Serum procalcitonin value is useful for predicting severity of Kawasaki disease.

Department of Pediatrics, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
The Pediatric Infectious Disease Journal (Impact Factor: 3.14). 12/2011; 31(5):523-5. DOI: 10.1097/INF.0b013e3182463879
Source: PubMed

ABSTRACT We measured serum procalcitonin concentrations in 160 patients suffering from Kawasaki disease. Serum procalcitonin was significantly higher in nonresponders to an initial intravenous immunoglobulin treatment than in responders. A cutoff value of procalcitonin (0.5 ng/mL) for nonresponders showed that the sensitivity was 85% and the accuracy was 64%. Multivariate logistic regression analysis revealed that procalcitonin-positive cases showed the highest risk for nonresponders.

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    ABSTRACT: Henoch-Schönlein purpura (HSP) is a vasculitic disorder resulting from autoinflammatory-mediated tissue injury. Procalcitonin (PCT) and C-reactive protein (CRP) are two biomarkers of the immune response that recognize bacterial infection and inflammation, respectively. This study tested whether levels of PCT and CRP were associated with selected clinical features, disease severity, and organ damage in HSP. Eighty-nine pediatric patients with HSP were analyzed for clinical manifestations and organ damage. Serum CRP, PCT, and occult blood in the urine and stool (prior to steroid therapy) were measured. Disease severity was classified according to previously established clinical classifications. Sixty patients (67.4 %) had a low clinical score (LCS) of <4 (group A) while 29 patients (32.5 %) had a high clinical score (HCS) of ≥4 (group B). When patients were then classified by the presence of gastrointestinal bleeding, 66 (74.2 %) cases lacked alimentary tract hemorrhage (group C) while 23 (25.8 %) cases presented with gastrointestinal bleeding (group D). There were no significant differences in CRP (group A: median = 5.26, range = 1.00-77.60 vs. group B: median = 8.59, range = 1.00-144.00 mg/l; u = 1.397) or PCT levels (group A: median = 0.05, range = 0.05-0.24 vs. group B: median = 0.08, range = 0.05-1.02 ng/ml; u = 1.709) between groups A and B. When serum PCT levels were examined in relation to gastrointestinal bleeding, the levels of serum PCT were higher in group D than group C patients (group D: median = 0.09, range = 0.05-1.02 vs. group C: median = 0.05, range = 0.05-0.32 ng/ml; u = 2.849). It is important to note that the average PCT level was below the threshold for a systemic bacterial infection (0.5 ng/ml). We did not observe a correlation between CRP levels and the absence or presence of GI bleeding in groups C or D (group C: median = 4.66, range = 1.00-144.00 vs. group D: median = 9.44, range = 1.06-124.00 mg/l; u = 1.783), respectively. In all patients, there was a significant correlation between the concentrations of PCT and CRP (r = 0.721, p = 0.002). In patients with HSP, inflammatory markers are not uniformly associated with the disease and instead, show variable association depending on the clinical severity and level of organ damage. In patients with severe HSP, elevated serum PCT was significantly associated with gastrointestinal bleeding. In contrast, CRP was not a specific predictor for different clinical classifications of HSP, despite a similar pattern of concentration changes to PCT.
    Clinical Rheumatology 10/2014; DOI:10.1007/s10067-014-2773-1 · 1.77 Impact Factor
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    ABSTRACT: OBJECTIVE: To conduct a systematic review and meta-analysis of the performance of the procalcitonin (PCT) diagnostic test for identifying infectious complications after hematopoietic stem cell transplantation (HSCT). METHODS: We searched EMBASE, MEDLINE, the Cochrane database, and reference lists of relevant articles, with no language restrictions, through December 2011. We selected original articles that reported diagnostic performance of PCT alone or compared with other biomarkers for identifying serious infections in HSCT recipients. We quantitatively evaluated test accuracy parameters with the use of forest plots, hierarchical summary receiver operating characteristic curves, and bivariate random effect models. RESULTS: We found 6 qualifying studies (studying 1344 episodes of suspected infection with confirmed infectious episodes) from 3 countries. These 6 studies examined both PCT and C-reactive protein (CRP) test performance. Bivariate pooled sensitivity, specificity, positive likelihood ratios, and negative likelihood ratios were 0.66 (95% confidence interval [CI] 0.60-0.72), 0.72 (95% CI 0.65-0.79), 2.39 (95% CI 1.84- 3.09), and 0.47 (95% CI 0.39-0.57) for PCT, and 0.80 (95% CI 0.54-0.93), 0.73 (95% CI 0.56-0.86), 3.00 (95% CI 1.86-4.84), and 0.27 (95% CI 0.11-0.65) for CRP. In terms of area under the curve (AUC), CRP was superior to PCT in detecting infectious complications, with an AUC of 0.82 for CRP versus an AUC of 0.69 for PCT. CONCLUSION: The pooled accuracy estimates of 6 different studies indicated only a moderate rule-out diagnostic value of both PCT and CRP in discriminating infection from other inflammatory complications following allogeneic HSCT.
    Transplant Infectious Disease 02/2013; 15(3). DOI:10.1111/tid.12055 · 1.98 Impact Factor
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    ABSTRACT: Previously, we reviewed biological evidence that mercury could induce autoimmunity and coronary arterial wall relaxation as observed in Kawasaki syndrome (KS) through its effects on calcium signaling, and that inositol 1,4,5-triphosphate 3-kinase C (ITPKC) susceptibility in KS would predispose patients to mercury by increasing Ca(2+) release. Hg(2+) sensitizes inositol 1,4,5-triphosphate (IP3) receptors at low doses, which release Ca(2+) from intracellular stores in the sarcoplasmic reticulum, resulting in delayed, repetitive calcium influx. ITPKC prevents IP3 from triggering IP3 receptors to release calcium by converting IP3 to inositol 1,3,4,5-tetrakisphosphate. Defective IP3 phosphorylation resulting from reduced genetic expressions of ITPKC in KS would promote IP3, which increases Ca(2+) release. Hg(2+) increases catecholamine levels through the inhibition of S-adenosylmethionine and subsequently catechol-O-methyltransferase (COMT), while a single nucleotide polymorphism of the COMT gene (rs769224) was recently found to be significantly associated with the development of coronary artery lesions in KS. Accumulation of norepinephrine or epinephrine would potentiate Hg(2+)-induced calcium influx by increasing IP3 production and increasing the permeability of cardiac sarcolemma to Ca(2+). Norepinephrine and epinephrine also promote the secretion of atrial natriuretic peptide, a potent vasodilator that suppresses the release of vasoconstrictors. Elevated catecholamine levels can induce hypertension and tachycardia, while increased arterial pressure and a rapid heart rate would promote arterial vasodilation and subsequent fatal thromboses, particularly in tandem. Genetic risk factors may explain why only a susceptible subset of children develops KS although mercury exposure from methylmercury in fish or thimerosal in pediatric vaccines is nearly ubiquitous. During the infantile acrodynia epidemic, only 1 in 500 children developed acrodynia whereas mercury exposure was very common due to the use of teething powders. This hypothesis mirrors the leading theory for KS in which a widespread infection only induces KS in susceptible children. Acrodynia can mimic the clinical picture of KS, leading to its inclusion in the differential diagnosis for KS. Catecholamine levels are often elevated in acrodynia and may also play a role in KS. We conclude that KS may be the acute febrile form of acrodynia.
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