Soluble Intercellular Adhesion Molecule 1 and Soluble Vascular Cell Adhesion Molecule 1 in Sudden Hearing Loss

Quaranta, Nicola; Ramunni, Alfonso; Brescia, Paola; D’Elia, Alessandra; Vacca, Angelo; Ria, Roberto

doi:10.1097/mao.0b013e318170b650

Cited by 45 publications

(47 citation statements)

References 24 publications

(23 reference statements)

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“…In the literature, the association between MTHFR C677T mutation and hyperhomocysteinemia has been confirmed by various authors [Almawi et al, 2009;Fujimaki et al, 2009;Husemoen et al, 2009;Oterino et al, 2010;Szamosi et al, 2009;Yamada et al, 2001] although in another study [Antoniades et al, 2009] the same mutation showed a stronger correlation with low folate levels. In our study we did not analyze folate levels; however, according to several studies, low levels of folate are inversely related to homocysteine levels [Cadoni et al, 2004;Quaranta et al, 2008;Schuknecht et al, 1973;Suckfüll et al, 2002]. The association between homozygosity for the MTHFR C677T mutation and hyperhomocysteinemia suggests that this combination of variables may be involved, along with other factors, in the onset of SSHL.…”

Section: Discussionmentioning

confidence: 99%

Role of Genetic and Acquired Prothrombotic Risk Factors in Genesis of Sudden Sensorineural Hearing Loss

Fusconi¹,

Chistolini

Angelosanto

et al. 2010

Audiol Neurotol

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The methylenetetrahydrofolate reductase C677T mutation, factor V G1691A (factor V Leiden) mutation, prothrombin G20210A mutation and 8 other laboratory values associated with increased thrombotic risk were analyzed in 40 patients with sudden sensorineural hearing loss (SSHL). The results were compared with those obtained from 120 controls not affected by SSHL. We found a statistically significant higher frequency of hyperhomocysteinemia in the SSHL group compared with controls, and that this was also associated with the presence of homozygosity for the MTHFR C677T mutation. The study results suggest that SSHL might be caused, among other factors, by a combination of these 2 variables. We suggest that this analysis of the MTHFR C677T mutation should be further investigated to establish the etiology of SSHL, and that the same analysis should be taken into account in those patients with high levels of homocysteine.

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Section: Discussionmentioning

confidence: 99%

Role of Genetic and Acquired Prothrombotic Risk Factors in Genesis of Sudden Sensorineural Hearing Loss

Fusconi¹,

Chistolini

Angelosanto

et al. 2010

Audiol Neurotol

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“…The role of proinfl ammatory cytokine expression has been studied in patients with various ear disorders, including SSNHL (Quaranta et al, 2008;Suslu et al, 2009). During in vitro experiments, 24 h of hypoxia decreased the levels of mRNAs encoding IL-1 β and IL-6 and increased the levels of mRNA encoding TNF α in the stria vascularis and spiral ligament compared with normoxia.…”

Section: Mode Of Inheritancementioning

confidence: 98%

Polymorphisms in Genes Involved in Inflammatory Pathways in Patients with Sudden Sensorineural Hearing Loss

Hiramatsu

Teranishi

Uchida

et al. 2012

Journal of Neurogenetics

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Although the etiology of idiopathic sudden sensorineural hearing loss (SSNHL) remains unclear, the pathologically increased permeability of blood vessels, elucidated by gadolinium-enhanced magnetic resonance imaging (MRI), suggests the involvement of inflammation. Because SSNHL is considered a multifactorial disease, possibly caused by interactions between genetic factors and environmental factors, the authors investigated the associations of polymorphisms of inflammatory mediator genes with susceptibility to SSNHL. The authors compared 72 patients affected by SSNHL and 2010 adults (1010 men and 1000 women; mean age 59.2 years; range 40-79) who participated in the National Institute for Longevity Sciences Longitudinal Study of Aging. Multiple logistic regression was used to obtain odds ratios (ORs) for SSNHL in subjects with polymorphisms in the genes IL-6 C - 572G, IL-4R G1902A, IL-10 A - 592C, TNFα C - 863A, TNFRSF1B G593A, VEGF C936T, VEGF C - 2578A, and VEGF G - 1154A, with adjustment for age, gender, and any history of hypertension, diabetes, or dyslipidemia. The per-allele OR for the risk of SSNHL in subjects bearing IL-6 C - 572G was 1.480 (95% confidence interval [CI], 1.037-2.111) in model 1 (no adjustment), 1.463 (CI, 1.022-2.094) in model 2 (adjusted for age and gender), and 1.460 (CI, 1.016-2.097) in model 3 (adjusted for age, gender, and a history of hypertension, diabetes, or dyslipidemia). Under the dominant model of inheritance, the ORs were 1.734 (CI, 1.080-2.783) in model 1, 1.690 (CI, 1.050-2.721) in model 2, and 1.669 (CI, 1.035-2.692) in model 3. The remaining seven polymorphisms failed to show any associations with the risk of SSNHL. These data need to be confirmed on larger series of patients. In conclusion, the IL-6 C - 572G polymorphism is associated with a risk of SSNHL. Because permeability of blood vessels in the inner ear is frequently increased in patients with SSNHL, inflammation of the inner ear might be involved.

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“…However, its etiopathogenesis has not yet been clearly delineated [3][4][5][6] . In studies performed during recent years, systemic stress and inflammation have mainly been held responsible [7][8][9] .…”

Section: Introductionmentioning

confidence: 99%

New Inflammation Parameters in Sudden Sensorineural Hearing Loss: Neutrophil-to-Lymphocyte Ratio and Platelet-to-Lymphocyte Ratio

İkincioğulları¹,

Köseoğlu²,

Kılıç³

et al. 2015

Int Adv Otol

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OBJECTIVE:The etiopathogenesis of sudden sensorineural hearing loss (SSNHL) is not clearly defined. Inflammation is being emphasized in its etiology. Neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) are the parameters that show inflammation that can be obtained easily without additional cost. In this study, we aimed at delineating the relationship between SSNHL and the inflammation markers NLR and PLR. MATERIALS and METHODS:This study was performed with 102 patients diagnosed with SSNHL and 119 sex-and age-matched controls. All subjects in the study and the control group had their complete blood count (CBC) results, which were evaluated retrospectively to calculate NLR and PLR values. All patients underwent an audiological examination on the 1 st , 3rd, 10 th , and 30 th days of the hearing loss. All patients received 1 mg/kg IV prednisolone treatment in tapered amounts to be completed in 15 days. Based on the improvements seen in the audiograms, the patients were divided into two groups: responders and non-responders to treatment. RESULTS:PLR and NLR values of the patient group were significantly higher than in the control group (p<0.001, p<0.001). Furthermore, patients who responded to treatment had significantly higher NLR values than those who did not respond (p=0.010). CONCLUSION:In this study, NLR and PLR values were found to be significantly high in SSNHL patients. PLR value was investigated for the first time in the literature in SSNHL patients. NLR and PLR values are parameters that aid in the diagnosis of SSNHL. Moreover, SSNHL patients who had higher NLR values responded to the treatment better.

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Soluble Intercellular Adhesion Molecule 1 and Soluble Vascular Cell Adhesion Molecule 1 in Sudden Hearing Loss

Cited by 45 publications

References 24 publications

Role of Genetic and Acquired Prothrombotic Risk Factors in Genesis of Sudden Sensorineural Hearing Loss

Role of Genetic and Acquired Prothrombotic Risk Factors in Genesis of Sudden Sensorineural Hearing Loss

Polymorphisms in Genes Involved in Inflammatory Pathways in Patients with Sudden Sensorineural Hearing Loss

New Inflammation Parameters in Sudden Sensorineural Hearing Loss: Neutrophil-to-Lymphocyte Ratio and Platelet-to-Lymphocyte Ratio

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