N, OkabeY, et al.Vitamin E and vitamin C in the treatment of idiopathic sudden sensorineural hearing loss ［J］. Acta Otolaryngol. 2008, 128: 116-1121. 14 Kojima Y, Ito S, Furuya N, et al. Hearing improvement after therapy for hyperlipidemia in patients with chronic-phase sudden deafness［J］. Ann Otol Rhinol Laryngol. 2001, 110: 105-108. 15 Suckfull M, Thiery J, Wimmer C, et al. Hypercholesteremia and hyperfibrinogenemia in sudden deafness［J］. Laryngorhinoot⁃ ologie. 1997, 76: 453-457. 16 Lv JG, Liang SL. The association between coronary heart dis⁃ ease and uric acid［J］. Chinese Journal of Cardiovascular Medi⁃ cine. 1998, 3: 288-289. 17 Hink HU, Santanam N, Dikalov S, et al. Peroxidase proper⁃ ties of extracellular superoxide dismutase: role of uric acid in mod⁃ ulating in vivo activity［J］. Arterioscler Thromb Vasc Biol. 2002, 22: 1402-1408. 18 Ban JH, Jin SM, Seoul, et al. A clinical analysis of psychogen⁃ ic sudden deafness［J］. Otolaryngology-Head and Neck Surgery. 2006, 134: 970-974. （Received November 26, 200９）
Vol. 4
No. 1
·55·
Original Article Relationship between Sudden Sensorineural Hearing Loss and Vascular Risk Factors ZHU Wen-yan1, DAI Yan-hong1, SHE Wandong1, WANG Lu2, Gao Xia1
1
Department of Otolaryngology-Head and Neck Surgery, Drum Tower Clinical Medical School, 2
Nanjing Medical University, Nanjing 210008, China Department of Medical English, School of Foreign Language, Nanfang Medical University, Guangzhou 510510, China
Abstract Objective To explore the relationship between sudden sensorineural hearing loss（SSNHL）and vascular risk factors（including serum lipids and uric acid）. Method This is a retrospective analysis of 100 cases of SSNHL seen at the Drum Tower Hospital, Nanjing Medical University, between Jan. 2007 and Apr. 2008。Patient history, blood test results and imaging scans were analyzed. Levels of triglyceride（TG）, cholesterols（CHO）, high density lipoprotein-cholesterol（HDL-CH）, low density lipoprotein-cholesterol（LDL-CH）, apolipoprotein AI（ApoAI）, apolipoprotein B（ApoB）and uric acid（UA）from these patients were compared with a control group of 56 patients treated for vocal cord polyps or nasal septum deviation during the same period. Patients with hypertension, diabetes, heart, brain, liver or kidney disorders are excluded from the present investigation. Results HDL-CH level was higher and UA level lower in the study group than the control group（P < 0.05）. HDL-CH and UA showed no significant differences among different age-groups（P > 0.05）. There were no significant differences in the levels of TG, CHO, LDL-CH, ApoAI and ApoB（P > 0.05）. Conclusion These data indicate that metabolic disturbances of serum lipids and/or uric acid may be potential risk factors for SSNHL Key words Sudden Sensorineural Hearing Loss; Lipid; Uric Acid; Age Introduction Sudden sensorineural hearing loss（SSNHL） has been defined as sensorineural hearing loss of 20 dB over at least 3 contiguous audiometric frequencies, occurring within 3 days ［1］. Approximately15, 000 new cases of SSNHL occur annually worldwide, accounting for 1% of all cases of sensorineural hearing loss［2,3］. Being a typi⁃ cal acute（mostly unilateral）inner ear disorder with un⁃ known etiology, SSNHL is assumed to be a multi-factori⁃ al disorder with different underlying etiologies. At pres⁃ ent, SSNHL remains one of the refractory diseases to otologist. Efforts by many experts to find its causes have Corresponding Author: SHE Wan-dong, Department of Otolaryn⁃ gology-Head and Neck Surgery, the Affiliated Drum Tower Hospi⁃ tal, Nanjing Medical University, Nanjing 210008, China. Email: [email protected]
failed to yield results. Etiologies can be identified in about 10-15% of all cases, including microcirculatory disturbance, infection, autoimmune disorders, but the majority of cases are idiopathic. Microcirculation distur⁃ bance in the cochlea as the cause of SSNHL has always been a research hotspot. The deep position of the co⁃ chlea within the temporal bone makes it difficult to di⁃ rectly study cochlear microcirculation disturbance or embolism in SSNHL patients. But there seem to be simi⁃ larities between cochlear microcirculation disturbance and cardio- or cerebrovascular embolism. In recent years, many studies have been directed to evaluating the role of various cardiovascular risk factors and blood vessel embolism in SSNHL［3-7］. High serumcholesterol, anticardiolipin antibodies, plasminogen acti⁃ vator inhibitor, blood plasma viscosity, increased fibrino⁃ gen, and decreased red blood cell filtration rate have
· 56 · been suggested to be associated with SSNHL, although not without controversies［5，6］. Uric acid, as purine metab⁃ olites, can stimulate proliferation of vascular smooth muscle cell and generation of local thronboxane after en⁃ tering the cell［8］, with possible effects on the process of cochlear microvascular embolization. The present study is aimed at studying the relationship between SSNHL and vascular risk factors through retrospective case anal⁃ ysis. 1
Material and Methods
1.1 Subjects 1.1.1 SSNHL Group Subjects were 100 patients seen at the Department of Otolaryngology-Head and Neck surgery, the Affiliat⁃ ed Drum Tower Hospital of Nanjing Medical University between Jan. 2007 and Apri.2008 with a diagnosis of SSNHL. There were 50 males and 50 females in this group with a mean age of 42.23 years（ranging from 15 to 69 years）. Diagnosis of SSNHL was made based upon the criteria established at Jinan Conference［1］. All cases were unilateral, of which 50 were on right ears and 50 on left. All patients underwent complete audiometric evaluation. Evaluation also included detailed history, physical examination, imaging studies and blood tests. Collected history covered time interval between onset of hearing loss and hospital admission, associated symp⁃ toms, emotional disturbances and demographic informa⁃ tion including occupation. Body weight was also taken. 1.1.2 Control Group he control group included 56 patients treated for na⁃ sal septum deviation or vocal cord polyps during the same period of time as the SSNHL patients. There were 30 males and 26 females with a mean age of 33 years （ranging from 17 to 60 years）. All individuals in this group had normal hearing Exclusion criteria included diseases such as hyperten⁃ sion, diabetes mellitus, cardiac or cerebral diseases, liv⁃ er and kidney diseases, and neoplasm. 1.2 Methods 1.2.1 Blood test indices Fasting venous blood specimens were sent to the labo⁃ ratory for testing. Levels of triglyceride（TG）, cholesterol （CHO）, high density lipoprotein-cholesterol （HDL-CH）, low density lipoprotein-cholesterol
Journal of Otology 2009 Vol. 4 No. 1
（LDL-CH）, apolipoprotein AI（ApoAI）, apolipoprotein B （ApoB） and uric acid（UA） were tested. Patients were divided into four age groups（≤20, 21-40, 41-60, and >60）. 1.2.2 Statistical Analysis Covariance analysis was conducted using the SPSS10.0 software. Statistical significance was accepted when p < 0.05. 2 Results 2.1 Subject population Of the 100 patients, 56% had office jobs, 35% were manual laborers and 9% were in non-specified profes⁃ sions. Events at the onset of SSNHL included fatigue （71.43%）, mood changes（84%）, and life style changes （16%）such as smoking and drinking. Associated symp⁃ toms included vertigo（51%）, tinnitus（96%）, nausea （34%）, and vomiting（24%）. The average Body Mass in⁃ dexes（BMI）was 22.10 ± 2.38 kg/m2 in the control group and 22.30 ± 2.27 kg/m2 in study patients, respectively （t = 0.62）. 2.2 Serum Lipid and Uric Acid Table 1 shows results of the tested parameters. Be⁃ cause age distribution was different between SSNHL pa⁃ tients and the control group（t = 0.000）, age factor was not included in the disease-control comparison analy⁃ sis. Covariance analysis was used to mitigate the influ⁃ ence of age factor. When compared between the two groups, the differences of HDC-CH and UA levels reached statistical significance （p=0.0010 and p= 0.0008, respectively）, and those of the rest indexes did not. The combined 156 cases were divided into 4 age groups（see methods） and one-factor analysis of vari⁃ ance was used to test influence of age on the indexes. The comparison among the age groups showed no statis⁃ tically significant differences with HDL-CH, LDC-CH, ApoAI, ApoB and UA（p > 0.05）, indicating no age ef⁃ fects on lipid or UA metabolism. 3 Discussion The pathogenesis of SSNHL remains unknown, and is generally believed to be related with virus infection and vascular embolism. There are numerous factors affecting cochlea microcirculation and many studies have focused
Journal of Otology 2009
Vol. 4 Table 1
Item（unit）
TG（mmol/L）
CHO（mmol/L）
HDC-CH（mmol/L）
LDC-CH （mmol/L） ApoAI（g/L）
ApoB（g/L）
UA（umol/L）
No. 1
·57·
Comparison between the SSNHL and control groups（x ± s） SSNHL Group
Control Group
Fvalue
4.41 ± 0.98
4.11 ± 1.00
0.23
1.13 ± 0.80 1.12 ± 0.31 2.34 ± 0.73 1.35 ± 0.32 0.76 ± 0.26
332.02 ± 74.96
on the mechanism of its disturbance recently. However, the studies have been inconclusive. As one of the risk factors for atherosclerosis, hypercholesterolemia contrib⁃ utes to heart/brain/aorta occlusion. Similar effects on the cochlear ischemia-reperfusion injury from hypercholes⁃ terolemia have been suspected. Marcucci and his col⁃ leagues［4］ concluded that hypercholesterolemia was an independent risk factor for SSNHL through his study on the relationship between SSNHL and risk factors for car⁃ diovascular and thrombosis. LU Yuan-yuan's research ［7］ showed that Total CHO, TG, and lipoprotein A in SSNHL group were higher than the control group. Gabriella Cadoni and his colleagues ［9］ were not able to confirm the association between congenital and acquired thrombus risk factors and SSNHL. Like⁃ wise, Claudia Rudack and his colleagues ［10］ found no correlation between HDL，CHO，LDL and CHO and SSNHL. Our study shows that total CHO was not differ⁃ ent between the SSNHL and control groups, but the HDL-CH level in SSNHL group was lower than the con⁃ trol group. HDL-CH is a type of CHO carried by HDL and indirectly reflects HDL levels. It is well known that HDL drives CHO to counter transport, eliminates extra cholesterol from blood and organs and eventually slows the process of atherosclerosis［11］. HDL can also reverse endothelial dysfunction, inhibit LDL oxidation, stimu⁃ late endothelial cell proliferation and prostacyclin gener⁃ ation（a vasodilative and anti-thrombosis agent）, reduce platelet aggregation ［12］, and much more. Lowered HDL levels diminish these benefits and increase the risk for thrombosis. Improved therapeutic results have been re⁃ ported when blood lipoid adjustment is included in the SSNHL treatment protocol, probably from decreased co⁃
1.39 ± 0.90
Pvalue
3.49
0.0638
1.30 ± 0.29
11.22
0.0010
1.19 ± 0.26
0.48
2.18 ± 0.66 0.76 ± 0.36
284.73 ± 91.15
0.26 0.00 7.24
0.6320 0.6094 0.4907 0.9901 0.0080
chear ischemia-reperfusion injury［13］ and blood viscosity . The higher blood UA level in the SSNHL group than the control group seen in this study suggests a possible relationship between UA and SSNHL. Increased blood UA level may lead to UA deposits in vascular intima, re⁃ sulting in local damage and inflammation, aggravated ar⁃ teriosclerosis and accelerated formation of thrombosis ［16］ . However, some researchers insist that UA is the most important antioxidant in blood that can prevent cells from tyrosine residue nitration and prevent extra⁃ cellular superoxide dismutase from degradation［17］, thus exerting protective effects in heart and cerebral vascular conditions. More than 80% of our patients experienced signifi⁃ cant mood swings at the onset of SSNHL, similar to re⁃ ports by Jae-Ho Ban and Yuan-yuan Lu［6，18］. Job pres⁃ sure, emotional and physical stress can lead to anxiety, overexcitation in the nervous system and excessive re⁃ lease of catecholamine, which in turn may result in in⁃ ner ear vasospasm, increased platelet aggregation and a tendency to thrombosis. In conclusion, our study indicates a relationship be⁃ tween the occurrence of SSNHL and a number of vascu⁃ lar risk factors including blood lipids and uric acid me⁃ tabolism disorder. Further studies are needed to investi⁃ gate pathopoiesis of HDL-C and UA in SSNHL. ［14，15］
Acknowlegment This study was supported by a grant from Nanjing Medi⁃ cal Development Foundation（NO: YKK05098）
References
· 58 · 1 Society for Otorhinolaryngology-Head and Neck Surgery of Chinese Medical Association. Diagnosis criteria and treatment guideline for Sudden Sensorineural Hearing Loss. Chinese J of Otorhinolaryngology-Head and Neck Surgery. 2006, 41:325. 2 Olzowy B, Osterkorn D, Suckfull M. The incidence of senso⁃ neurinal sudden hearing loss is greater than previously presumed. MMW Fortschr Med. 2005, 147: 37-38. 3 Cadoni G，Scipione S, Agostino S,et al. Coenzyme Q 10 and cardiovascular risk factor in idiopathic sudden sensorineural hear⁃ ing loss patients [J]. Otol Neurotol. 2007, 28: 878-883. 4 Marcucci R, Sodi A, Giambene B, et al. Cardiovascular and thrombophilic risk factors for idiopathic sudden sensorineural hearing loss［J］. Thromb Haemost, 2005, 3: 929-934. 5 Markus Suckfüll, Christoph Wimmer, Oliver Reichel, et al. Hyperfibrinogenemia as a Risk Factor for Sudden Hearing Loss [J]. Otology & Neurotology. 2002, 23: 309-311. 6 Cadoni G, Agostino S, Scipione S, et al. Low serum foliate lev⁃ els: a risk factor for sudden sensorineural hearing loss? [J]. Acta Otolaryngol. 2004, 124: 608-611. 7 Lu YY, Tong BS, Yang JM, et al. Relationship between dis⁃ turbed microcirculation and sudden deafness.Chinese Journal of Otology［J］. 2007, 5: 45-48. 8 Johnson RJ, Kang DH, Feig D, et al. Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal dis⁃ ease?［J］. Hypertension. 2003, 41: 1183-1190. 9 Cadoni G, Scipione S, Rocca B, et al. Lack of association be⁃ tween inherited thrombophilic risk factors and idiopathic sudden sensorineural hearing loss in Italian patients［J］. Ann Otol Rhinol Laryngol. 2006, 115: 195-200.
Journal of Otology 2009 Vol. 4 No. 1 10 Rudack C, Langer C, Stoll W, et al. Vascular risk factors in sudden hearing loss［J］. Thromb Haemost. 2006, 95: 454-461. 11 Toth PP. Reverse cholesterol transport high-density lipopro⁃ tein′ s magnificent mile［J］. Current Arteriosclerosis Reports. 2003, 5: 386-393. 12 Nofer J, Kehrel B, Fobker M, et al. HDL and arteriosclerosis: beyond reverse cholesterol transport［J］. Atherosclerosis. 2002, 161: 1-16. 13 Hatano M, Uramoto N, OkabeY, et al.Vitamin E and vitamin C in the treatment of idiopathic sudden sensorineural hearing loss ［J］. Acta Otolaryngol. 2008, 128: 116-1121. 14 Kojima Y, Ito S, Furuya N, et al. Hearing improvement after therapy for hyperlipidemia in patients with chronic-phase sudden deafness［J］. Ann Otol Rhinol Laryngol. 2001, 110: 105-108. 15 Suckfull M, Thiery J, Wimmer C, et al. Hypercholesteremia and hyperfibrinogenemia in sudden deafness［J］. Laryngorhinoot⁃ ologie. 1997, 76: 453-457. 16 Lv JG, Liang SL. The association between coronary heart dis⁃ ease and uric acid［J］. Chinese Journal of Cardiovascular Medi⁃ cine. 1998, 3: 288-289. 17 Hink HU, Santanam N, Dikalov S, et al. Peroxidase proper⁃ ties of extracellular superoxide dismutase: role of uric acid in mod⁃ ulating in vivo activity［J］. Arterioscler Thromb Vasc Biol. 2002, 22: 1402-1408. 18 Ban JH, Jin SM, Seoul, et al. A clinical analysis of psychogen⁃ ic sudden deafness［J］. Otolaryngology-Head and Neck Surgery. 2006, 134: 970-974. （Received November 26, 200９）