Background: Adiponectin, one of the adipocytokines, is postulated to play a key role in fetal growth, probably enhancing the growth-promoting effect of insulin through insulin-sensitizing action. Objectives and Methods: To examine how different intrauterine or postnatal growth patterns relate to adiponectin secretion, we measured serum adiponectin concentrations in 30 appropriate-for-gestational-age (AGA) and 19 small-for-gestational-age (SGA) preterm infants on the first day of life and at term-equivalent age. Results: The serum levels of adiponectin increased significantly in all preterm infants from birth to term-equivalent age. The adiponectin levels at term-equivalent age were significantly higher in the AGA than in the SGA group [mean (SD) 40.4 (12.3) vs. 28.4 (10.4) µg/ml; p < 0.01] after adjustment for gestational age or term-equivalent body weight. The increase in adiponectin levels from birth to term-equivalent age was significantly higher in the AGA than in the SGA group, and was positively correlated with the weight gain rate (g/kg/day) in the combined groups (r = 0.37, p < 0.01). A multiple regression analysis with the adiponectin increase from birth to term-equivalent age as the dependent variable for all the subjects revealed that only weight gain rate was independently associated with the adiponectin increase. Conclusions: Our results suggest that the change in serum adiponectin levels may reflect postnatal growth from birth to term-equivalent age in preterm infants.

Mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) is a clinico-radiological syndrome with a very particular clinical course. Three patients with MERS were evaluated by various sequences of magnetic resonance imaging with diffusion tensor imaging. Initial diffusion-weighted imaging showed reduction in the apparent diffusion coefficient values in the lesions, which completely resolved with the elimination of symptoms. However, diffusion anisotropy of the lesions showed no remarkable abnormalities in the early or delayed phases. These results may indicate that white matter architecture is preserved in both early and delayed phases in MERS.

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Our results suggest that hypoadiponectinaemia in short SGA children without catch-up growth may reflect insulin resistance and imply a higher risk of developing type 2 diabetes mellitus. Additionally, adiponectin may be a more sensitive indicator for latent insulin resistance than IGFBP-1 in short SGA children.

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We confirmed that resistin was an acute inflammatory protein, but its concentrations were unlikely to predict the prognosis of disease in acute KD patients.

<b><i>Background:</i></b> About twice as many boys as girls undergo growth hormone (GH) therapy in GH deficiency (GHD). However, this sex difference may not correctly reflect a real incidence. <b><i>Objectives:</i></b> We analyzed the evidence of a selection bias whereby more boys seek treatment at short stature clinics. <b><i>Subjects and Methods:</i></b> The present study included 3,902 children who visited 17 short stature clinics with a height SD score of −2 SD or less. The percentage of children who underwent the GH stimulation test was compared between boys and girls, as was the percentage of children ultimately diagnosed with GHD. <b><i>Results:</i></b> The children comprised 2,390 boys (61.3%) and 1,512 girls (38.7%), with a boy:girl ratio of 1.58:1. The percentage of children who underwent the GH stimulation test did not differ between boys (45.7%) and girls (49.8%). Among the children who underwent the GH stimulation test, the percentage diagnosed with GHD did not differ significantly between boys (22.0%) and girls (20.1%). The boy:girl ratio of children diagnosed with GHD was 1.59:1. <b><i>Conclusions:</i></b> The boy:girl ratio of children with short stature (1.58:1) did not differ significantly from that of children diagnosed with GHD (1.59:1). These results indicate that the predominance of boys in GHD does not reflect a real incidence, but rather a selection bias whereby a higher proportion of boys with short stature seek treatment at clinics. This difference arises because parents are more concerned about boys’ height, and because boys reach adult height at an older age.

Isolated adrenocorticotropic hormone defi ciency (IAD) is a rare pituitary disease in childhood and is considered to be a differential diagnosis in cases of ketotic hypoglycemia. 1 Although a few patients have an infl ammation or organic lesion in the pituitary gland, the etiology of this disorder has remained unclear in the majority of cases. Adrenocorticotropic hormone (ACTH) is produced from the ACTH precursor, proopiomelanocortin (POMC), by prohormone convertase 1 (PC1), and POMC gene expression requires a cell-restricted transcription factor, TPIT. Recently, mutations in the TPIT gene have been reported in cases of early onset IAD, 2 -5 and loss-of-function mutations of the POMC gene have been found in patients with ACTH defi ciency, obesity and hair pigmentation. 6 Furthermore, PC1 gene mutation has been described in a woman with both ACTH and gonadotropin defi ciency. 7 We describe a sporadic case of congenital IAD with psychomotor retardation and report our investigations of the TPIT , POMC , and PC1 genes in the patient. Case reportThe patient was a 3-year-old Japanese boy who had been born at term weighing 3574 g, by normal vaginal delivery after an uncomplicated pregnancy. Apgar score was 9 and 10 at 1 and 5 min, respectively. The mother had a past history of hyperthyroidism and epilepsy, and his parents were unrelated. There were no neonatal or infant deaths in his family history. He exhibited neither persistent jaundice nor hypoglycemic episodes in the neonatal period. After 9 months of age, he sometimes exhibited drowsiness in the morning, which was resolved after drinking milk. Because he was barely able to sit independently and was not able to stand even with support at 10 months of age, he was admitted to Tsukuba Medical Center Hospital for examination. Laboratory tests, brain magnetic resonance imaging (MRI), electroencephalography and auditory brainstem response were all within normal limits. Chromosomal analysis indicated the 46,XY karyotype. During an episode of acute gastroenteritis at 3 years of age, the diagnosis of ketotic hypoglycemia was fi rst established because of consciousness disturbance, with a blood glucose level of 41 mg/dL and ketonuria; his condition rapidly improved with i.v. glucose infusion. At the same time, the level of plasma cortisol was low and the patient was hospitalized for further examination. On admission his height was 98 cm (+0.5 SD), bodyweight 15 kg (+0.3 SD), and head circumference 50 cm (−0.1 SD). He showed no facial dysmorphism, minor anomalies, dyspigmentation, hepatomegaly, or neurological abnormalities. He could walk without support but could not run, climb stairs, or speak even two-word sentences. His developmental quotient was 38, equivalent to 15 months of age. Laboratory tests ( Table 1 ) showed reduced plasma ACTH, cortisol, and urine 17-hydroxycorticosteroids (17-OHCS), and no circadian cycle of cortisol secretion was found. The plasma level of corticotropin-releasing hormone (CRH) measured by radioimmunoassay was within a normal range. Anti-pituit...