Commentary: Thiamine Deficiency in Tropical Pediatrics: New Insights into a Neglected but Vital Metabolic Challenge

A commentary on Thiamine deficiency in tropical pediatrics: new insights into a neglected but vital metabolic challenge Although there have been health-care improvements in recent decades, it is a fact that nutritional deficiencies persist in children worldwide (1, 2). One of these is thiamine deficiency (TD). In a comprehensive review, Hiffler et al. (3) have addressed two relevant questions for the management of TD in resource-poor settings that are as follows: (1) the early diagnosis of TD depends on clinical awareness and (2) the need for early thiamine supplementation during the refeeding of malnourished children. The review adds significant insight into the problem and gives the opportunity to discuss diagnosis, management, and the rationale for including thiamine in children nutritional support. Thiamine deficiency is less common than in the past but still occurs endemically as beriberi in children and nursing mothers living in rural areas of Southeast Asia (4–9) and as outbreaks in different parts of the world (10–12). The clinical spectrum of TD may vary according to the clinical setting, age, and individual susceptibility (13). Infantile beriberi typically presents as heart failure, dysphonia, and increased irritability (5, 14, 15). However, the classical diagnostic criteria for infantile beriberi may be non-specific for diagnosis of TD in endemic regions, where the disease may often be clinically unapparent (5). As early symptoms are non-specific, biochemical analysis is unavailable in resource-limited settings, and food intake records are usually inaccurate for a timely diagnosis of deficiency, it is not known just how widespread subclinical TD is. An issue not addressed in this review is that the clinical expression of a micronutrient deficiency is a result of a progressive process whose duration is variable, dependent on reserves, consumption, and food intake. In an initial phase, there is a depletion of the reserves followed by decreased intracel-lular concentration. If inadequate intake persists, metabolic changes occur, followed by non-specific functional defects (subclinical deficiency). The end result of this process will be a clinical deficiency state and ultimately death (16). Given its very limited body stores, the time taken to pass through these different phases are shorter for thiamine (13). This can be particularly worrying in the case of malnourished and critically ill patients. A comment should be made on the laboratory diagnosis of TD. Hiffler et al. refer to the limitations of serum or whole blood thiamine as a marker of thiamine status during the systemic inflam-matory …