Homozygous mutations in the CARD9 gene, with a premature termination codon, are associated with chronic mucocutaneous candidiasis in an Iranian family. Dysfunction of CARD9 impairs the innate signaling of dectin-1, an antifungal pattern-recognition receptor.

In this 3-year multicenter trial, patients with suboptimal glycated hemoglobin levels while receiving metformin and sulfonylurea therapy were randomly assigned to add biphasic, prandial, or basal insulin. During the first year, sulfonylurea therapy was replaced by additional insulin for unacceptable hyperglycemia or subsequently for a glycated hemoglobin level of more than 6.5%. Basal- or prandial-based insulin regimens more often achieved glycated hemoglobin targets. Fewer hypoglycemic episodes and less weight gain occurred with regimens initiated with basal insulin.

This study from four Australian centers examined whether low-dose, continuous oral antibiotic therapy would prevent urinary tract infection in children (under the age of 18 years) who had already had one or more microbiologically proven urinary tract infections. Long-term, low-dose trimethoprim–sulfamethoxazole was associated with a modest decrease in the number of urinary tract infections in predisposed children.

A family with recurrent mucocutaneous candidiasis was evaluated for a potential genetic cause. An early-stop-codon mutation in the β-glucan receptor dectin-1 was found in the affected family members. These data suggest an important role of dectin-1 in mucosal antifungal defense.