Adolfo José da Mota

Oral microbial colonization in children with sickle cell anaemia under long-term prophylaxis with penicillin

BACKGROUND AND OBJECTIVE Sickle cell anaemia (SCA) is the most frequent haematological hereditary disease. Children with SCA are submitted to long-term prophylactic therapy with penicillin, but little is known about its impact on oral microflora. The aim of this study was to evaluate the oral microbial colonization of paediatric patients with SCA. DESIGN Forty children (4-11yrs old) with SCA (genotype SS) under long-term prophylactic treatment with penicillin were included in the study. Age/gender-matched control group of healthy children was also included. Scores of dmft/DMFT (number of decayed (D), missing (M), or filled (F) teeth; dmft, for primary dentition; DMFT, for permanent dentition) were obtained and stimulated saliva was sampled. Salivary flow rate and buffering capacity were evaluated. Counts of microorganisms (mutans streptococci, lactobacilli and yeasts) were determined by plating method. Yeasts were identified by API 20C AUX and PCR. RESULTS Mean dmft/DMFT values were similar in the studied groups (SCA 2.13/1.60 and control 2.38/1.3). Although no significant differences between cariogenic microorganism counts were observed, significantly higher yeasts oral levels were observed in SCA group. Controls showed lower salivary buffering capacity. Candida albicans was the most frequently isolated species in both groups. Candida famata, Candida parapsilosis and Candida tropicalis were also isolated from controls. Candida dubliniensis, Candida rugosa and Candida sphaerica were found only in SCA group. CONCLUSIONS Based on the results, it could be concluded that paediatric patients with SCA showed significantly higher oral level of yeasts. Uncommon fungal species were found in SCA group. Similar caries prevalence and counts of lactobacilli and streptococci in relation to controls were observed.

Integrated actions of assistance to the diabetic patient

Background WHO alerts to the epidemic behavior of diabetes (DM): more than 190 million people worldwide suffer from diabetes and this number will double by 2030 (Brasilsus, 2014). In Brazil, IDF estimated in 2014 that the number of diabetics was 11.6 million. Aging, urbanization, sedentary lifestyle, high fat diet and obesity are seen as responsible for this situation. In addition to the cost of treatment, complications of the syndrome, overtax and overwhelm the health care system. Thus, only public policies are insufficient, being essential the efforts of researchers and health teams to carry out projects for the guidance of the population, who often have no basic knowledge, compromising the effectiveness of treatment.

Could one splicing-site single nucleotide polymorphism cause the MODY2 disease?

Background Maturity-onset Diabetes of the Young (MODY; OMIM# 606391) is often related to a single gene mutation and characterized by dominant inheritance and non-insulindependent DM with a young age at diagnosis (Fajans et al., 2001). The most frequent subtype, MODY2, Results from SNPs in the glucokinase gene (Osback et al., 2009). Mapped to human chromosome 7p15.3-p15.1, the GCK gene consists of 10 exons and roughly 45 Kb. More than 600 SNPs were reported to this gene and among those, around 200 are related to the disease (Osback et al., 2009).

Indentification of single base mutations in the GCK gene of patients with diagnosis of MODY2

Background Diabetes mellitus (DM) refers to a group of common metabolic disorders, with multiple causes, that share a common phenotype: hyperglycemia (Kota, 2012). The concept of multiple etiologies is recent and a third group of DM is proposed today, a monogenic form with autosomal dominant inheritance: MODY. There are 13 subtypes described for MODY, which in MODY2 is one of the most common, although the relative frequency varies according to the study population (Corrales et al., 2010). MODY2 is provoked by mutations in the glucokinase gene (GCK) located on human chromosome 7p15.3-p15.1, which consists of 10 exons that span 45.169 bp and encode a 465-amino-acid protein (Tinto et al., 2008).