Prevalence of growth hormone deficiency in middle-age adults recovering from stroke.

Objective: The prevalence of chronic growth hormone deficiency (GHD) and its association with other hormonal deficiencies was determined in middle-aged patients post-stroke with and without consideration of body mass index (BMI).Methods: Clinical records were reviewed to determine pituitary function at least 3 months post-stroke. Patients with a history of endocrine anomalies were excluded. GHD was determined by utilizing standard peak GH cutoffs following the glucagon stimulation test. A secondary analysis was conducted with stricter BMI-adjusted cutoffs. The accuracy of IGF-1 in predicting GHD was also examined.Results: GHD was diagnosed in 54% of patients (≥5.0 µg/L), with 32% falling into the severe (≤3 µg/L) category. Patients with GHD had lower levels of FSH, T3, LH, and SHBG. Analyzes of BMI-adjusted GH levels, revealed that 14% of patients were GHD. These patients had higher prolactin. IGF-1 values were not predictive of GHD. Latency to be admitted to post-acute rehabilitation was greater in patients with GHD.Conclusions: Evidence suggests patients with stroke may be at risk for developing GHD. GHD was associated with decreased levels of other hormones. Co-morbidities for stroke and neuroendocrine dysfunction overlap and may have implications for recovery following stroke.

Altered Fecal Microbiome Years after Traumatic Brain Injury.

Patients with chronic traumatic brain injury (TBI) requiring long-term, permanent care suffer a myriad of clinical symptoms (i.e., impaired cognition, fatigue, and other conditions) that persist for years beyond the acute brain injury. In addition to these comorbid clinical symptoms, chronic TBI patients exhibit altered amino acid and hormonal profiles with distinct cytokine patterns suggesting chronic inflammation. This metabolic link suggests a role of the gut-brain axis in chronic TBI. Thus, we utilized a two-site trial to investigate the role of the gut-brain axis in comorbidities of chronic TBI. The fecal microbiome profile of 22 moderate/severe TBI patients residing in permanent care facilities in Texas and California was compared to 18 healthy age-matched control subjects working within the participating facilities. Each fecal microbiome was characterized by 16S(V4) ribosomal RNA (rRNA) gene sequencing and metagenomic genome sequencing approaches followed by confirmatory full 16S rRNA gene sequencing or focused tuf gene speciation and specific quantitative polymerase chain reaction evaluation of selected genera or species. The average chronic TBI patient fecal microbiome structure was significantly different compared to the control cohort, and these differences persisted after group stratification analysis to identify any unexpected confounders. Notably, the fecal microbiome of the chronic TBI cohort had absent or reduced Prevotella spp. and Bacteroidies spp. Conversely, bacteria in the Ruminococcaceae family were higher in abundance in TBI compared to control profiles. Previously reported hypoaminoacidemia, including significantly reduced levels of l-tryptophan, l-sarcosine, ß-alanine, and alanine, positively correlated with the reduced levels of Prevotella spp. in the TBI cohort samples compared to controls. Although the sequelae of gut-brain axis disruption after TBI is not fully understood, characterizing TBI-related alterations in the fecal microbiome may provide biomarkers and therapeutic targets to address patient morbidity.

Adrenal vein sampling with and without cosyntropin stimulation for detection of surgically remediable aldosteronism.

CONTEXT AND OBJECTIVE: Bilateral adrenal vein sampling (AVS), the diagnostic standard for identifying surgically remediable aldosteronism (SRA), is commonly performed after cosyntropin stimulation (post-ACTHstim). The role of AVS without cosyntropin stimulation (pre-ACTHstim) has not been established. The selectivity index (SI), the adrenal vein (av) serum cortisol concentration divided by that in a peripheral vein, confirms av sampling. The minimally acceptable SI is controversial. The objectives of this study were to determine the role of pre-ACTHstim AVS and a predetermined SI. DESIGN: Using biochemical cure as the endpoint, we performed a retrospective head-to-head comparison of pre-ACTHstim AVS to post-ACTHstim AVS. The specificity of a predetermined minimum SI of 1.5 in pre-ACTHstim AVS was determined. PATIENTS: At a regional AVS referral centre, we analysed 32 patients who had undergone simultaneous bilateral AVS both pre- and post-ACTHstim and had returned for postadrenalectomy evaluation. MEASUREMENTS: Simultaneous bilateral AVS was performed with measurements of venous concentrations of aldosterone and cortisol. End points were postadrenalectomy plasma renin activity, serum aldosterone concentration, and number of antihypertensive medications. RESULTS: All 32 patients achieved a biochemical cure following adrenalectomy. The two AVS protocols were complementary. Notably, seven patients (22%; CI = 11-38) were found to have SRA by a lateralization index (LI) > 4 on the pre-ACTHstim AVS, but not on the post-ACTHstim AVS. SI pre-ACTHstim was divided into tertiles. Specificity was 100% in all. CONCLUSIONS: Simultaneous bilateral AVS performed both pre-ACTHstim and post-ACTHstim maximizes SRA identification. A SI of 1.5 pre-ACTHstim does not reduce specificity.

Nicotinamide reverses behavioral impairments and provides neuroprotection in 3-nitropropionic acid induced animal model ofHuntington's disease: implication of oxidative stress- poly(ADP- ribose) polymerase pathway.

Huntington's disease (HD) is characterized by cognitive and psychiatric impairment caused by neuronal degeneration in the brain. Several studies have supported the hypothesis that oxidative stress is the main pathogenic factor in HD. The current study aims to determine the possible neuroprotective effects of nicotinamide on 3-nitropropionic acid (3-NP) induced HD. Male Wistar albino rats were divided into six groups. Group I was the vehicle-treated control, group II received 3-NP (20 mg/kg, intraperitoneally (i.p.) for 4 days, group III received nicotinamide (500 mg/kg, i.p.). The remaining groups received a combination of 3-NP plus nicotinamide 100, 300 or 500 mg/kg, i.p. respectively for 8 days. Afterward, the motor function and hind paw activity in the limb withdrawal were tested; rats were then euthanized for biochemical and histopathological analyses. Treatment of rats with 3-NP altered the motor function, elevated oxidative stress and caused significant histopathological changes in the brain. The treatment of rats with nicotinamide (100, 300 and 500 mg/kg) improved the motor function tested by locomotor activity test, movement analysis, and limb withdrawal test, which was associated with decreased oxidative stress markers (malondialdehyde, nitrites) and increased antioxidant enzyme (glutathione) levels. In addition, nicotinamide treatment decreased lactate dehydrogenase and prevented neuronal death in the striatal region. Our study, therefore, concludes that antioxidant drugs like nicotinamide might slow progression of clinical HD and may improve the motor functions in HD patients. To the best of our knowledge, this study is the first to explore the neuroprotective effects of nicotinamide on 3-NP-induced HD.

Comparison of Visual Prostate Symptom Score and International Prostate Symptom Score in the evaluation of men with benign prostatic hyperplasia: A prospective study from an Indian population.

BACKGROUND: Lower urinary tract symptoms (LUTSs) due to benign prostatic hyperplasia (BPH) are common conditions in middle-age or older men. The International Prostate Symptom Score (IPSS) is a useful and validated questionnaire to evaluate LUTS secondary to BPH. Van der Walt et al have developed an alternative questionnaire named the Visual Prostate Symptom Score (VPSS) questionnaire. This study aimed to evaluate the relationship between the VPSS and IPSS in the evaluation of men with LUTSs due to BPH in an Indian population. MATERIALS AND METHODS: This was a prospectively designed study conducted at Sri Sathya Sai Institute of Higher Medical Sciences, Prashanthigram (Anantapur, Andhra Pradesh, India). A total of 121 patients who presented to the urology outpatient department with LUTS due to BPH were enrolled in the study. Patients were followed up at 1-month and 3-month intervals. All patients were given both questionnaires. The correlation test was used to assess the correlation between two symptom scores and various parameters. Observations with a P value < 0.05 were considered statistically significant. RESULTS: There was a statistically significant difference in the number of patients requiring assistance to fill the questionnaires according to their education level. There was a positive correlation between IPSS total score and VPSS total score (r = 0.7235; P < 0.0001), VPSS total score and VPSS quality of life (Qol; r = 0.70753; p < 0.0001), IPSS total versus IPSS Qol (r = 0.65583; P < 0.0001), and IPSS Qol versus VPSS Qol (r = 0.84093; P < 0.0001). A negative correlation was observed between total VPSS with Qmax, total IPSS with Qmax, IPSS total versus Qavg (r = -0.479; P < 0.0001), and VPSS total versus Qavg (r = -0.5; P < 0.0001). All VPSS questions showed statistically significant correlation with the corresponding IPSS questions. CONCLUSION: There is a statistically significant correlation between the VPSS and IPSS and it can be completed by a greater number of patients without assistance.

Hypoaminoacidemia Characterizes Chronic Traumatic Brain Injury.

Individuals with a history of traumatic brain injury (TBI) are at increased risk for a number of disorders, including Alzheimer's disease, Parkinson's disease, and chronic traumatic encephalopathy. However, mediators of the long-term morbidity are uncertain. We conducted a multi-site, prospective trial in chronic TBI patients (∼18 years post-TBI) living in long-term 24-h care environments and local controls without a history of head injury. Inability to give informed consent was exclusionary for participation. A total of 41 individuals (17 moderate-severe TBI, 24 controls) were studied before and after consumption of a standardized breakfast to determine if concentrations of amino acids, cytokines, C-reactive protein, and insulin are potential mediators of long-term TBI morbidity. Analyte concentrations were measured in serum drawn before (fasting) and 1 h after meal consumption. Mean ages were 44 ± 15 and 49 ± 11 years for controls and chronic TBI patients, respectively. Chronic TBI patients had significantly lower circulating concentrations of numerous individual amino acids, as well as essential amino acids (p = 0.03) and large neutral amino acids (p = 0.003) considered as groups, and displayed fundamentally altered cytokine-amino acid relationships. Many years after injury, TBI patients exhibit abnormal metabolic responses and altered relationships between circulating amino acids, cytokines, and hormones. This pattern is consistent with TBI, inducing a chronic disease state in patients. Understanding the mechanisms causing the chronic disease state could lead to new treatments for its prevention.