Adiponectin is an adipocytokine with insulin-sensitizing and antiatherogenic properties. Reduced concentrations of adiponectin precede the onset of type 2 diabetes and the development of atherosclerosis. Our aim was to quantify adiponectin concentrations in small for gestational age (SGA) children. Fifty-one SGA children, 24 obese, and 17 short-normal children with birth weight appropriate for gestational age (short-AGA) were studied. The statures of the SGA children were corrected for their midparental height and subdivided into two groups according to their corrected height: catch-up growth group, children with corrected height of 0 z-score or greater (n = 17); and noncatch-up growth group, subjects with corrected height less than 0 z-score (n = 34). SGA children showed adiponectin levels significantly lower than short- normal children (35.2 +/- 3.5 vs. 80.4 +/- 26.6 micro g/ml; P < 0.0001) and obese children (77.5 +/- 39.4 micro g/ml; P < 0.0001). Catch-up growth children showed adiponectin levels significantly lower than noncatch-up growth subjects (29.4 +/- 10.3 vs. 38.1 +/- 11.5 micro g/ml; P = 0.01). Adiponectin concentrations were inversely related to height z-score, corrected stature, weight, and body mass index and were positively related to birth weight. Our results suggest that adiponectin levels are reduced in SGA children and are even lower in those with postnatal catch-up growth. Whether this finding implies a higher risk of developing type 2 diabetes and atherosclerosis remains to be established.

Carbapenemase-producing Enterobacterales constitute a serious public health threat; however, information on the oxacilinasa (OXA-48)-type is limited. The objective of the study was to evaluate the risk factors associated with 14-day mortality for patients with bacteremia due to OXA-48 carbapenemase-producing Klebsiella pneumoniae . We conducted a retrospective, single-center observational study of adult patients with K. pneumoniae bacteremia, classifying the strains as carbapenem-susceptible K. pneumoniae (CSKp) and carbapenem-resistant K. pneumoniae (CRKp). All of the CRKp strains were the OXA-48-type. The study included 202 cases of bacteremia: 114 due to CSKp and 88 due to CRKp. The clinical cure rate was higher for the patients with CSKp (85% vs 69% for CSKp and CRKp, respectively; P = .010), while the 14-day mortality rate was lower (13% vs 30%, P = .005). An INCREMENT-CPE score ≥7 (HR 3.05, 95% CI 1.50–6.25, P = .002) was the only independent factor associated with 14-day mortality for the patients with Klebsiella spp. bacteremia. Other factors related to 14-day mortality were a rapidly fatal prognosis (McCabe) (HR 7.1, 95% CI 2.75–18.37, P < .001), dementia (HR 5.9, 95% CI 2.0–7.43, P = .001), and a high-risk source of infection (HR 2.7, 95% CI 1.06–6.82, P = .038). The most important factors associated with 14-day mortality for the patients with K. pneumoniae bacteremia was an INCREMENT-CPE score ≥7, dementia, a McCabe score indicating a rapidly fatal prognosis and a high-risk source of infection. We found no relationship between a poorer outcome and CRKp isolation or inadequate antibiotic therapy.

We have previously described severe hyperparathyroidism during the pubertal growth spurt in three uremic adolescents treated with recombinant human growth hormone (rhGH). Here we investigate the possible role of puberty in the genesis of hyperparathyroidism during rhGH treatment of a large cohort of patients. Data from 67 uremic patients treated with rhGH from five Italian pediatric nephrology centers were retrospectively recorded every 3 months starting 1 year before rhGH administration. The mean (+/-SD) rhGH treatment observation period was 19.9+/-5.9 months. The mean age at the start of rhGH treatment was 8.3+/-3.6 years. Of the 67 patients, 15 reached pubertal stage 2 during the 1st year of rhGH treatment and 12 of these 15 progressed to pubertal stage 3. The relative increase in parathyroid hormone (PTH) levels after rhGH initiation was greater in pubertal [1.95, 95% confidence interval (CI) 1.43-2.66] than in prepubertal patients (1.19, 95% CI 1.01-1.40). Increases in PTH levels were significantly different between the two groups (Delta=1.64, 95% CI 1.16-3.19, P=0.007). Multiple regression analysis showed an inverse correlation between PTH and calcium levels and a positive correlation between PTH and pubertal stage 3. There was no correlation with phosphate levels and calcitriol dosage. In conclusion, these results suggest that in uremic adolescents treated with rhGH puberty may influence PTH levels.