No abstract

We evaluated the GH response to combined administration of pyridostigmine (PD), a cholinergic agonist, and GH-releasing hormone (GHRH) (60 mg PD given orally 60 min before the GHRH bolus) as well as baseline IGF-I concentrations in 10 patients (5 males and 5 females, age 6.0-24 years) with Prader-Labhard-Willi (PLW) syndrome, 8 prepubertal obese children (4 males and 4 females, age 5.6-12.0 years) and 9 prepubertal short normal children (7 males and 2 females, age 8.0-12.8 years). Mean GH responses to PD + GHRH were significantly lower (p < 0.0001) in the PLW patients (13.8 ± 3.3 µg/l) than in the short normal children (52.2 ± 9.0 µg/l) and similar to those of the obese children (14.3 ± 3.2 µg/l). Mean serum IGF-I levels were significantly lower (p < 0.05) in the PLW patients (117.5 ± 26.4 µg/l) than in the obese (329.3 ± 88.0 µg/l) and the short normal children (214.3 ± 38.3 µg/l). Two of the PLW patients had absent GH responses to PD + GHRH associated with subnormal IGF-I concentrations, indicating pituitary GH deficiency. When these 2 cases were excluded from the statistical calculation, mean peak GH responses to PD + GHRH remained significantly lower (p < 0.0001) in the PLW patients (17.1 ± 3.0 µg/l), while their mean serum IGF-I concentrations (143.4 ± 71.5 µg/l) were not significantly different from those of the other two groups. These results indicate that patients with the PLW syndrome have a reduced or absent GH secretory reserve associated in some cases with low levels of IGF-I. Whether these findings are involved in the pathogenesis of their short stature remains to be confirmed.

à 112 à /120 à Protein intake (g/kg) on day 21/28 4.1 à /4.3 Ãà 3.8 à /4.0 Ãà BUN (mg/dL) on day 21/28 14 à /11 Ãà 17 à /16 Ãà z score: 2010 Fenton growth curves. Standard deviation for each variable omitted for clarity (available from author). BUN ¼ blood urea nitrogen; FOC ¼ fronto-occipital circumference; L ¼ length; W ¼ weight. à P < 0.05; Ãà P < 0.01. Student t test used.

No abstract

Background: Holder pasteurization (HoP) is the recommended method of pasteurization for donor human milk (DHM). The aim of the present study was to compare nutritional and microbiological impact on DHM of a new technique of pasteurization based on technical changes of HoP. Methods: We analyzed milk samples from 25 donors. Each sample, derived from one breast milk expression, was subdivided into three aliquots according to pasteurization: The first was not pasteurized, the second pasteurized by HoP, and the third was pasteurized by modified HoP (MHoP). Each aliquot was assessed as to its microbiological and nutritional profile. Nutritional profile included calcium and triglycerides concentrations detected by spectrophotometry and amino acid levels assessed by high-performance liquid chromatography (HPLC). Results: Triglycerides were significantly lower in pasteurized, by both methods, than in not pasteurized aliquots, while calcium and amino acids concentration were similar. Microbiological profile did not differ between HoP and MHoP aliquots. Conclusions: HoP and MHoP seem to have similar efficacy in preserving some nutritional characteristics of DHM and to confer similar microbiological safety. MHoP is time-saving and potentially costs-effective when compared to HoP, and it is; therefore, potentially of more interest from a practical point of view. Further studies are needed to confirm these findings.

We have evaluated the effect of pyridostigmine (PD), a cholinergic agonist, on the growth hormone (GH) response to physical exercise (EXC) in nine healthy volunteers. PD administration and EXC caused a similar increase of GH secretion to mean (+/- SE) peak values of 5.3 +/- 0.9 and 6.5 +/- 1.2 micrograms/l, respectively. Pretreatment with PD caused a significant augmentation of the EXC-induced GH release evaluated both as maximum peak (13.5 +/- 2.1 micrograms/l, p < 0.01 vs EXC) and as area under the secretory curve (EXC = 292.6 +/- 41.9 micrograms.min.l; PD + EXC = 587.3 +/- 68.9 micrograms.min.l, p < 0.005). The action of PD on GH secretion was additive to that of EXC since the sum of the GH responses to PD and EXC was not significantly different from the response obtained during PD + EXC. Whether PD and EXC act through a common final pathway, i.e. inhibition of endogenous somatostatin release, or the EXC-induced GH secretion involves stimulation of endogenous GHRH remains matter of investigation.

No abstract

The role of somatostatinergic tone (SST) in growth hormone (GH) neuroregulation in children with chronic renal failure (CRF) and short stature (mean height standard deviation score -3.47) was investigated. Ten children (9 males, 1 female), mean age 13.4 years (range 8-17 years), five with renal transplants (TP) and five on chronic haemodialysis (HD), underwent three separate investigations: (1) measurement of spontaneous GH secretion: (2) measurement of GH after infusion of GH releasing hormone (GHRH); (3) measurement of GH following treatment with pyridostigmine bromide (PD) and subsequent infusion of GHRH. All patients showed normal or exaggerated spontaneous nocturnal GH secretion (mean concentration values ranging between 3.8 and 19.07 ng/ml). In four of ten patients GHRH was not able to cause an increase in GH levels (mean peak GH 7.35 +/- 2.05 ng/ml) while PD pretreatment reinstated the GH response to GHRH (mean peak GH 55.25 +/- 17.23 ng/ml) in these children. In the other patients in whom GHRH-induced GH release was normal or exaggerated (mean peak GH 42.0 +/- 13.8 ng/ml). PD did not potentiate the GH response to GHRH (mean peak GH 54.83 +/- 7.88 ng/ml). These different types of responses were observed both in TP and HD patients. Our data indicate that: (1) PD potentiates the response to GHRH only when GHRH alone is not able to cause GH release, suggesting that SST is already reduced in patients with a normal or exaggerated GH response to GHRH; (2) in CRF patients the SST can be either reduced or increased, at least during the daytime.