Sleep is a cardinal biological process that backstops central nervous system function, which also plays a crucial role in regulating systemic homeostasis, including immune activities. Cytokines, particularly interleukin-1β and tumor necrosis factor-α, act as mediators bridging sleep and inflammation, also influencing both sleep architecture and sleep–wake cycle. Sleep deprivation and sleep disorders such as insomnia, narcolepsy, hypersomnia, or obstructive sleep apnoea may disrupt cytokine production, alter their circadian rhythm of release, and shift secretion peaks from night to day. These changes contribute to daytime fatigue, impaired cognitive and physical performance, increased susceptibility to infections and/or systemic inflammation. Molecular studies indicate that insufficient sleep primes immune cells to enhance pro-inflammatory responses, creating a feedback loop with neuroendocrine pathways that further exacerbates sleep patterns and inflammatory dysregulation. Understanding the bidirectional relationship between sleep and cytokines may highlight the role of sleep as an active component of immunity regulation and underscore the potential usefulness of multilevel interventions that include complementary and integrative health approaches restoring sleep, normalizing cytokine rhythms and mitigating inflammation.

Background: Growth hormone deficiency (GHD) in childhood impairs linear growth and may affect body composition, metabolism, and quality of life; recombinant human growth hormone (rhGH) therapy improves outcomes, but response is highly variable, especially in idiopathic GHD (IGHD). Objective: To summarize current evidence on predictors of growth response to rhGH therapy in children with IGHD, focusing on clinical, biochemical, and treatment-related determinants. Methods: This is a narrative review dealing with studies assessing clinical, auxological, biochemical and treatment-associated factors that may influence response to rhGH in IGHD. Results: Early treatment initiation, baseline short stature, prepubertal status, and higher early height growth velocity are strong clinical predictors; biochemical markers, including GH peak, IGF-1, and IGFBP-3, provide complementary information. Modifiable factors such as GH dose, adherence to therapy, and therapy duration also influence outcomes. Integrated predictive models improve accuracy but require further validation. Conclusions: Growth response to rhGH in IGHD is multifactorial and could be individualized: early identification of suboptimal responders and personalized treatment strategies that integrate clinical, biochemical, and treatment-related data may optimize the final outcome. Future research studies should focus on validated predictive models incorporating genetic and molecular markers.

Pertussis remains a potentially severe respiratory illness in pediatric populations, especially in vulnerable groups. A severe outbreak has been reported in the post pandemic era, but it is uncertain if risk factors for severe disease may have changed compared with pre-pandemic years. We conducted a retrospective analysis of children diagnosed with Bordetella pertussis infection at a single tertiary pediatric center, from January 2023 to May 2024 Clinical and demographic variables were compared between outpatients and hospitalized patients to identify factors associated with disease severity. A total of 71 patients were included. Younger age (p < 0.001), lower body weight, (p = 0.0005) and lack of vaccination (p < 0.00001) were significantly associated with hospitalization. No significant differences were found regarding clinical symptoms, oxygen saturation, fever, or viral co-infection. Conclusion: Unvaccinated status, younger age, and lower weight appear to be key risk factors for hospitalization in pediatric pertussis, underlining the protective role of vaccination and the vulnerability of younger infants. These findings support targeted vaccination efforts and early risk stratification to prevent severe disease in vulnerable infants.

Background: Growth hormone (GH) stimulation testing remains the diagnostic gold standard for GH deficiency (GHD), but body mass index (BMI) inversely influences peak GH levels, creating a risk of overdiagnosis. We evaluated the association between BMI standard deviation score (SDS) and peak GH response in children undergoing diagnostic work-up for suspected GHD. Methods: This is a retrospective single-center study of 298 children (55.4% male, mean age 9.5 ± 2.9 years) evaluated for growth failure with arginine or clonidine stimulation testing. GHD was confirmed in 114 patients (38.3%). Multivariable linear and logistic regression models evaluated associations after adjustment for age, sex, and pubertal status. Results: BMI SDS negatively correlated with peak GH levels in the overall cohort (r = −0.299, p < 0.001) and in GHD patients (r = −0.322, p < 0.001), but not in non-GHD controls (r = −0.102, p = 0.167; Fisher’s z p = 0.050). On multivariable analysis, each 1-SDS increase in BMI SDS was independently associated with a 1.63 ng/mL reduction in peak GH (β = −1.63, 95% CI −2.20 to −1.07; p < 0.001) and 2.10-fold higher odds of GHD diagnosis (OR 2.10, 95% CI 1.60–2.74; p < 0.001). Across BMI SDS quartiles (Q1 to Q4), mean peak GH progressively decreased from 11.14 to 6.93 ng/mL (p < 0.0001), while GHD prevalence increased from 22.4% to 62.7% (p < 0.0001). Conclusions: BMI SDS significantly blunts peak GH response and increases the likelihood of a GHD diagnosis. This inverse relationship was evident primarily in children with confirmed GHD, suggesting that adiposity predominantly impairs an already compromised somatotropic axis. Adiposity should be accounted for when interpreting GH stimulation tests.

Growth hormone deficiency (GHD) is a frequent cause of impaired linear growth and may also affect skeletal development and bone mass acquisition. This narrative review summarizes the current evidence on bone health in pediatric GHD, with a focus on clinical findings, response to recombinant human growth hormone (rhGH) therapy, and practical approaches to bone assessment. Available pediatric studies consistently show decreased BMD and bone mineral content at diagnosis, often involving the lumbar spine and total body, together with alterations in bone structure. During rhGH treatment, gradual improvements in bone turnover markers and BMD are generally observed, although responses are variable and may depend on age, growth response, and treatment intensity. Full normalization is achieved only in a subset of patients, highlighting heterogeneity in skeletal recovery. Given these findings, a structured clinical approach is recommended. An integrated algorithm for bone health evaluation in children with GHD should include biochemical assessment (IGF-1, calcium-phosphate metabolism, vitamin D status, and bone turnover markers) plus imaging evaluation, primarily using dual-energy X-ray absorptiometry (DXA) with appropriate pediatric and size-adjusted interpretation. Early initiation of rhGH therapy, alongside optimization of calcium and vitamin D intake, is essential to support bone accrual. Overall, pediatric GHD is associated with impaired skeletal development, but timely diagnosis and standardized monitoring through a combined clinical, biochemical, and imaging algorithm can improve the final bone outcomes. Further prospective studies are needed to refine assessment tools and optimize long-term management strategies.