[Sudden infant death syndrome (SIDS) caused by ATP-depletion following hyperventilation, tissue-hypoxia and hypermetabolism--a hypothesis].
BACKGROUND
Despite a decreasing incidence, sudden infant death syndrome (SIDS) is still the most frequent cause of death in industrial nations during the first year of life. Hypoxia plays a major role in the pathogenesis, but the exact mechanism is not fully understood.


METHODS
This study was based on personal considerations and a selective online literature search.


OBJECTIVE
SIDS is the result of a frequently protracted ATP-depletion.


CONCLUSIONS
Especially in combination, all risk factors for SIDS favour an ATP-deficiency by increasing ATP-catabolism and/or by diminishing ATP-synthesis. Prenatal chronic hypoxaemia and an insufficient supply with nutrients lead to low birth-weight, reduced adipose tissue, elevated haemoglobin F, increased sympathetic activity, hypermetabolism, and diminished hypoxia tolerance in the neonates. Because of reduced adipose tissue, more energy for thermogenesis is needed after birth. In reaction to hypoxaemia, infants with risk factors show hyperventilation instead of hypoxic hypometabolism and respiratory depression. Enhanced breathing, however, requires additional ATP and causes increasing oxygen affinity, which is elevated physiologically during the first months of life. Thereby, tissue-hypoxia and diminished ATP-synthesis may arise. Besides, enhanced sympathetic activity leads to hypermetabolism and increased ATP-catabolism. While innate risk factors may reduce ATP-production in burdening situations, like food deprivation, postnatal hyperthermia and stress augment ATP-catabolism by hyperventilation and hypermetabolism and empty energy stores. For term newborns, the peak incidence of SIDS might be explained by the haemoglobin nadir of physiological anaemia and by the therefore reduced capacity for oxygen transport. Thereby, the risk of tissue-hypoxia, which follows increased oxygen affinity and vanishing ability to hypoxic hypometabolism, is further enhanced. The almost identical symptoms of SIDS and ATP-deficiency diseases like hypophosphataemia, heat stroke, and carbon monoxide poisoning support the presented hypothesis.
Deixler
E
E
IV. Medizinische Abteilung, Rheumatologie und Klinische Immunologie, Städtisches Klinikum München GmbH, Krankenhaus München-Bogenhausen, Akademisches Lehrkrankenhaus der Technischen Universität München. e.deixler@gmx.de
D000255:Adenosine Triphosphate / Q000172:deficiency*; D006801:Humans; D006985:Hyperventilation / Q000150:complications* / Q000503:physiopathology; D000860:Hypoxia / Q000150:complications* / Q000503:physiopathology; D007223:Infant; D007231:Infant, Newborn; D008659:Metabolic Diseases / Q000150:complications* / Q000503:physiopathology; D008954:Models, Biological; D010100:Oxygen / Q000378:metabolism*; D013398:Sudden Infant Death / Q000209:etiology*
D000255:Adenosine Triphosphate; D010100:Oxygen