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Tumour necrosis factor (TNF) receptor-associated periodic syndrome (TRAPS) is an autoinflammatory disorder characterized by periodic attacks of fever and inflammation, due to mutations in the gene coding for the TNF type I receptor (TNFRSF1A). A 16-year-old patient with the diagnosis of TRAPS was admitted to hospital because of fever and abdominal pain. Initially, the symptoms were interpreted as manifestations of another TRAPS attack, but the patient's condition worsened, despite treatment with corticosteroids and antibiotics. A repeated computer tomography revealed an intra-abdominal abscess, which necessitated urgent surgical intervention. This case stresses the importance of differential diagnostic vigilance when dealing with patients with rare genetic diseases.

Background Hydrocortisone (HC) has been reported to rapidly improve hemodynamics and reduce the time to vasopressor cessation in septic shock, but none has focused on this effect in acute pancreatitis. We therefore performed a study to assess the effects of hydrocortisone on catecholamine-dependent shock among patients with severe acute pancreatitis. Methods A retrospective, case-controlled study among 10 patients with severe acute pancreatitis and HC treatment for catecholamine-dependent shock was performed. The control group comprised 11 conventionally treated patients with the same severity of pancreatitis and circulatory shock according to the norepinephrine support required. In focus were the first 48 h from the start of HC administration in the HC group and from the reference point in the control group, respectively. The reference point for the control group was the time point at which doses of norepinephrine exceeded 0.3 microg kg(-1) min(-1). Results Patients in the HC group were weaned off norepinephrine in a significantly shorter time (61 h in HC group vs. 141 h, P = 0.016). The HC group received significantly less norepinephrine (area under curve of norepinephrine dose, P = 0.041). The reduction in norepinephrine dose was comparable at 24 h, being -0.051 (-0.208-0.022) microg kg(-1) min(-1) in the HC group vs. -0.026 (-0.150-0.030) microg kg(-1) min(-1) in the controls (P = 0.307), and at 48 h with respective figures of -0.206 (-0.317 to -0.102) microg kg(-1) min(-1) and -0.103 (-0.178-0.029) microg kg(-1) min(-1) (P = 0.072), from the start of HC administration. Conclusion According to our data it seems reasonable to formulate a hypothesis that low doses of HC shorten the time to vasopressor cessation and rapidly reduce the need for norepinephrine support in patients with shock associated with severe acute pancreatitis without sepsis.

Acute pancreatitis (AP) is a common disease with wide variation of severity. The diagnosis of AP is usually based on high serum amylase or lipase values but the accuracy of these methods is considered unsatisfactory. One in five of the patients develops a severe disease and carries a considerable risk of development of organ failure and high mortality. Early detection of patients with severe AP and especially those with increased risk of organ failure is importance since such patients seem to benefit from treatment in an intensive care unit started as soon as possible after presentation. In addition to enzymological methods, increasing interest has been focused on laboratory markers reflecting the level of inflammatory response in AP. At present, in routine clinical work the most commonly used severity marker is serum C-reactive protein, the concentration of which rises too slowly to be used for early prediction of severity. New therapies aiming at modifying the course of systemic inflammation in AP are being developed and therefore monitoring the patient's immune inflammatory status is needed. In this review article we present the current knowledge of laboratory tests, which has been evaluated for diagnostic and prognostic purposes in AP.

Background: Serum amyloid A (SAA) is an early and sensitive marker of the extent of tissue trauma and inflammation. The aim of this study was to compare the early prognostic accuracy of SAA with that of serum C-reactive protein (CRP) in acute pancreatitis. Methods: In a prospective multicentre trial, plasma SAA and CRP levels were measured in patients with severe and mild acute pancreatitis, and in a control group with acute abdominal pain. Plasma samples were collected on admission and at 6-h intervals for 48 h, every 12 h between 48 and 72 h, then daily for 5 days. Plasma SAA was measured by a new enzyme-linked immunosorbent assay and CRP was measured by immunoturbidometry. Results: There were 137 patients with mild and 35 with severe acute pancreatitis, and 74 control patients. SAA levels were significantly higher in patients with severe acute pancreatitis than in those with mild acute pancreatitis, on admission, at 24 h or less after symptom onset, and subsequently. Whereas plasma CRP concentration was also significantly higher in patients with severe acute pancreatitis on admission, it failed to distinguish mild from severe acute pancreatitis until 30–36 h after symptom onset. SAA levels predicted severity (sensitivity 67 per cent, specificity 70 per cent, negative predictive value 89 per cent, mean(s.d.) area under curve 0·7(0·05)) significantly better than CRP (57 per cent, 60 per cent, 84 per cent, 0·59(0·06) respectively) on admission (P = 0·02) and at 24 h following symptom onset (area under curve 0·65(0·09) versus 0·58(0·09) respectively; P ≤ 0·02). Conclusion: Plasma SAA concentration is an early marker of severity in acute pancreatitis and is superior to CRP estimation on hospital admission and at 24 h or less after symptom onset. This study suggests that plasma SAA concentration is clinically useful, with the potential to replace CRP in the management of acute pancreatitis. © 2002 British Journal of Surgery Society Ltd