Cerebrospinal Fluid Leaks: A Case Series of Sinus Opacification on Computed Tomography (CT) Imaging.

Introduction: Cerebrospinal fluid (CSF) leaks occur when fluid seeps through a dural or skull base defect, typically in the nose or ear. CSF leaks commonly are identified and diagnosed by use of computed tomography (CT) and CT cisternogram. CT findings suggestive of a CSF leak include a skull-based bone defect along with opacification of the contiguous sinus. This study examined a series of CSF leaks on CT imaging to document imaging findings. Methods: A single-institution retrospective review of cases of CSF leak diagnosed by CT maxillofacial or CT cisternogram from January 1, 2008 to March 12, 2018 was performed. Patient demographics, history, imaging findings, and treatment were recorded. Results: Thirty-nine patients met the inclusion criteria for the study. The average age was 51, and a large majority were female (76.9%). Among the 25 patients in which it was reported, the mean size of skull base defect was 0.472 cm. Of the 39 total cases, 27 patients (69.2%) presented with sinus opacification on CT imaging. Conclusions: Radiologists should be aware of the possibility of notable sinus opacification observable on CT when investigating a potential CSF leak. Opacification may vary in both location and size depending on the nature and location of a CSF leak. Further research is needed to draw a correlation between sinus opacification seen on CT scan and the diagnosed origin of a CSF leak.

Adiponectin Levels Differentiate Metabolically Healthy vs Unhealthy Among Obese and Nonobese White Individuals.

CONTEXT: Adiponectin levels (ADPN) are lower in individuals with central obesity and cardiometabolic diseases. Conversely, studies have shown paradoxical hyperadiponectinemia (HA) in metabolically healthy obese (MHO) individuals of non-European descent. Moreover, individuals with higher sc to visceral adipose tissue (ie, higher peripheral adiposity) distribution have higher ADPNs. However, it is not known whether metabolically healthy individuals have predominantly peripheral adiposity along with higher ADPNs. OBJECTIVE: This study aimed to evaluate the association of ADPN and adiposity distribution with metabolic health in white individuals. DESIGN AND SETTING: This was a cross-sectional study of members of "Take Off Pounds Sensibly" weight loss club and their relatives. PARTICIPANTS: We recruited 2486 (72% women, 61% obese) individuals. They were defined as metabolically healthy by absence of hypertension, diabetes, and dyslipidemia; and they were further classified into metabolically healthy nonobese (MHNO), metabolically unhealthy nonobese (MUNO), metabolically healthy obese (MHO), and metabolically unhealthy obese (MUO). Waist-to-hip ratios (WHRs) were used as markers of adiposity distribution. Insulin resistance was measured using homeostasis model assessment. RESULTS: Among the four groups, MHNO had the lowest WHRs (higher peripheral adiposity) and highest ADPN, and MUO had highest WHRs (higher central adiposity) and lowest ADPN (P < .001). Among both nonobese and obese, metabolically healthy individuals had higher ADPN than metabolically unhealthy individuals (P < .05) after adjustment for age, sex, and body mass index. MHNO also had lower WHRs compared with MUNO (P < .01). Although WHRs were lower among MHO compared with MUO, the difference was not significant. In addition, nonobese and obese individuals with HA (defined using sex-specific cutoffs) had lower homeostasis model assessment and dyslipidemia compared with individuals without HA. CONCLUSIONS: Higher ADPN and lower WHRs (higher peripheral adiposity) are associated with better metabolic health in both nonobese and obese white individuals. These results suggest that ADPN and peripheral adiposity play a key role in determining the metabolic health independent of body mass index.

Adiposity distribution influences circulating adiponectin levels.

Thirty percent of obese individuals are metabolically healthy and were noted to have increased peripheral obesity. Adipose tissue is the primary source of adiponectin, an adipokine with insulin-sensitizing and anti-inflammatory properties. Lower adiponectin levels are observed in individuals with obesity and those at risk for cardiovascular disease. Conversely, higher levels are noted in some obese individuals who are metabolically healthy. Our objective was to determine whether abdominal adiposity distribution, rather than body mass index (BMI) status, influences plasma adiponectin level. A total of 424 subjects (female, 255) of Northern European ancestry were recruited from "Take Off Pounds Sensibly" weight loss club members. Demographics, anthropometrics, and dual-emission x-ray absorptiometry of the whole body, and computed tomography scan of the abdomen were performed to obtain total body fat content and to quantify subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT), respectively. Laboratory measurements included fasting plasma glucose, insulin, lipid panel, and adiponectin. Age- and gender-adjusted correlation analyses showed that adiponectin levels were negatively correlated with BMI, waist circumference, triglycerides, total fat mass, and VAT. A positive correlation was noted with high-density lipoprotein cholesterol and fat-free mass (P < 0.05). SAT-to-VAT ratios were also significantly associated with adiponectin (r = 0.13, P = 0.001). Further, the best positive predictors for plasma adiponectin were found to be SAT-to-VAT ratios and gender by regression analyses (P < 0.01). Abdominal adiposity distribution is an important predictor of plasma adiponectin and obese individuals with higher SAT-to-VAT ratios may have higher adiponectin levels.

Effects of body temperature maintenance on glucose, insulin, and corticosterone responses to acute hypoxia in the neonatal rat.

One of the biggest challenges of premature birth is acute hypoxia. Hypothermia during acute hypoxic periods may be beneficial. We hypothesized that prevention of hypothermia during neonatal hypoxia disrupts glucose homeostasis and places additional metabolic challenges on the neonate. Pups at PD2 and PD8 were exposed to 8% O2 for 3 h, during which they were allowed to either spontaneously cool or were kept isothermic. There was also a time control group that was subjected to normoxia and kept isothermic. Plasma glucose, insulin, C-peptide, corticosterone, and catecholamines were measured from samples collected at baseline, 1 h, 2 h, and 3 h. In postnatal day 2 (PD2) rats, hypoxia alone resulted in no change in plasma glucose by 1 h, an increase by 2 h, and a subsequent decrease below baseline values by 3 h. Hypoxia with isothermia in PD2 rats elicited a large increase in plasma insulin at 1 h. In PD8 rats, hypoxia with isothermia resulted in an initial increase in plasma glucose, but by 3 h, glucose had decreased significantly to below baseline levels. Hypoxia with and without isothermia elicited an increase in plasma corticosterone at both ages and an increase in plasma epinephrine in PD8 rats. We conclude that the insulin response to hypoxia in PD8 rats is associated with an increase in glucose similar to an adult; however, insulin responses to hypoxia in PD2 rats were driven by something other than glucose. Prevention of hypothermia during hypoxia further disrupts glucose homeostasis and increases metabolic challenges.

Adrenocorticotropic hormone and corticosterone responses to acute hypoxia in the neonatal rat: effects of body temperature maintenance.

The corticosterone response to acute hypoxia in neonatal rats develops in the 1st wk of life, with a shift from ACTH independence to ACTH dependence. Acute hypoxia also leads to hypothermia, which may be protective. There is little information about the endocrine effects of body temperature maintenance during periods of neonatal hypoxia. We hypothesized that prevention of hypothermia during neonatal hypoxia would augment the adrenocortical stress response. Rat pups separated from their dams were studied at postnatal days 2 and 8 (PD2 and PD8). In one group of pups, body temperature was allowed to spontaneously decrease during a 30-min prehypoxia period. Pups were then exposed to 8% O(2) for 3 h and allowed to become spontaneously hypothermic or externally warmed (via servo-controlled heat) to maintain isothermia. In another group, external warming was used to maintain isothermia during the prehypoxia period, and then hypoxia with or without isothermia was applied. Plasma ACTH and corticosterone and mRNA expression of genes for upstream proteins involved in the steroidogenic pathway were measured. Maintenance of isothermia during the prehypoxia period increased baseline plasma ACTH at both ages. Hypothermic hypoxia caused an increase in plasma corticosterone; this response was augmented by isothermia at PD2, when the response was ACTH-independent, and at PD8, when the response was ACTH-dependent. In PD8 rats, isothermia also augmented the plasma ACTH response to hypoxia. We conclude that maintenance of isothermia augments the adrenocortical response to acute hypoxia in the neonate. Prevention of hypothermia may increase the stress response during neonatal hypoxia, becoming more pronounced with increased age.