Purpose A reduction in hearing sensitivity is often considered to be a normal age-related change. Recent studies have revisited prior ways of thinking about sensory changes over time, uncovering health variables other than age that play a significant role in sensory changes. Method In this cross-sectional study, cardiovascular (CV) health, pure-tone thresholds at 1000 to 4000 Hz, and distortion product otoacoustic emissions (DPOAEs), with and without contralateral noise, were measured in 101 participants age 10–78 years. Results Persons in the “old” age category (49–78 years) had worse pure-tone hearing sensitivity and DPOAEs than persons in the younger age categories ( p < .05), affirming an age effect. Although hearing decline occurred in all persons in all CV fitness categories of every age group, those with low CV fitness in the old age group had significantly worse pure-tone hearing at 2000 and 4000 Hz ( p <.05). Otoacoustic emission measurements were better for the old high-fit group but not significantly influenced by CV fitness level across age groups. Conclusions Results of the current study elucidate the potentially positive impact of CV health on hearing sensitivity over time. This finding was particularly robust among older adults.
Abstract Protein and immunofixation (IFIX) electrophoresis are used to diagnose and monitor monoclonal gammopathies. While IFIX detects clonal production of intact immunoglobulins and free light chains (FLC), the latter can also be quantified using a serum free light chain (SFLC) assay, in which polyclonal antisera detects epitopes specific for free kappa (KFLC) or lambda light chains (LFLC). An abnormal KFLC: LFLC ratio (KLR) serves as a surrogate for clonality. While the SFLC assay is highly sensitive, normal LFLC (<2.63mg/dL) and KLR results (>0.26 & <1.65) were found in samples with distinct lambda monoclonal free light chains visualized by IFIX (X-LMFLC). To investigate this discordance, contemporaneous SFLC or KLR values were evaluated for their ability to accurately classify monoclonal FLCs identified by IFIX. We performed a retrospective analysis of serum and urine IFIX (Sebia Hydrasys) and SFLC (Freelite®, Binding Site) results from our institution between July 2010 through December 2020, using R 4.0.2 and Tidyverse packages. From among 9,594 encounters in which a single monoclonal component was initially identified by IFIX, 157 X-LMFLC and 131 X-KMFLC samples were analyzed. Elevated LFLC with normal KFLC was identified in 105/157 X-LMFLC samples (67%), while both LFLC and KFLC were elevated in 42/157 samples (27%). Concordance between X-KMFLC and KFLC was markedly higher, where 122/131 samples (93%) displayed elevated kappa FLC (>1.94mg/dL) with normal LFLC, and only 7/131 X-KMFLC samples (5%) possessed both elevated KFLC and LFLC. The use of KLR to identify pathogenic monoclonal free light chains improved lambda concordance to 85%; however, 19/157 (12%) of X-LMFLC samples still exhibited normal KLR. High concordance of 98% was again observed for X-KMFLC with abnormal KLR. When samples were segregated according to normal or impaired renal function (eGFR > or ≤60mL/min/1.73m², respectively), this disparate identification of X-LMFLC and X-KMFLC by the SFLC assay persisted, suggesting that renal dysfunction (as measured by eGFR) does not underlie this phenomenon. Lastly, we corroborated the above findings in a larger sample population by examining patients with urine Bence Jones FLC identified by IFIX who had free or intact monoclonal components in serum (N=724), grouped by lambda or kappa light chain involvement. The cause(s) of the discrepant performance by the Freelite® SFLC assay, relative to the Sebia Hydrasys IFIX assay, for identifying lambda FLC components is currently unclear. Possible contributory factors include assay reference range cutoffs, other patient disease parameters, and differences in assay-specific polyclonal antisera. Future analyses of these factors will help to further characterize SFLC assay performance and elucidate how interpretation of composite serum FLC test results can be improved to better guide patient management.
Abstract Background The 2019 classification criteria for systemic lupus erythematosus (SLE) includes an initial criterion requiring the presence of an antinuclear antibody (ANA), positive at a titer of at least 1:80 on HEp-2 cells, or equivalent. However, results of ANA tests performed on HEp-2 cells vary when tested in different laboratories. Calibration of ANA assays by achieving a common specificity in healthy control populations offers the possibility of achieving harmonization via population interrogation, but the expected specificity in a healthy control population is not known. Methods The studies used to determine the use of ANAs performed by immunofluorescence microscopy on HEp-2 cells as the entry criterion for classification of SLE were reanalyzed by a meta-analysis to determine the expected frequency of positive ANAs in healthy control populations at serum dilutions of 1:40 and 1:80. Results Our meta-analysis demonstrated that the expected specificity in a healthy control population of ANA performed using serum diluted 1:80 is 91.3% (CI 86.1–94.7%). The expected specificity of ANA performed at 1:40 serum dilution is 79.2% (CI 72.3–84.8%). Conclusion One approach to achieving harmonization of ANA assays from different laboratories with each other and with expected performance would involve adjusting assays so that about 10% of a healthy control population has a positive ANA when tested at 1:80 dilution, and about 20% of the healthy control population has a positive ANA when tested at 1:40 dilution. This pragmatic approach to calibration and harmonization adjustment via population interrogation offers an opportunity for individual laboratories to be aligned with each other and with ANA performance expected for consistent categorization of patients with SLE.
Persons with healthy cardiovascular (CV) fitness have more acute hearing than persons with below-average CV fitness. Possible mechanisms include enhanced circulation, healthier blood lipid profiles, and different sympathetic activity. Muscle strength (MS) and conditioning programs may influence hearing acuity via similar proposed mechanisms. But studies have only examined the relationship of cardiovascular fitness and hearing. This study compared pure tone hearing levels and otoacoustic emissions for 4 groups categorized as high CV-high MS (n = 11), high CV-low MS (n = 10), low CV-high MS (n = 7), and low CV-low MS (n = 15). Twenty-four women and 19 men, mean (±SD) age = 21 ± 4 years underwent hearing tests at 3 frequencies: 2, 3, and 4 kHz. Each group's Vo2max; strength by leg curl, leg extension, bench press, and hand grip; blood lipid profile; body composition; and diet recall were assessed. Pure tone hearing results showed that at 2 kHz, the high CV-high MS group had better hearing than the low CV-high MS group (F = 4.31, p = .04). Otoacoustic emission results demonstrated similar patterns. The fitness-hearing relationship appears to be specifically related to cardiovascular fitness. High MS has an additive effect with CV on hearing.
Sixteen adults cycled for 10 min at low and high intensities--with and without noise. The noise consisted of a 1/3 octave band-filtered noise with a 2,000 Hz center frequency at 104 dB SPL. Regardless of whether or not noise was present, systolic blood pressure increased 14% and 40% above rest during low- and high-intensity exercise, respectively. Heart rate also increased above rest (36% and 90%) during low- and high-intensity exercise, respectively. Temporary threshold shifts (TTS) at 3,000, 4,000 and 6,000 Hz could not be differentiated following low- and high-intensity exercise when noise was not present. We report significant TTS at the three frequencies following 10 min of noise exposure with or without low- or high-intensity exercise. TTS was not influenced by either the 14-40% increase in blood pressure or the 36-90% increase in heart rate induced by exercise. The inability of noise alone to influence either blood pressure or heart rate appears to implicate systems other than the cardiovascular in the regulation of hearing sensitivity.
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