Pediatric norovirus infection.

Noroviruses (NoVs) are among the most frequent causes of acute pediatric gastroenteritis. Although the disease is often self-limiting and recovery is the rule, it constitutes an important health problem because of its highly contagious nature and the high rate of morbidity. NoVs are responsible for 47-96 % of outbreaks of acute pediatric gastroenteritis, and 5-36 % of sporadic cases. NoV-induced gastroenteritis is a frequent cause of hospitalization, and severe and sometimes fatal cases have been reported in immunocompromised children. The increasing recognition of NoVs as the cause of pediatric disease and the limited success in preventing outbreaks have led to consideration of vaccines. However, while awaiting the development of a vaccine, there is an urgent need for more epidemiological data concerning childhood NoV infection, including the impact of NoVs on different age groups, the possible etiological role of NoVs in infections other than gastroenteritis, and the socioeconomic impact of NoVs on households.

Current advances in the understanding and treatment of mevalonate kinase deficiency.

Mevalonate kinase deficiency (MKD) is a rare autosomal recessive autoinflammatory metabolic disease that is caused by mutations in the MVK gene. Patients with MKD typically have an early onset in infancy. MKD is characterized by recurrent episodes of high fever, abdominal distress, diffuse joint pain, and skin rashes. In a subset of patients, MKD is also associated with elevated serum immunoglobulin D (IgD) levels (hyperimmunoglobulinemia D syndrome, HIDS). The clinical phenotype of MKD varies widely and depends on the severity of the impaired mevalonate kinase activity. Complete impairment results in the severe metabolic disease, mevalonic aciduria, while a partial deficiency results in a broad spectrum of clinical presentation, including HIDS. The precise molecular mechanisms behind the elevated serum IgD levels and inflammation that occurs in MKD remain unknown. Children who exhibit symptoms of MKD should be tested for mutations in the MKD gene. However, the complexity of MKD often results in delays in its definitive diagnosis and the outcome in adult age is not completely known. Therapeutic options for MKD are based on limited data and include non-steroidal anti-inflammatory drugs, corticosteroids, and biological agents that target specific cytokine pathways. In recent years, some studies have reported promising results for new biological drugs; however, these cases have failed to achieve satisfactory remission. Therefore, further studies are needed to understand the pathogenesis of MKD and identify innovative therapeutic tools for its management.