Neonatal sepsis is a frequent occurrence in the nursery. The morbidity associated with this condition is still significant despite the availability of antibiotics (1). This is due to factors other than the mere presence of an organism. In sepsis, liver mitochondria can increase rates of hydrogen peroxide and hydroxyl radical production via alterations in complex II activity (2). Cytokine release and resultant transcriptional activation of various genes can also result in increased reactive oxygen species (3). Some reports indicate that septic neonates have altered antioxidant status and several investigators have demonstrated increased oxidative stress in septic adults (2, 4). Based on this premise, Gitto and colleagues (5) evaluated the protective effects of melatonin therapy in neonates with sepsis by measuring a marker of oxidative stress.

In this small study involving only 20 newborns with sepsis, melatonin dissolved in 1:90 ethanol was administered orally to neonates within 24 -48 h diagnosis. Melatonin treated infants were less often classified as septic and demonstrated a reduction in markers of lipid peroxidation [malondialdehyde and 4-hydroxynonenal (4-HNE)]. This study provides encouraging evidence for the use of melatonin as an adjunct therapy in the treatment of neonatal sepsis. However, this study population is small and the criteria used for defining sepsis did not necessarily require that a blood culture be positive. Although we do not always identify the bacterial organisms responsible for neonatal sepsis, the lack of absolute confirmation of sepsis raises concerns about the nature of the illness in these patients. Would the infants have improved even if they were not given melatonin? Additionally, a change in serum malondiadldehyde and 4-HNE in the first four hours of life is difficult to reconcile with a change in clinical status 24 to 48 h later. We are not told whether this change persists or whether this difference was only transient. In either case, the association of decreased oxidative markers and improved clinical status is not necessarily causative.

Log in or create a free account to read this content

Gain free access to this article, as well as selected content from this journal and more on nature.com

Access through your institution

or

Sign in or create an account
Continue with Google
Continue with ORCiD