Hyperandrogenemia is prevalent in autistic patients and increases with autistic severity. Thus, androgen levels should be assessed in autistic patients with signs of early puberty. Further studies are warranted regarding trials of anti-androgen therapy in such patients.

Adrenal suppression is an inevitable consequence of ALL therapy. Monitoring of cortisol levels and steroid coverage during stress is recommended, and gradual steroid tapering is suggested.

Background/Aims: It was suggested that serum pentraxin 3 (PTX3) levels could differentiate obese children with nonalcoholic steatohepatitis (NASH) from those with simple steatosis. Thus, we aimed to evaluate the clinical utility of serum PTX3 fragment levels in the diagnosis of NASH and the assessment of its severity in obese children with suspected nonalcoholic fatty liver disease (NAFLD). Methods: Fifty obese children were compared to 25 matched controls. All were subjected to history taking, anthropometric measurements, and abdominal ultrasonography, as well as laboratory assessments of liver functions, fasting lipid profile, fasting blood glucose, fasting insulin, homeostasis model assessment (HOMA) index, fasting glucose/insulin ratio, and serum PTX3. Results: PTX3 was higher in obese cases than controls (p = 0.0001). Eighty percent of the cases had NAFLD with progressive increases in PTX3 levels as the severity of fatty liver increased (p = 0.0001). Moreover, PTX3 was higher in cases with elevated liver enzymes (3.205 ± 0.77 U/l) than those with normal liver enzymes (2.77 + 0.69 U/l, p < 0.0001). A cutoff value of 3.03 U/l differentiated fatty liver from NASH with a sensitivity of 89% and a specificity of 86%. Conclusion: Noninvasive monitoring of serum PTX3 fragment levels in obese patients with suspected NAFLD may be used as a reliable tool for differentiating NASH from simple fatty liver.

Dyslipidemia and HI were frequent findings in patients with CLD, which worsened with increased severity of CLD.

Because ghrelin is one of the key hormones in regulating feeding behavior and caloric status, it was suggested that ghrelin behavior might be closely associated with malnutrition state of patients with chronic liver disease (CLD). Thus, we aimed to assess serum ghrelin levels in children with CLD and its relation to anthropometric parameters and severity of CLD. Forty CLD patients were studied in comparison to 40 controls. All subjects were subjected to history, anthropometric, and laboratory assessment of liver functions and serum acylated ghrelin. Ghrelin was higher in patients than controls being higher with progress of Child's grade and with deterioration of liver functions. Hyperghrelinemia was detected in 62.5% of cases. Ghrelin correlated negatively with body mass index standard deviation score (BMISDS ( = −0.95, < 0.001)), triceps skin fold thickness (TSFT ( = −0.88, < 0.001)), and subscapular skin fold thickness (SSFT ( = 0.83, < 0.001)) percentiles. In conclusion, hyperghrelinemia may represent a compensatory mechanism trying to overcome malnutrition state complicating CLD and can be used as a parameter for early detection and assessment of the severity of malnutrition in children with CLD.