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Mild asthma is prevalent in childhood and causes as many as 30%–40% asthma exacerbations requiring emergency visits. The management of "intermittent" and "mild persistent" asthma phenotypes is still a matter of debate, even if the role of inhaled corticosteroids, both continuous and intermittent, is a cornerstone in this field. Recent updates of the guidelines on the strategies to manage these patients are coming, since the role of inflammation in these asthma phenotypes is crucial, as well as the potential side effect and risks of short‐acting beta 2 agonists overuse, prescribed as the only "as‐needed" treatments. In this paper, we overview the new (r)evolution regarding intermittent and mild persistent asthma management.

We present a case of an 11-month-old girl who was referred to our unit for an erythematous rash that appeared on the face and extremities. Personal and family history was not relevant. Laboratory tests were normal. During recovery, diameter and colour intensity of the cutaneous lesions increased, but after some weeks, lesions had a self-limited resolution without any treatment. Based on clinical and laboratory findings, a diagnosis of acute hemorrhagic edema of infancy (AHEI) was made. AHEI is a rare cutaneous leukocytoclastic vasculitis that usually affects children aged between 4 and 24 months. Etiology is unknown but almost of 75% of cases are preceded by infectious episodes, vaccinations or use of medications. In contrast to the dramatic cutaneous eruption, clinical conditions are usually optimal. Classically, AHEI is characterized by a triad of symptoms: fever, edema and purpura. Skin lesions are erythematous, annular, medallion-like, purpuric plaques that have a rapid onset and appear on the face and extremities, sparing trunk and mucosal membranes. Initially interpreted as a variant of Henoch-Schönlein purpura, now it is considered a distinct disease. In the majority of cases the disease is benign and self-limited without a visceral involvement, so a conservative approach is most often chosen.PubMed Abstract | Publisher Full Text 3.Homme JL, Block JM: Acute hemorrhagic edema of infancy and common mimics. Am J Emerg Med. 2016; 34(5): 936.e3-6. PubMed Abstract | Publisher Full Text 4. Cunha DF, Darcie AL, Benevides GN, et al.: Acute Hemorrhagic Edema of Infancy: an unusual diagnosis for the general pediatrician. Autopsy Case Rep. 2015; 5(3): 37-41. PubMed Abstract | Publisher Full Text | Free Full Text 5. Fotis L, Nikorelou S, Lariou MS, et al.: Acute hemorrhagic edema of infancy: a frightening but benign disease. Clin Pediatr (Phila). 2012; 51(4): 391-3. PubMed Abstract | Publisher Full Text 6. Miorin E, Meneghini A, Don B, et al.: Edema emorragico acuto del lattante, descrizione di un caso clinico e revisione della letteratura. Medico e Bambino pagine elettroniche. 2002; 5(3). Reference Source 7. Alhammadi AH, Adel A, Hendaus MA: Acute hemorrhagic edema of infancy: a worrisome presentation, but benign course. Clin Cosmet Investig Dermatol. 2013; 6: 197-9. PubMed Abstract | Publisher Full Text | Free Full Text 8. Krause I, Lazarov A, Rachmel A, et al.: Acute haemorrhagic oedema of infancy, a benign variant of leucocytoclastic vasculitis. Acta Paediatr. 1996; 85(1): 114-7. PubMed Abstract | Publisher Full Text 9. Savino F, Lupica MM, Tarasco V, et al.: Acute hemorrhagic edema of infancy: a troubling cutaneous presentation with a self-limiting course. Pediatr Dermatol. 2013; 30(6): e149-52. PubMed Abstract | Publisher Full Text 10. Tagliabue A, Bettinelli A, Cogliati F: Edema acuto emorragico della prima infanzia (porpora di seidlmayer). Medico e Bambino pagine elettroniche. 2009; 12(6). Reference Source

Background: Congenital hypothyroidism (CH) is reported to be more common in preterm infants than in term infants, especially in sick preterm infants. Though a frequent possibility of transitory thyroidal alterations in this category of neonates, the evolution of CH to transient or permanent forms is unpredictable. Methods: We retrospectively analyzed medical records of 28 preterm infants (<37 weeks gestation) who had exhibited a positive screening for CH at birth during the period 2000 e2015 followed in our Center. Children were divided into three groups: permanent CH (PCH) with thyroid dysgenesis, PCH with eutopic normal-sized thyroid gland, and transient CH (TCH) with eutopic normal-sized thyroid gland. In all groups we described clinical and biochemical characteristics. Secondly, we analyzed the differences between patients with thyroid dysgenesis and patients with eutopic normal-sized gland and we compared PCH and TCH groups with normal-sized thyroid gland in order to identify clinical or biochemical data for early detection of transient forms.Results: Of all patients, 21.4% showed thyroid dysgenesis while 78.6% presented eutopic normal-sized gland. Infants with thyroid dysgenesis had higher median (IQR) baseline s-TSH and levothyroxine (L-T4) dose per weight at 12 months (12 m-dose) than patients with eutopic normal-sized gland. At re-evaluation of the patients with eutopic normal-sized gland, 36% showed PCH and 64% had TCH. The age of the patients at the beginning of L-T4 treatment, gestational age (GA), birth weight, blood thyroid stimulating hormone levels (b-TSH) at first newborn screening (NBS), baseline serum thyroid stimulating hormone (s-TSH), and L-T4 12 m-dose were statistically different between the two groups. Conclusions: Our results demonstrate that factors as GA, birth weight, b-TSH levels at first NBS, baseline s-TSH, L-T4 12 m-dose and age at the start of the treatment may be considered useful predictive elements for the evolution of CH.

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