To assess the growth‐promoting effect of different doses of growth hormone‐releasing hormone(1–29)‐NH, (GHRH(1–29)‐NH2) in GH deficiency (GHD) of hypothalamic origin, 43 prepubertal children aged between 4.3 and 18.9 years (mean 10.4 k 2.9 years) were randomly assigned to three treatment regimens: low‐dose GHRH(1–29)‐NH2 (LD group; n = 15), high‐dose GHRH(1–29)‐NH, (HD group; n = 12) and GH (GH group; n = 16). The LD group received GHRH(1–29)‐NH, at 30 yglkglday S.C. in three daily doses, the HD group received 60 μg/kg/day S.C. in three daily doses and the GH group received GH, 0.1 IU/kg/day S.C. once daily. All children were treated for a period of 6 months. Evaluation included anthropometry, bone age, intravenous and subcutaneous GHRH(1–29)‐NHZ tests and determination of insulin‐like growth factor I (IGF‐I) levels. An increase in height velocity of 2 cm/year or more was observed in all except two children. Height velocity during treatment was lowest in the LD group, but comparable in the HD and GH groups. An increase in height SDS for bone age occurred only in the GH‐treated group. GH responses to intravenous GHRH(1–29)‐NH, showed a priming effect of the LD GHRH(1–29)‐NH, treatment, while a decrease in response occurred in the GH‐treated group. Following a subcutaneous test dose of one‐third of the daily dose of GHRH(1–29)‐NH, GH levels remained unchanged in both the LD and HD groups. There was accumulation of GHRH immunoreactivity over time in the HD group, but there was no correlation between measured GHRH and GH levels. IGF‐I levels increased in the HD and GH‐treated groups. Antibodies to GHRH were detected in 54% and 58% of children in the LD and HD groups, respectively. None of these variables correlated with changes in height velocity. The results indicate that 6 months of GH and high‐dose GHRH(1–29)‐NH, treatment have similar growth‐promoting effects.

Fibrinogen (Fgn) and haemorheologic parameters were serially measured in 44 pts (38 males, age 59+/−7) with claudicatio intermittens due to peripheral arterial obliterative disease (PAOD) treated for 24 months with Ticlopidine (T group, 250 mg b.i.d. p.os), or placebo (P group), in a double blind randomized controlled study, part of a larger clinical trial. Fgn (immunodiffusion), haematocrit (Ht, micromethod), whole blood viscosity (BV, Contraves LS 30, at 37 C) at high (94.5) and low (0.2 sec-1) shear rates (s.r.) and plasma viscosity (PV, Contraves LS 30) were measured three-monthly. The data were evaluated by means of ANOVA and Student's t test. The values in groups T and P did not differ at baseline except for greater BV at high s.r. in group P (p< 0.05). During the observation period circannual variations appeared especially in group T, where summer-time values for most parameters (Fgn, Ht, PV, low s.r. BV) were lower (significance from p<0.05 to <0.01) than the correspondent winter-time values, while a similar pattern was observed in group P only for PV (p<0.01). Fgn (p<0.05), Ht (p<0.01), and low s.r. BV (p<0.001) were significantly lowered in group T versus group P but only in the summer months (after about 1 year of treatment). In conclusion, this study proves that long-term Ticlopidine treatment in PAOD is associated with significant lowering of fibrinogen and “improvement” in haemoreologic tests although limited to the summer observations. Ticlopidine while positively interfering with haemorheology in PAOD may not counteract other mechanisms of rheologic deterioration probably occurring during winter. Long-term evaluation of drug effects should therefore take into account spontaneous or drug-enhanced seasonal changes of the investigated values.