Is there an acute-phase response in steady-state sickle cell disease?

Metabolic and serum changes during steady-state homozygous sicle cell (SS) disease are consistent with an acute-phase response and raise the possibility that inflammation occurs in SS disease even during the steady state. To test this hypothesis, we measured concentrations of acute phase reactants in patients with SS disease, in patients with sickle cell haemoglobin C (SC) disease, and in normal (AA) control subjects. The concentrations of C-reactive protein and serum amyloid A were increased above 10 mg/L and 5mg/L, respectively (our definition of an acute-phase response) in 18 percent (26/143) of subjects with SS disease even when they were symptom free, in 17 percent (6/35) of subjects with SC disease, and in 1 percent (1/80) of AA controls (p<0.001). We suggest that subclinical vaso-occlusion may generate a covert inflammatory response and that the cytokine mediators of this response may contribute to the metabolic abnormalities and growth failure in sickle cell disease.(AU)

The acute phase response in severely malnourished children - abstract

The acute phase response is a non-specific reaction to tissue injury, in which the liver plays a central role. We examined the acute phase response in 52 severely malnourished children by measuring the serum levels of C-Reactive Protein (CRP) and Serum Amyloid A (SAA), using an ELISA technique. Blood was taken both at admission and following a controlled stress, namely, Triple (DPT) Vaccine. Four children died. The surviving children received DPT either at admission (n=16) or early in recovery (time B) (n=32). All the children received a second vaccination with DPT once they had regained > 90 percent weight-for-height (discharge) (n=48). Both acute phase proteins responded in tandem. The admission values were elevated in only 44 percent of the children for CRP and 20 percent for SAA, despite clinical evidence of infection. The magnitude of the response of both acute phase proteins to DPT given at admission or at time B was significantly less than at discharge (p < 0.05). Even at discharge, approximately 20 percent of the children did not have the expected response. Children with oedematous malnutrition were less likely to respond than non-oedematous children. We suggest that, firstly, severly malnourished children are unable to mount an effective acute phase response, which may have functional implications. Secondly, that the inability to synthesize acute phase proteins represents one manifestation of the hepatic dysfunction that occurs in severe malnutrition (AU)