Vestibular function in Lermoyez syndrome at attack

Lermoyez syndrome (LS) has been regarded as a variant of Ménière’s disease (MD), but so far there have been very few cases of LS reported in the literature, so such a conclusion is debatable. Specifying the pattern of auditory and vestibular changes at attack using objective quantitative measures is important for understanding the mechanism responsible for MD and LS. Here we report the first objective measures of dynamic otolith function and dynamic semicircular canal function in an LS patient at the time of the attack as well as at quiescence, documenting the fluctuation in otolith and semicircular canal function in the patient. The very rapid changes in dynamic vestibular function at the time of the LS attack appear to complement some of the rapid changes in auditory and vestibular function at the attack in Ménière’s disease, supporting the contention that LS is a variant of MD.     

Enlarged vestibular aqueduct (EVA) related with recurrent benign paroxysmal positional vertigo (BPPV)

The vestibular aqueduct is a bony canal related to the bony labyrinth of the inner ear and represents the non-sensory components of the endolymph-filled, closed, membranous labyrinth. The association of congenital sensorineural hearing loss with a large or enlarged vestibular aqueduct is well known as the large vestibular aqueduct syndrome (LVAS). The enlarged VA (EVA) comprises abnormalities not only in the structure of the inner ear, but also in the physiology of the auditory and vestibular systems. The clinical picture of this clinical entity is variable [Yetiser S, Kertment M, Ozkaptan Y. Vestibular disturbance in patients with Large Vestibular Aqueduct Syndrome (LVAS). Acta Otolaryngol (StochK) 1999;119: 641-646]. Signs and symptoms of the auditory impairment are more commonly described in the literature: hearing loss ranges from mild to profound, arising from fluctuating to stepwise progressive or sudden. Vestibular disturbances, ranging from mild imbalance to episodic vertigo, are rarely described in the literature. Benign paroxysmal positional vertigo (BPPV) is a labyrinthine disorder with a typical behavior: intense crises of rotational vertigo induced by postural changes of the head, with short duration and usually good responsiveness to rehabilitative maneuvers. These maneuvers are effective in about 80% of patients with BPPV. BPPV often recurs. About 1/3 of patients have a recurrence in the first year after treatment, and by five years, about half of all patients have a recurrence. Vestibular aqueduct has been demonstrated by conventional tomography and computed tomography (CT), however, CT scans cannot show the membranous labyrinth itself. On MR images it is not the vestibular aqueduct that is visualized but its contents, the endolymphatic duct and sac, and can show the abnormalities of the fluid spaces related to the membranous labyrinth. It is proposed that recurrent benign paroxysmal positional vertigo (BPPV) is related with volumetric abnormalities of vestibular aqueduct. This verifiable hypothesis tries to define this rapport and explore new diagnostic and therapeutic possibilities.     

Rehabilitation and quality of life in patients undergoing surgery for esophageal cancer

The impact of esophageal cancer surgery, postoperatively as well as on quality of life (QoL) is still largely unknown. Clinical experience and the scarce existing literature concur that these patients show difficulty in returning to their original lifestyles and previous social activities, not just due to the difficulties common to all tumor pathologies but also for the specific dietary and digestive disturbances which characterize esophageal cancer therapy. As specific rehabilitation protocols are nonexistent in the literature, in this study a rehabilitation planning program, is proposed based on evaluation of postoperative and long-term problems which can be tackled with rehabilitation.     

EGFR and KRAS mutations detection on lung cancer liquid-based cytology: a pilot study

In advanced non-small-cell lung carcinomas epidermal growth factor receptor (EGFR) and KRAS testing is often performed on cytology. Liquid-based cytology (LBC), which eliminates the need for slide preparation by clinicians, may be very useful. In 42 LBC DNA was extracted twice. One sample was obtained directly from CytoLyt solution, whereas the other DNA sample was derived after smear preparation and laser capture microdissection (LCM) of Papanicolaou-stained cells. EGFR and KRAS mutational analyses were performed by direct sequencing. On CytoLyt-derived DNA four EGFR (9%) and five KRAS (12%) gene mutations were found. When direct sequencing was performed after LCM, the rate of cases that displayed either EGFR or KRAS mutations increased from 21% to 40%. Although time-consuming, LCM makes direct sequencing highly sensitive even on LBC preparations containing only a few cells.     

Low baseline and subsequent higher aortic abdominal aneurysm FDG uptake are associated with poor sac shrinkage post endovascular repair

Purpose

The growth phases of medically treated abdominal aortic aneurysms (AAA) are frequently associated with an ¹⁸F–fluorodesoxyglucose positron emission tomography (FDG-PET) pattern involving low baseline and subsequent higher FDG uptake. However, the FDG-PET patterns associated with the endovascular aneurysm repair (EVAR) of larger AAA are presently unknown. This study aimed to investigate the relationship between serial AAA FDG uptake measurements, obtained before EVAR and 1 and 6 months post-intervention and subsequent sac shrinkage at 6 months, a well-recognized indicator of successful repair.

Methods

Thirty-three AAA patients referred for EVAR (maximal diameter: 55.4?±?6.0 mm, total volume: 205.7?±?63.0 mL) underwent FDG-PET/computed tomography (CT) before EVAR and at 1 and 6 months thereafter, with the monitoring of AAA volume and of a maximal standardized FDG uptake [SUVmax] averaged between the axial slices encompassing the AAA.

Results

Sac shrinkage was highly variable and could be stratified into three terciles: a first tercile in which shrinkage was absent or very limited (0–29 mL) and a third tercile with pronounced shrinkage (56–165 mL). SUVmax values were relatively low at baseline in the 1st tercile (SUVmax: 1.69?±?0.33), but markedly increased at 6 months (2.42?±?0.69, p?=?0.02 vs. baseline). These SUV max values were by contrast much higher at baseline in the 3rd tercile (SUVmax: 2.53?±?0.83 p?=?0.009 vs. 1st tercile) and stable at 6 months (2.49?±?0.80), while intermediate results were documented in the 2nd tercile. Lastly, the amount of sac shrinkage, expressed in absolute values or in percentages of baseline AAA volumes, was positively correlated with baseline SUVmax (p?=?0.001 for both).

Conclusion

A low pre-EVAR FDG uptake and increased AAA FDG uptake at 6 months are associated with reduced sac shrinkage. This sequential FDG-PET pattern is similar to that already shown to accompany growth phases of medically treated AAA.

     

Immunogenicity of two doses of BNT162b2 and mRNA-1273 vaccines for solid cancer patients on treatment with or without a previous SARS-CoV-2 infection

Previous studies on the immunogenicity of SARS-CoV-2 mRNA vaccines showed a reduced seroconversion in cancer patients. The aim of our study is to evaluate the immunogenicity of two doses of mRNA vaccines in solid cancer patients with or without a previous exposure to the virus. This is a single-institution, prospective, nonrandomized study. Patients in active treatment and a control cohort of healthy people received two doses of BNT162b2 (Comirnaty, BioNTech/Pfizer, The United States) or mRNA-1273 (Spikevax, Moderna). Vaccine was administered before starting anticancer therapy or on the first day of the treatment cycle. SARS-CoV-2 antibody levels against S1, RBD (to evaluate vaccine response) and N proteins (to evaluate previous infection) were measured in plasma before the first dose and 30 days after the second one. From January to June 2021, 195 consecutive cancer patients and 20 healthy controls were enrolled. Thirty-one cancer patients had a previous exposure to SARS-CoV-2. Cancer patients previously exposed to the virus had significantly higher median levels of anti-S1 and anti-RBD IgG, compared to healthy controls (P = .0349) and to cancer patients without a previous infection (P < .001). Vaccine type (anti-S1: P < .0001; anti-RBD: P = .0045), comorbidities (anti-S1: P = .0274; anti-RBD: P = .0048) and the use of G-CSF (anti-S1: P = .0151) negatively affected the antibody response. Conversely, previous exposure to SARS-CoV-2 significantly enhanced the response to vaccination (anti-S1: P < .0001; anti-RBD: P = .0026). Vaccine immunogenicity in cancer patients with a previous exposure to SARS-CoV-2 seems comparable to that of healthy subjects. On the other hand, clinical variables of immune frailty negatively affect humoral immune response to vaccination.     

Inverse correlation between VEGF and soluble VEGF receptor 2 in POEMS with AIDP responsive to intravenous immunoglobulin

POEMS (polyneuropathy, organomegaly, endocrinopathy, M‐band, and skin changes) syndrome is characterized by chronic progressive polyneuropathy and plasma‐cell dyscrasia. A major diagnostic criterion of POEMS is elevation of circulating vascular endothelial growth factor (VEGF), which is believed to play a pathogenic role in this disease. We report a case of POEMS that presented as relapsing acute inflammatory demyelinating polyneuropathy, in which complete remission after intravenous immunoglobulin (IVIg) treatment was unexpectedly observed. At clinical nadir, the VEGF level was 30‐fold higher, and the soluble form of VEGF receptor 2 (sVEGFR2), which acts as a decoy for VEGF, was 2.7‐fold lower than normal. These changes combined might contribute to the pathogenesis of POEMS, inducing vascular permeability and tissue edema. At 9‐month follow‐up, during clinical remission, VEGF and sVEGFR2 were near normal values. sVEGFR2 reduction is a new finding in POEMS. IVIg treatment may benefit POEMS patients with acute neuropathy by downgrading VEGF release induced by inflammatory cytokines. Muscle Nerve, 2010