Vestibular Assessment with the vHIT and Skull Vibration-Induced Nystagmus Test in Patients with Nonprogressive Vestibular Schwannoma.

Background: Our primary objective was to monitor nonprogressive unilateral vestibular schwannomas (VSs) to assess the efficiency of rapid bedside examinations, such as the video head impulse test (vHIT) and skull vibration-induced nystagmus test (SVINT), in identifying vestibular damage. Methods: An observational study was conducted from March 2021 to March 2022 on all adult patients (>18 years old) with a confirmed nonprogressive VS (no active treatment). The SVINT (using a 100 Hz vibrator with two (SVINT2) or three (SVINT3) stimulation locations) and vHIT (for the six semicircular canals (SCCs)) were performed on all patients. The asymmetry of function between the vestibules was considered significant when the gain asymmetry was greater than 0.1. Rapid and repeatable assessment of VSs using two- and three-stimulation SVINT plus vHIT was performed to quantify intervestibular asymmetry. Results: SVINT3 and SVINT2 triggered VIN in 40% (24/60) and 65% (39/60) of patients, respectively. There was significant asymmetry in the vestibulo-ocular reflex (VOR), as shown by a VS-side gain < healthy-side gain in 58% (35/60) of the patients. Among the patients with significant gain asymmetry between the two vestibules according to the vHIT (VS-side gain < healthy-side gain), the proportion of patients expressing vestibular symptomatology was significantly greater than that of patients without any symptoms [67% (29/43) vs. 35% (6/17), respectively; p = 0.047]. Conclusions: The SVINT2 can be combined with the vHIT to form an interesting screening tool for revealing vestibular asymmetry. This work revealed the superiority of mastoid stimulation over vertex stimulation for SVINT in patients with unilateral vestibular loss.

Transoral Laser Microsurgery versus Robot-Assisted Surgery for Squamous Cell Carcinoma of the Tongue Base (Oncological and Functional Results)-A Retrospective GETTEC Multicenter Study.

The base of the tongue (BOT) is the second most common site for squamous cell carcinoma (SCC) in the oropharynx. There are currently no clear guidelines for the management of BOT SCC. Our main objective was to compare the oncological outcomes of two minimally invasive approaches, transoral laser microsurgery (TLM) and transoral robot-assisted surgery (TORS). This was a retrospective French GETTEC (Groupe d'Études des Tumeurs de la Tête et du Cou) multicenter study of patients with BOT SCC removed surgically either by TLM or TORS between 2005 and 2021. The study group included 16 patients treated by TLM and 38 by TORS, with median follow-up times of 14.4 and 37.2 months, respectively. The overall survival (OS) rates at 2 and 3 years were 67% in the TLM group and 90% at 2 years and 86% at 3 years in the TORS group (p = 0.42, p = 0.20). There was no significant difference in recurrence-free survival (RFS) between the two techniques after 2 and 3 years. The tumors removed by TORS were significantly larger. Operative times were significantly shorter in the TLM group. There were no differences in feeding resumption; none of the patients in the TLM group required a tracheotomy. Postoperative hemorrhagic complication rates were similar in the two groups (12% for TLM and 13% for TORS). Both TORS and TLM showed encouraging oncological, functional, and safety results in BOT SCC even in recurrence or second primary cancer patients, without a technique being found superior in terms of OS or RFS. Tumors removed by TORS were larger without an increase in postoperative bleeding, extending the possibilities of transoral treatment.

Systematic MRI in persistent post-Covid-19 olfactory dysfunction should be reassessed.

BACKGROUND: Magnetic resonance imaging (MRI) is the gold standard in the etiological assessment of a persistent olfactory dysfunction (OD). While the utility of imaging in COVID-19-related OD has yet to be established, MRI is recommended in all patients with persistent OD. The high prevalence of the latter after SARS-CoV-2 infection means evaluating this strategy is an important public health matter. METHODS: The main objective was to examine the impact of systematic MRI on the management of patients with OD. All adult patients consulting for persistent OD (>2 months) after primary SARS-COV-2 infection (PCR) between March 2020 and December 2021 were included (n = 67). The secondary objective was to evaluate the relationship between the severity of the OD as measured by psychophysical testing (ETOC) and the volume of the olfactory bulb (OB) measured by MRI. RESULTS: All patients underwent MRI, and none led to a change in diagnosis or treatment. Among them, 82% (55/67) were considered normal by the radiologist on initial interpretation. There were no significant differences (visual analysis or OB volume) between groups (mild, moderate, and severe hyposmia). CONCLUSION: Systematic MRI may be unnecessary in patients whose persistent OD began soon (a few days) after confirmed SARS-CoV-2 infection.

Controversy on high density lipoprotein raising therapy.

Decreased high density lipoproteins (HDL) plasma levels are a recognized independent risk factor for atherosclerotic cardiovascular disease. Attempts were therefore initiated to pharmacologically raise plasma HDL cholesterol, and the most impressive increase was obtained by inhibiting cholesteryl ester transfer protein (CETP) by means of the synthetic compound torcetrapib. Clinical trials were however disappointing, as torcetrapib increased mortality and did not reduce the progression of atherosclerosis. According to some view, it was claimed that CETP inhibition is unfavourable and that development of this class of compounds should be abandoned. Controversy nevertheless stimulated research on HDL structure, heterogeneity and functions which are not limited to reverse cholesterol transport and exert antioxidant and antiinflammatory actions. It could also be demonstrated that the deleterious effects of torcetrapib are compound specific, including its tight binding to CETP on HDL particles, thereby blocking both neutral lipids and phospholipid transfer from HDL to other lipoproteins, and would also exert an off-target effect by increasing plasma sodium and decreasing potasium concentrations (an aldosterone-like effect). As the structure of CETP was elucidated, it became possible to design CETP inhibitors that lack such off-target toxicity and may successfully slow the progression of atherosclerosis. Noteworthy, mice and rats naturally lacking CETP are resistant to diet induced atherosclerosis, while rabbits with high CETP levels are very susceptible. Families with deficient activity and exceptional longevity had also been reported.

Lipolytic enzymes, metablic syndrome and atherosclerosis (revisiting and revising a 40 years old study).

More than 40 years ago, our laboratory reported that post-heparin lipolytic activity was decreased in patients with severe atherosclerotic disease, while values recorded in obese and hyperlipidemic subjects without clinically detectable atherosclerotic lesions did not significantly differ from normal weight normolipidemic controls. Because in 1967 data on pathophysiology of lipolytic enzymes were rather scarce, and mainly because our information facilities were limited in those years, we had difficulties in interpreting these results, and the study was to some extent awkwardly approached, as the investigated subjects were not considered according to their gender, body fat patterning and type of hyperlipoproteinemia, and the lipolytic activities of lipoprotein lipase and hepatic lipase had not been selectively assessed. Reviewing recent data in the literature it was noted that pre-heparin lipoprotein lipase mass assessed by ELISA was indeed significantly lower in insulin resistant coronary patients than in patients with no lesions, and correlated negatively with the severity of atherosclerotic lesions. Noteworthy hypoadiponectinemia, a hallmark of insulin resistance, was associated with decreased lipoprotein lipase and increased hepatic lipase activities. Clustering of increased plasma VLDL-triglyceride, cholesteryl-ester transfer protein and hepatic lipase would remodel HDL and LDL particles, generating an atherogenic lipoprotein profile. In opposition to atherogenic dyslipidemia related to an enhanced hepatic secretion of VLDL, cases with important hypertriglyceridemia subsequent to deficient lipolytic clearance are at a rather low risk for coronary artery disease. It may therefore be suggested that the decreased lipoprotein lipase noted in atherosclerotic patients is not a major pathogenic link, being rather related to the inflammatory component of the disease, its expression being reduced by proinflammatory cytokines.

Pathogenic role of abnormal fatty acids and adipokines in the portal flow. Relevance for metabolic syndrome, hepatic steatosis and steatohepatitis.

Evidence has been provided that increased levels of non esterified fatty acids (NEFA) in the portal flow would produce insulin resistance and would also stimulate the hepatic protein synthesis, thereby explaining the increased plasma levels not only of apolipoprotein B, but also of other liver-derived enzymes and proteins occurring in overweight and hypertriglyceridemic patients. The high plasma concentration of triglyceride-rich lipoprotein would facilitate the transfer of cholesteryl esters from HDL and LDL to VLDL in exchange for triglycerides, a process mediated by liver-derived cholesteryl ester transfer protein (CETP). The triglyceride thereby acquired in HDL and LDL would then be hydrolyzed by hepatic lipase. The resulting association of increased triglycerides, low HDL cholesterol and small dense LDL is considered to be an atherogenic profile. The prothrombotic state, another feature of the metabolic syndrome, may also be explained by an enhanced hepatic synthesis of clotting factors and of the inhibitors of fibrinolysis. It was recently shown that adipocyte synthesized adiponectin reduces the release of fatty acids from the adipose tissue and would also enhance their uptake and oxidation in the muscle, thereby limiting their uptake in the liver. Decreased adiponectin production in obesity would therefore promote the development of insulin resistance, of atherogenic dyslipidemia and of the prothrombotic state. Because adiponectin also exerts an antiinflammatory activity by antagonizing TNFalpha, hypoadiponectinemia may be involved in atherogenesis and in the progression of hepatic steatosis to steatohepatitis.