Introduction:
Tinnitus is hearing sounds of different frequencies and qualities in the ear without any external stimulus [1]. Tinnitus is evaluated in two main groups as objective and subjective. Objective tinnitus is mostly caused by temporomandibular joint disorder, arteriovenous malformations, and spasm of the tensor timpani muscle, and in this form, the person performing the test hears the sound together with the patient [2]. In subjective tinnitus, the sound is only heard by the patient, not the person conducting the test. Subjective tinnitus may develop for many reasons, such as hearing impairment, insomnia, medication use, depression, chronic diseases, anxiety, and difficulty concentrating, and it has a negative impact on the quality of life of patients [3]. Tinnitus can have various frequencies and qualities, as well as various intensities. It can reach disturbing levels that seriously affect the daily life and social performance of the sufferer.
Despite the abundance of studies on the etiology and treatment of tinnitus, most do not present definitive conclusions. However, it is a known fact that although the majority of tinnitus sounds heard are considered to originate from the cochlea, tinnitus continues even after the auditory nerve has been completely resected [4]. This situation shows that tinnitus can originate not only from the cochlea but also from all auditory pathways, and can be seen after the formation of some inappropriate neural plasticities in the central nervous system. Although these changes in the central nervous system are both structural and functional, they can be seen in different parts of the brain, as well as the auditory pathways [5, 6]. Among all these factors, vascular and hematological abnormalities can be defined as an important etiology when tinnitus cases are evaluated, and there may even be underlying many structural and functional problems. In sudden hearing loss and facial paralysis, the vascular and hematological dimensions of tinnitus have been the subject of many studies, but a clear result has not yet been determined. Among these possible hematological causes, the neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio (PLR) have been associated with the inflammatory process and some thrombotic events [7]. The effect of these parameters on tinnitus has been investigated in many publications, and results have been reported based on different levels of evidence. However, considering that the main function in thrombosis risk is related to thrombocytes, they should be examined more carefully. In these thrombotic events, the platelet mass index (PMI), which is considered to be very effective at the microvascular level, comes to the fore. This is especially important in organs with endarteria, such as the ear cochlea. Any microvascular thrombotic event caused by platelets in these endarteria causes serious problems in organ functions. This situation cannot always be revealed by angiographic methods and it is vital to consider the possibility of transient ischemic attacks, and thus tissue damage. In addition, in the literature, it has been emphasized that the increase in the mean platelet volume (MPV) is effective in inflammatory processes and that increased MPV values are directly related to the activation of platelets [8]. Although MPV is a parameter that has been previously investigated, its evaluation alone may not be sufficiently reliable since the number of platelets is at least as important as their volume. Therefore, in this study, we aimed to explore whether there was a correlation between PMI and tinnitus. To our knowledge, this is the first study investigating the effect of platelet mass on tinnitus.
Material and method:
After obtaining the approval of the ethics committee of Harran University, dated June 29, 2020 and numbered HRU/20.12.09, the detailed medical records (examination notes, drug use, radiological evaluations, audiological evaluations, and previous surgical procedures) of 1,079 tinnitus patients presenting to our clinic between January 2019 and May 2020 were examined, and the hemogram data of 177 cases meeting the inclusion criteria were analyzed. Following a detailed evaluation of medical records, patients with chronic tinnitus (continuing for at least three months) in the 18-60 age group were included in the study. In line with the medical records, cancer patients, patients with chronic disease, those with a history of cardiac or vascular surgery in the head and neck region, and those with platelet dysfunction were excluded from the study to determine the independent effect of platelet mass. Further excluded were patients with acute inflammation or infection, diabetes mellitus, systemic hypertension, hyperlipidemia, coronary artery disease, chronic liver disease, acute or chronic renal failure, chronic obstructive pulmonary disease, connective tissue disease, inflammatory bowel disease or a history of acoustic trauma, current smokers, patients with a personal or family history of hearing loss due to noise, those with a hearing loss above 20 dB caused by any otological disease, such as chronic otitis media, otosclerosis and Meniere’s disease, and those with chronic diseases. For the patients included in the study, age, gender, hemoglobin, neutrophil, lymphocyte, platelet, and MPV were examined. This was followed by the assessment of the distribution of age, gender and hemoglobin level, NLR, PLR, and PMI (calculated as platelet number x MPV/1000). The values ​​of the tinnitus group were compared with the data of 192 patients without a history of temporary (lasting less than two weeks) or permanent tinnitus. The control group consisted of patients daily presenting to the outpatient clinic for any reason other than otologic complaints. Cancer patients with chronic diseases, those with a history of cardiac or vascular surgery in the head and neck region, and those with platelet dysfunction were not included in this group. The medical history of this group were evaluated at the same sensitivity as the tinnitus group in terms of chronic diseases.