The Hypothalamic-Pituitary-Adrenal—Immune Axis

Lilly, Michael; Gann, Donald S.

doi:10.1001/archsurg.1992.01420120097017

Cited by 43 publications

(20 citation statements)

References 192 publications

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“…In the brain, GCs feed back negatively onto the hypothalamus (Figure 1), thereby inhibiting their own overproduction and maintaining homeostasis (Jacobson and Sapolsky, 1991;Lilly and Gann, 1992). Although most cells in the brain predominantly express GRs, principal cells of the limbic system often contain MRs as well as GRs (Joels, 2001).…”

Section: Adverse Glucocorticoid Effects In the Central Nervous Systemmentioning

confidence: 99%

Glucocorticoids and Central Nervous System Inflammation

2002

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Glucocorticoids (GCs) are well known for their anti-inflammatory and immunosuppressive properties in the periphery and are therefore widely and successfully used in the treatment of autoimmune diseases, chronic inflammation, or transplant rejection. This led to the assumption that GCs are uniformly anti-inflammatory in the periphery and the central nervous system (CNS). As a consequence, GCs are also used in the treatment of CNS inflammation. There is abundant evidence that an inflammatory reaction is mounted within the CNS following trauma, stroke, infection, and seizure, which can augment the brain damage. However an increasing number of studies indicate that the concept of GCs being universally immunosuppressive might be oversimplified. This article provides a review of the current literature, showing that under certain circumstances GCs might fail to have anti-inflammatory effects and sometimes even enhance inflammation. Journal of NeuroVirology (2002) 8, 513-528.

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Section: Adverse Glucocorticoid Effects In the Central Nervous Systemmentioning

confidence: 99%

Glucocorticoids and Central Nervous System Inflammation

2002

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“…15 These responses allow provision of adequate conditions for tissue repair and infection control and eventually promote survival. 16 Many investigators have described the metabolic events associated with burns, trauma, and sepsis.…”

Section: Figurementioning

confidence: 99%

Energy Metabolism of Infants and Children with Systemic Inflammatory Response Syndrome and Sepsis

Turi¹,

Petros²,

Eaton³

et al. 2001

Annals of Surgery

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ObjectiveTo evaluate whether critically ill children with systemic inflammatory response syndrome (SIRS) or sepsis have altered resting energy expenditure (REE) and substrate utilization. Summary Background DataStudies in adults with sepsis have shown increased energy expenditure and mobilization of endogenous fat. In infants and children, energy metabolism and substrate utilization during sepsis have not been characterized. MethodsMetabolic studies were performed in 21 critically ill children with SIRS or sepsis. Twenty-one stable control children, matched for weight, were also studied. Seven patients required inotropic support and 17 received mechanical ventilation. Fifteen patients with SIRS had evidence of bacterial, fungal, or viral infection and were considered septic. Respiratory gas exchange was measured by computerized indirect calorimetry for 1 to 2 hours continuously. ResultsThe REE of patients with SIRS or sepsis was not different from that of controls. Similarly, there were no differences in carbon dioxide production and oxygen consumption. Resting energy metabolism was not different between patients with SIRS and patients with sepsis. In addition, the presence of low platelet count or inotropic support did not affect resting energy metabolism. The median respiratory quotient of patients with SIRS or sepsis was 0.88 (range 0.75-1.12), indicating mixed utilization of fat and carbohydrate; this was not significantly different from that of controls. The Pediatric Risk of Mortality Score was not significantly correlated with REE or respiratory quotient. ConclusionsThe energy requirements of children with SIRS or sepsis are not increased. Their resting metabolism is based on both carbohydrate and fat utilization. The authors speculate that these children divert the energy for growth into recovery processes.Studies in adults have shown that the metabolic response to trauma and sepsis is characterized by hypermetabolism and increased tissue catabolism.1 Plank et al 2 have found that resting energy expenditure (REE) in adults with severe sepsis resulting from peritonitis increases up to 49% above normal and remains high for at least 3 weeks from the onset of disease. Hypermetabolism in these patients is associated with lipolysis and catabolism despite increased caloric intake.1,2 The energy requirement of adult patients with critical illness or those undergoing severe stress is thought to be increased by 30% above normal.3 Van Lanschot et al 4 have shown that energy expenditure measured by indirect calorimetry in these patients is greater than energy expenditure predicted on the basis of body size and age.There is little information on the metabolic response to critical illness in infancy and childhood. Preliminary studies 5,6 have not demonstrated a hypermetabolic response similar to that described in adults.2,4 Chwals et al 5 measured REE by indirect calorimetry in critically ill ventilated infants and young children and showed that the measured

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“…While laboratory studies often involve highly controlled and specific noxious stimulation, real life tissue trauma usually involves a spectrum of afferent activity, and the pattern of activity may be a greater determinant of the stress response than the specific receptor system involved (Lilly & Gann, 1992). Traumatic injury, for example, might initiate complex signaling from the site of injury, including inflammatory mediators, baroreceptor signals from blood volume changes, and hypercapnia.…”

Section: Figmentioning

confidence: 99%