The Role of Fibrinogen, Homocysteine and Metabolic Syndrome’s Alterations in Sudden Sensorineural Hearing Loss (SSHL): A Narrative Review

Abstract

Fibrinogen and homocysteine (HCY) are molecules known to play a role in vascular homeostasis, and their blood levels are often elevated in patients with metabolic syndrome. Recent evidence suggests that sudden sensorineural hearing loss (SSHL) may have a vascular origin. This has led many authors to advocate that fibrinogen, homocysteine, and metabolic syndrome (MetS) may play a direct role in SSHL. The aim of this brief review is to examine the role and influence of these molecules and MetS on the mechanisms of SSHL. Elevated fibrinogen levels have been associated with a worse prognosis in SSHL, possibly due to increased blood viscosity and decreased blood flow. Similarly, HCY has been associated with vascular damage, particularly in hyperhomocysteinemia, although the exact association with SSHL remains controversial. MetS has been demonstrated to function both as a causative factor and as a contributor to poorer recovery in cases of SSHL. However, although some studies suggest a possible role for these biomarkers and MetS in the prognosis and treatment of SSHL, specific therapeutic and preventive strategies based solely on these factors have yet to be developed. Given their potential role in prognosis and treatment and the global epidemic of metabolic syndrome, this issue needs to be analyzed comprehensively. Thus, further quality studies need to be conducted, even though it is difficult to determine the actual impact of MetS on the development of SSHL, as it is a multifactorial disease affecting multiple organs.

The relationship between cysteine, homocysteine, and osteoporosis

“…Elevated plasma levels of homocysteine, known as hyperhomocysteinemia, are a risk factor for various pathological disorders. Homocysteine metabolism is influenced by B vitamins, and there have been suggestions for vitamin treatments to lower Hcy concentration [4,5]. However, clinical trials have not yet established a consensus on the effectiveness of vitamin supplements in reducing homocysteine levels and improving pathological conditions [6].…”