Anti-Human IgD polyclonal antibody [FITC]

Objectives: GH-releasing hormone (GHRH) exerts hypnotic actions increasing the non-rapid eye movement (NREM) sleep. Conversely, GH stimulates the REM sleep. GH deficiency (GHD) often leads to sleep problems, daytime fatigue and reduced quality of life (QoL). GHD may be due to lack of hypothalamic GHRH or destruction of somatotroph cells. We have described a cohort with isolated GHD (IGHD) due to GHRH resistance caused by a homozygous null mutation (c. 57 + 1G > A) in the GHRH receptor gene. They have normal QoL and no obvious complaints of chronic tiredness. The aim of this study was to determine the sleep quality in these subjects. Methods: A cross-sectional study was carried out in 21 adult IGHD subjects, and 21 age-and gender-matched controls. Objective sleep assessment included polygraphic records of the awake, stages NREM [N1 (drowsiness), N2 and N3 (already sleeping)] and REM (R). Subjective evaluation included the Pittsburgh Sleep Quality Index, the Insomnia Severity Index and the Epworth Sleepiness Scale. Results: IGHD subjects showed a reduction in sleep efficiency (P = 0.007), total sleep time (P = 0.028), duration of N2 and R in minutes (P = 0.026 and P = 0.046 respectively), but had increased duration and percentage of N1 stage (P = 0.029 and P = 0.022 respectively), wake (P = 0.007) and wake-time after sleep onset (P = 0.017). There was no difference in N3 or in sleep quality questionnaire scores. Conclusion: Patients with IGHD due to GHRH resistance exhibit objective reduction in the sleep quality, with changes in NREM and REM sleep, with no detectable subjective consequences. GHRH resistance seems to have a preponderant role over GHD in the sleep quality of these subjects.

OBJECTIVE The serum level of sex hormone binding globulin (SHBG) changes inversely with that of both insulin and insulin-like growth factor (IGF-I), during several nutritional conditions, as well as in response to GH treatment. However, with exogenous IGF-I administration, endogenous IGF-I increases, while insulin decreases. In order to study the separate roles of these hormones in controlling SHBG metabolism, we compared SHBG levels in patients treated with IGF-I and GH. DESIGN AND PATIENTS Serum levels of IGF-I, insulin and SHBG were measured before and during the treatment of patients with IGF-I or GH. Blood samples were drawn in the fasting state, prior to and during therapy, 24 hours after drug administration. Sixteen children and adults with Laron syndrome (LS) received daily s.c. injections of IGF-I (120-150 mu g/kg) for up to 5 months. Three adults with isolated GH deficiency (IGHD) received daily s.c. injections of GH (0.03-0.06 U/kg) for 16 months. Two groups of nine prepubertal children with constitutional short stature (CSS) received GH (0.1 U/kg/day) for 3 months. MEASUREMENTS Serum levels of insulin and acid extractable IGF-I were determined by RIA, and that of SHBG by IRMA. RESULTS Basal insulin and SHBG levels were within normal range in the LS, IGHD and CSS patients. IGF-I levels were low in LS and IGHD patients, and normal in the CSS children. The mean peak response to chronic therapy was as follows: in LS patients, IGF-I administration decreased insulin levels to 62%, and increased SHBG levels by 64% above basal values. Chronic GH therapy in IGHD caused a marked rise in both IGF-I levels (473%), and insulin levels (96%), and a gradual decline of SHBG to 75% of the basal concentration. In GH treated CSS patients, serum IGF-I peaked at 80% and insulin levels at 102% above the respective basal levels, while SHBG decreased to 83% after 5 days of treatment. CONCLUSION The results obtained in Laron syndrome, isolated GH deficiency and constitutional shea stature patients treated with IGF-I or GH, indicate that serum insulin had consistently an inverse relation with the levels of circulating SHBG. No relation was found between IGF-I and SHBG levels.