Muscle electrolyte composition has been studied in 10 infants with marasmus and eight children with kwashiorkor. The presence of altered muscle salt and water concentrations was confined in the latter nutritional syndrome. The marasmic infant, with equivalent or more severe nutritional wasting than the child with kwashiorkor, maintained a more normal muscle electrolyte concentration as indicated by a number of criteria. The pathophysiology of the altered muscle composition in kwashiorkor remains unclear; however, it appears to be more specific than due just to a depletion of available fat and muscle stores. Although possible endocrine mechanisms can be postulated to explain the change in muscle chemistry, the existing evidence is inadequate. Clearly, continuing research is warranted.

Plasma concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), 17 alpha-hydroxyprogesterone (17 alpha-OHP), 17 beta-oestradiol (Oe2) and progesterone (P) were measured in 352 healthy girls aged 6.0 to 15.9 years, as a function of age (CA), weight, height and calculated lean body mass (LBM) and total body fat (TBF). The earliest hormonal changes were a fall in mean plasma FSH concentrations together with a small but significant rise in plasma Oe2 well in advance of any sign of pubertal development. The next changes were a progressive rise in plasma FSH and 17 alpha-OHP concentrations without further increments in plasma Oe2; these changes corresponded to a mean body weight of 29.8 kg, a mean height of 132.0 cm (initiation of the adolescent growth spurt), a mean LBM of 24.7 kg and a mean TBF of 5.1 kg. The last events were a progressive rise in plasma LH and Oe2 and less marked in P, which occurred in association with a mean body weight of 40.0 kg, a mean height of 142.0 cm (time of peak velocity of weight and height gain), a mean LBM of 31.8 kg and a mean TBF of 9.1 kg. Significant quadratic equations were disclosed between plasma FSH and LH versus CA, weight, height and LBM, and a significant linear correlation was observed between each gonadotrophin and TBF. These results show an association, not necessarily causal, between a 'critical level' of body composition and hormonal changes at the start of the adolescent growth spurt, as well as with late hormonal events at the time of peak velocity in weight and height gain. On the other hand, LBM rather than TBF seems more closely associated with the initiation and progression of puberty.

Abstract. Plasma concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), 17 alpha-hydroxyprogesterone (17α-OPH), androstenedione (Δ4) and testosterone (T) were measured in 543 healthy boys aged 6.0 to 15.9 years (with weight and height between the 3rd and 97th percentile for Mexican standards) as a function of chronologic age (CA), weight, height, surface area (SA) and calculated lean body mass (LBM) and total body fat (TBF). The earliest hormonal event was a clear rise in plasma 17α-OHP, either prior or simultaneously to at steady increase in plasma FSH, far ahead of any sign of puberty. These changes were closely followed by a continuous rise in plasma Δ4. Thereafter, there was a prolonged period of low but progressively increasing plasma FSH levels in the face of constantly low LH levels. However, a brisk rise in plasma LH and FSH occurred at a mean weight of 35.4 kg, at a height of 144.5 cm and when LBM was 32.0 kg. Simultaneously, plasma 17α-OHP began to fall, Δ4 reached a plateau and soon after, a marked rise in plasma T was documented. When plasma LH and FSH concentrations were plotted against CA, weight, height, SA and LBM a significant quadratic equation was disclosed in each case. Both gonadotrophins did not correlate with TBF. Multiple variance analysis demonstrated that LBM and SA had the most marked effect on LH, while LBM was the most important variable affecting plasma FSH concentrations. The present data suggest the association between a "critical level" of body composition and the major hormonal events in boys, regardless of a cause-effect relationship. A critical level of LBM (20–23 kg) and not of TBF was attained at time of the initial hormonal changes, as well as at the time of the major changes in plasma gonadotrophins (32–35 kg).

Five uremic (7.0 - 15.2 years), non-dialyzed children treated medically (group 1) had an intravenous glucose tolerance test (0.5 g/kg). Blood samples were obtained at frequent intervals and duplicate determinations of plasma glucose (glucose-oxidase method on Somogyi-Nelson protein-free filtrates), insulin and free fatty acids were performed. The same study was performed in eleven children (12.3 - 18.0 years) with chronic renal failure undergoing long-term hemodialysis (group 2), before and two hours after dialysis. Results were compared to a group (group 3) of eight healthy children (7.5 -- 17.5 years). In group 1 a "normal" insulin response was observed in the presence of hyperglycemia and the plasma glucose clearance was in the diabetic range. Twice weekly hemodialysis produced no beneficial acute effects on group 2, based on absolute glucose values or plasma glucose clearance rates, on groups as well as on individual basis; however, a clear hyperinsulinemia was present which was of even higher magnitude three and six months after the initial study. These results demonstrated that chronic hemodialysis had no beneficial acute effects on plasma glucose concentration or plasma glucose clearance rate. However, it may have obvious long term beneficial effects on glucose tolerance by enhancing pancreatic insulin release (to overcome peripheral insulin resistance) to such an extent as to maintain a normal carbohydrate tolerance.

The clinical characteristics and body composition of eight hypopituitary dwarfs (10.2−21.6 yr) were analyzed before and after 6 and 12 mo of growth hormone therapy, 2 IU 3 times/wk. Before treatment, growth rate was 1.8 ± 0.7 cm/yr, height age was 2.0−12.8 yr less, and bone age 2.0−11.1 yr less than chronologic age. Total body water (TBW), lean body mass (LBM), extracellular water (ECW), and intracellular water (ICW) were below normal for chronologic age, but normal for height. Muscle mass (MM) was below normal for age and height. During HGH therapy, growth rate was 7.1 ± 1.6 cm/yr in the first 6 mo and 7.8 ± 1.4 cm/yr during the next 6 mo; the ratio of change in height age to change in chronologic age was ≥ 1.0 in all patients and the ratio fo change in bone age to change in height age was 1.2 in one patient and ≤ 1.0 in the others. TBW, LBM, ECW, and ICW increased according to height increments; however, MM increased at a faster rate than expected from the height gains. Also, a relative or absolute loss of total body fat was recorded during the first 6 mo of therapy. It is suggested (1) that among the body composition parameters studied, muscle mass is the tissue most closely reflecting the lack of HGH and also its therapeutic benefits and (2) evaluation of body composition in hypopituitary dwarfs in response to HGH therapy shows striking changes not reflected by the determination of stature or weight alone.

ABSTRACT Serum thyrotrophin (TSH), triiodothyronine (T3) and thyroxine (T4) were measured by radioimmunoassay in 165 boys and 171 girls, clinically healthy, aged 6.1 to 16.0 years with normal weight and height, grouped at 12 months' intervals. The TSH values in boys ranged from 5.0 ± 0.6 to 6.1 ± 0.6 μU/ml without significant age differences. In girls, TSH level was 5.3 ± 0.5 μU/ml at the age of 6.0 to 7.0 and 7.4 ± 0.5 μU/ml at the age of 10.1 to 11.0 (P < 0.001). Girls had higher values than boys from 9.1 to 11.0 years (P < 0.025). In boys the T3 level was 182 ± 10 ng/100 ml at age 6.0 to 7.0 and 230 ± 15 ng/100 ml at age 11.1 to 12.0 (P < 0.025). Girls had higher values from the age of 9.1 on (215 ± 12 ng/100 ml), but after 13.1 years they decreased (P < 0.025). Girls had higher T3 levels than boys at age 10.1 to 11.0 (P < 0.025), but this difference disappeared when T3 concentrations in girls of this age were compared to boys aged 11.1 to 12.0. In boys and girls, T4 levels tended to be lower with increasing age (r = −0.860, P < 0.01) and there was a significant difference between the values seen up to 9.0 years and those after 13.1 years (P < 0.025 − < 0.001). Girls had lower values than boys at the age of 8.1 to 9.0; however, this difference disappeared when girls of this age were compared to boys 9.1 to 10.0 years old. It is concluded that previous to and around puberty initiation in both sexes, there is a rise in T3, followed by a progressive decrease in T4 with a rise in TSH only in girls. These changes occurred one year earlier in girls than in boys. These observations may represent transient adaptation responses to the increasing energy needs during periods of rapid growth.

Levels of haemoglobin (Hb), haematocrit (Ht) and mean corpuscular haemoglobin concentration (MCHC) were determined in 523 boys and 350 girls, clinically healthy, ages 6-0 to 13-5 years, middle socio-economic class living in Mexico City. In girls no significant differences according to age were observed in Hb or MCHC; however, Ht was significantly greater at 10-5 than at 10-0 years, without subsequent modifications. In boys, Hb and Ht had a first increase between 10-5 and 11-0 years and a second rise from 12-5 years on: MCHC remained unchanged. Boys were six to twelve months behind girls in regard to Ht increase; however, Ht increased when boys and girls reached similar mean weights (34 kg), heights (138 cm) and surface areas (1-15 m2); concomitantly, they had progressed to stage 2 of sexual development. Clear sex differences began to appear at age 11-5 when boys had higher Hb and Ht values than girls. These data suggest that Hb and Ht changes in these children are not related to chronological age but can be better interpreted if compared to weight, height, surface area or stage of sexual development.

A 3-hr glucose tolerance test was performed in 12 thyrotoxic patients before and after propranolol treatment for 30 days (120 mg/day). Plasma glucose, free fatty acid, insulin, and growth hormone levels were determined on each test and compared to each other and against nine clinically healthy volunteers. In eight thyrotoxic patients (subgroup A) an improvement in carbohydrate tolerance was observed after propranolol treatment, along with a fall in the previously elevated fasting FFA; no change in plasma insulin levels was observed. Plasma growth hormone levels were higher than normal both before and after propranolol; however, a 46% glucose-induced suppression was seen in both instances. In the other four patients (subgroup B) (who had had a marked and rapid weight loss) a deterioration of the previously normal glucosnificant changes in insulin levels. Elevated fasting plasma free fatty acids remained so despite propranolol treatment. Plasma growth hormone was higher than normal before and after propranolol; a late suppression (at 120 min) and no suppression at all were seen, respectively. After propranolol treatment, subgroup B had higher plasma free fatty acid than subgroup A in the fasting state and at 30 and 180 min. It is proposed that the improvement or deterioration in carbohydrate tolerance after propranolol treatment might be related to whether or not a satisfactory propranolol-induced lipolytic blockade is achieved, leading to a decrease in plasma free fatty acid levels, improved insulin sensitivity, and better peripheral glucose utilization. Therefore, a uniform dose of propranolol will not always be sufficient to obtain adequate lipolytic blockade, particularly if the thyrotoxic patient has had a marked and rapid weight loss.

Modifications in energy metabolism and endocrine homeostasis (plasma insulin and growth hormone values, glucose and free fatty acid levels, serum thyroxine and TSH, free thyroxine index, and urinary catecholamines) were investigated in eight children with edematous protein-calorie malnutrition. Caloric expenditure was low at admission and correlated linearly with increased caloric intake throughout the study. The hormonal changes at admission were characterized by a negligible insulin response to intravenous arginine or glucose and by markedly elevated growth hormone levels which were neither increased by arginine nor suppressed by intravenous glucose. Serum thyroxine values were low, but free thyroxine index and serum TSH levels were within normal limits. At admission to the study, 24-hour urinary excretion of dopamine and norepinephrine was relatively reduced in relation to the excretion of epinephrine. All these modifications were corrected at time of the recovery study. It is suggested that in edematous protein-calorie malnutrition, insulin acts as the primary regulator of peripheral fuel release and that the high, nonsuppressible growth hormone levels may form part of an important homeostatic mechanism to provide substrates for brain metabolism via lipolysis.