Introduction: Human parechovirus type 3 has been recognized as a cause of pediatric infection, occasionally associated with serious illness, including sepsis and meningitis, particularly among young infants. The aim of this study is to report the first known human parechovirus type 3 outbreak in Portugal.Material and Methods: Descriptive study of an outbreak that occurred between the 8th June to the 12th August 2016. Laboratory diagnosis was made by reverse transcription - polymerase chain reaction in the cerebrospinal fluid and/or in stools. Genotyping was made by reverse transcription - polymerase chain reaction and sequencing in stool samples from infants and family members.Results: Human parechovirus type 3 infection was detected in seven infants, of which six were male. Median age was 23 days (5 - 52). One had seizures, with a magnetic resonance imaging scan showing white matter diffusion restriction. The mean duration of admission was 5.6 days (3 - 11), with favourable outcome in all. In three cases there were symptomatic close family members. Human parechovirus type 3 was identified in the stools of three mothers.Discussion: Even though human parechovirus type 3 infection has been well described in the presented age group, most Portuguese hospitals do not have this laboratory diagnosis. Our results are comparable to those obtained in other countries. Besides detection of the virus in the cerebrospinal fluid, there were no raised local or systemic inflammatory markers.Conclusion: This study reports the first known outbreak, in infants, of human parechovirus type 3 in Portugal. Although there is no specific treatment, this diagnosis can avoid unnecessary empirical antibiotic treatment and prolonged admissions.

Background Postprandial hyperglycemia is one of the biggest challenges in children with type 1 diabetes (T1D). Ultra-fast-acting aspartic insulin (faster aspart) has a quicker onset of action and an earlier maximum activity. The aim of this study is to analyze the impact of faster aspart in metabolic control of pediatric patients with T1D in a “real-world” setting. Methods Retrospective analysis of 60 pediatric patients with T1D who changed their insulin analogue to faster aspart. Anthropometric data, insulin doses, capillary and interstitial glucose recordings and average glycated hemoglobin before and after insulin analogue’s switch were obtained. After all population analyses, patients were analyzed separately according to the type of treatment, multiple daily injections (MDI) and continuous subcutaneous insulin infusion (CSII), and according to age group. Results Faster aspart significantly improved metabolic control, increasing time in range (TIR) (42 vs.54%, respectively; P = 0.007) and decreasing time above range (TAR) (52 vs.40%, respectively; P = 0.009), without an increased time in hypoglycemia (7% before and after faster aspart’s introduction; P = 0.933). This was reassured in the adolescent years ( n = 45), with an increase in TIR (37 vs. 47%, respectively; P = 0.034) and decrease in TAR (51 vs. 45%, respectively; P = 0.022). Patients on CSII ( n = 47), also demonstrated an increase in TIR (38 vs. 50%, respectively; P = 0.010). The reduction of A1c was not statistically significant. Conclusion Although the advantage of faster aspart had already been demonstrated in pediatric patients under MDI, “real-world” studies, including patients under CSII, are still lacking. This study highlights the important impact of faster aspart on metabolic control in children with T1D, particularly among adolescents under CSII.

A 15-year-old girl was admitted to emergency department with an acute flaccid tetraparesis with no other symptoms. A history of recurrent similar episodes with spontaneous recovery was reported and no family history was known. Laboratory tests revealed severe hypokalaemia and hypokaluria. Symptoms resolution occurred after potassium replacement. The diagnosis of hypokalaemic periodic paralysis (HPP) was confirmed by genetic testing, which revealed a not previously described mutation in CACNA1S gene (c.3715C>G p.Arg1239Gly). HPP is a rare neuromuscular disorder that causes episodic attacks of flaccid paralysis with concomitant hypokalaemia. Primary forms of the disease are skeletal muscle ion channelopathies. HPP occurs due to a problem in potassium distribution rather than a total body potassium deficiency. Therefore potassium replacement should be carefully performed because of the risk of rebound hyperkalaemia. Knowing this rare entity is important in order to avoid diagnostic delays and so that proper treatment can be initiated to reduce morbidity and mortality.

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