The prevalence of Eustachian tube dysfunction symptoms in patients with chronic rhinosinusitis

Background

While Eustachian tube dysfunction (ETD) is a known comorbidity of chronic rhinosinusitis (CRS), the prevalence of ETD symptoms in the CRS population is poorly understood. We sought to determine the cross‐sectional prevalence of ETD in patients with CRS using the validated Eustachian Tube Dysfunction Questionnaire (ETDQ‐7) and to correlate ETDQ‐7 scores with 22‐item Sino‐Nasal Outcome Test (SNOT‐22) scores, endoscopy scores, and computed tomography (CT) scores.

Methods

A total of 101 patients with confirmed CRS completed the ETDQ‐7 and SNOT‐22 at their initial visit to our rhinology clinic. Lund‐Mackay CT and Lund‐Kennedy endoscopy scores were also obtained. Spearman's correlation coefficient (ρ) was calculated.

Results

Among the 101 patients, 49 patients (48.5%) had an ETDQ‐7 score of ≥14.5, signifying clinically significant ETD. The mean ± standard deviation (SD) ETDQ‐7 score of the entire cohort was 17.8 ± 10.1. There was a moderately strong correlation between ETDQ‐7 and the SNOT‐22 ear subdomain (ρ = 0.691, p < 0.001). The correlation coefficient between ETDQ‐7 and total SNOT‐22 scores was ρ = 0.491 (p < 0.001), indicating moderate correlation. ETDQ‐7 scores were poorly correlated to objective measures of sinonasal disease, including Lund‐Mackay CT score (ρ = ?0.055, p = 0.594) and Lund‐Kennedy endoscopy score (ρ = ?0.099, p = 0.334).

Conclusion

Symptoms of ETD are highly prevalent among patients with CRS as documented by patient‐reported outcome measures. The correlation between ETDQ‐7 scores and SNOT‐22 ear subdomain scores is moderately strong, while the correlation between ETDQ‐7 scores and SNOT‐22 scores is moderate. ETD severity does not correlate with CT score or nasal endoscopy score.

     

Long Term Effect of Intensive Lifestyle Intervention on Cerebral Blood Flow

Objectives

To determine whether long‐term behavioral intervention targeting weight loss through increased physical activity and reduced caloric intake would alter cerebral blood flow (CBF ) in individuals with type 2 diabetes mellitus.

Design

Postrandomization assessment of CBF.

Setting

Action for Health in Diabetes multicenter randomized controlled clinical trial.

Participants

Individuals with type 2 diabetes mellitus who were overweight or obese and aged 45 to 76 (N = 310).

Interventions

A multidomain intensive lifestyle intervention (ILI ) to induce weight loss and increase physical activity for 8 to 11 years or diabetes support and education (DSE ), a control condition.

Measurements

Participants underwent cognitive assessment and standardized brain magnetic resonance imaging (MRI ) (3.0 Tesla) to assess CBF an average of 10.4 years after randomization.

Results

Weight changes from baseline to time of MRI averaged ?6.2% for ILI and ?2.8% for DSE (P < .001), and increases in self‐reported moderate or intense physical activity averaged 444.3 kcal/wk for ILI and 114.8 kcal/wk for DSE (P = .03). Overall mean CBF was 6% greater for ILI than DSE (P = .04), with the largest mean differences between ILI and DSE in the limbic region (3.39 mL /100 g per minute, 95% confidence interval (CI ) = 0.07–6.70 mL /100 g per minute) and occipital lobes (3.52 mL /100 g per minute, 95% CI = 0.20–6.84 mL /100 g per minute). In ILI , greater CBF was associated with greater decreases in weight and greater increases in physical activity. The relationship between CBF and scores on a composite measure of cognitive function varied between intervention groups (P = .02).

Conclusions

Long‐term weight loss intervention in overweight and obese adults with type 2 diabetes mellitus is associated with greater CBF .

     

Biochemical Markers for Alcoholism

A panel of blood tests, purportedly markers for alcohol abuse, were examined in 543 relatively healthy alcoholics entering ambulatory rehabilitation treatment. Individual tests were too low in sensitivity: gamma-glutamyl transpeptidase was abnormally high in only 49%, then mean corpuscular volume (45%), high density lipoprotein cholesterol (HDLC) (25%), serum glutamic oxaloacetic transaminase (SGOT) (28%), and blood alcohol (21%). HDLC was of low sensitivity, generally unaffected by liver disease, and related to quantitation of recent alcohol consumed. Combining seven markers, 82% of males and 71% females had at least one abnormally high value. Histories of heavy recent drinking, positive blood alcohol levels on admission, and manifest liver disease on physical examination or by hyperbilirubinemia were associated with high sensitivities of individual and pooled markers. The biochemical markers studied can be useful to suggest alcohol abuse, especially in some populations of drivers. In other populations of alcoholics, especially with intermittent alcohol or recent abstinence, their sensitivities were so low as to discourage extensive reliance on their use. The diagnosis of alcoholism continues to depend on clinical history of alcohol-related problems, including social, familial, legal, medical, psychological, and economic.     

Increased susceptibility of rat gastric mucosa to ulcerogenic stimulation with aging

We examined the influences of aging on gastric damage and gastric mucosal blood flow (GMBF) responses induced by acid back-diffusion, following the barrier disruption, and investigated the relation of capsaicin-sensitive sensory nerves to these changes. Male Fischer rats 3, 13, and 24 months old were used. Under urethane anesthesia, a rat stomach was mounted on a chamber, and gastric potential difference (PD), luminal H⁺ loss, and GMBF were measured before, during, and after exposure to 20 mM sodium taurocholate (TC) for 30 min, in the presence of 50 mM HCl. Mucosal exposure to TC caused surface cell damage, PD reduction, and acid back-diffusion (luminal H⁺ loss) in all groups of rats; PD reduction and the amount of H⁺ loss were not significantly different between young and aged rats. In young rats, a marked increase of GMBF was observed with luminal acid loss following TC treatment, yet it resulted in less damage in the gastric mucosa. In aged rats, however, such GMBF responses were apparently mitigated, leading to a significant worsening of gastric mucosal lesions induced by TC. Mucosal application of capsaicin (0.1 mg/ml) caused an increase of GMBF in young rats, but this response was significantly attenuated in aged rats. In addition, the amount of calcitonin gene-related peptide (CGRP) released in the isolated stomach in response to capsaicin (1 × 10^–5 M) was significantly lower in aged animals when compared to young rats. These findings suggest that the gastric mucosa of aged rats is more vulnerable to acid back-diffusion following the barrier disruption, partly because of dysfunction of GMBF responses mediated by capsaicin-sensitive sensory neurons in the acidic conditions.     

Autoantibodies inhibit interleukin-7-mediated proliferation and are associated with the age-dependent loss of pre-B cells in autoimmune New Zealand Black Mice

Surface IgM+B220+ B cell precursors can be categorized as either leukosialin (CD43/S7) negative (late stage pre-B cells) or positive (pro-B/early pre-B cells). In autoimmune New Zealand Black (NZB) mice, bone marrow small pre-B cells (IgM-CD43-B220+) and pro-B/early pre-B cells (IgM-CD43+B220+) declined significantly with age. In particular, subpopulations of pro-B/early pre-B cells expressing the heat stable antigen (HSA) were found in lower proportions with age. Significant decreases in interleukin-7 (IL-7) colony forming units (CFU) were also seen in NZB mice by 6 to 8 months of age and accompanied alterations in the numbers of pro-B and pre-B cells in bone marrow. Concomitant with reduced numbers of B lineage precursor cells and IL-7 CFU in vivo, NZB mice produced serum IgM antibodies that strongly inhibited IL-7 CFU responses in vitro. Two monoclonal IgM antibodies (5G9, 2F5) derived from LPS stimulated 10-month-old NZB splenocytes recognized pre-B cell surface antigens on both pre-B cell lines and on IL-7 stimulated bone marrow pro-B/pre-B cells. However, these monoclonal antibodies (MoAb) failed to significantly stain ex vivo bone marrow cells. The 5G9 and 2F5 MoAbs also partially inhibited IL-7 CFU in vitro. These results suggest that NZB bone marrow becomes increasingly deficient in B cell precursors and especially in IL-7 responsive pre-B cells with age. IgM serum antibodies and monoclonal IgM antibodies derived from older NZB mice inhibit pre-B cell growth to IL-7. The production of such autoantibodies may interfere with B cell development in aging NZB mice by preventing IL-7-mediated proliferation.