Due to the current COVID-19 pandemic, worldwide population's lifestyle has changed dramatically, causing psychosocial consequences. Patients presenting a preexisting chronic condition, as Type 1 Diabetes (T1D), are the ones suffering the most from this situation. Moreover, people affected by diabetes are the ones with the worst prognosis, if infected by SARS-CoV-2. We analyzed why patients with T1D were poorly represented between the subjects hospitalized for COVID-19 and why the cases of diabetic ketoacidosis (DKA) were fewer and more severe compared with the past years. Furthermore, literature has showed how patients of all ages with T1D did not experience a deterioration in their glucose control throughout the lockdown. Among other causes, this is also due to the surging use of telemedicine. Finally, we tried to understand how the coronavirus tropism for endocrine tissues could influence the future epidemiology of T1D, focusing on the effects they have on pancreatic β-cells.

Background/Objectives: Biotinidase deficiency (BD) is a treatable autosomal recessive disorder included in many newborn screening (NBS) programs. The importance of early diagnosis and treatment is now well established. However, recent studies are emerging on the possibility of increased enzyme activity with age, an observation that raises questions about the long-term validity of the initial classification of these patients. This study aimed to assess the incidence, genetic and clinical features, and, notably, the longitudinal enzymatic trajectory of BD in a cohort identified by NBS in Emilia-Romagna, Italy, with implications for diagnostic re-evaluation and therapeutic decisions. Methods: A retrospective and prospective analysis was conducted on 64 infants recalled after NBS for suspected BD between 2016 and 2020. Biochemical, molecular, and clinical data were collected, and biotinidase (BTD) activity was monitored longitudinally. Affected individuals were supplemented with biotin and followed clinically for at least 5 years. Results: Thirty-one patients were diagnosed with BD (30 partial, 1 profound; incidence 1:5448). A significant and sustained increase in BTD activity was observed from diagnosis through early childhood (p < 0.001 up to 60 months), particularly among patients carrying the p.Asp444His variant. This enzymatic trend suggests a potential remodulation of biochemical classification over time. Genotype–phenotype concordance was high (92%), and clinical outcomes were favorable across the cohort. Conclusions: This study provides new evidence that BTD activity in patients with BD increases progressively, supporting the concept of age-dependent enzyme recovery. Our results support the need for systematic re-evaluation of diagnosis and treatment, especially at 12 months of age, and particularly in patients with evidence of partial activity deficiency and the p.Asp444His mutation.

Testicular tissue cryopreservation is increasingly offered to boys facing gonadotoxic therapies. Yet, its long-term clinical significance depends not only on future fertility-restoration technologies but also on how these patients evolve. This narrative review aims to synthesizes the available follow-up literature on boys who underwent testicular tissue cryopreservation, focusing on procedural safety, testicular growth, pubertal progression, endocrine function, semen outcomes in patients reaching adulthood, and the emerging question of whether cryopreserved tissue may ultimately be needed in all cases. We will compare follow-up strategies across centers, highlight the lack of standardized endpoints, and discuss how survivorship data may refine counseling, re-consent, and future management of cryopreserved tissue. The aim is to provide a clinically oriented overview of what current longitudinal cohorts can already tell us, while identifying the key evidence gaps that still limit harmonized follow-up protocols.

The authors would like to make the following correction to their published paper