Freshly isolated leukemic cells from patients with adult T-cell leukemia (ATL) produce high levels of interleukin-1 (IL-1), which is believed to play an important role in neutrophilia, elevation of C-reactive protein, osteolytic bone lesions, hypercalcemia, and fever in ATL.
Expression of IL-1alpha by HTLV-I productively infected cells may be important in the hypercalcemia, osteolytic bone lesions, neutrophilia, elevation of C-reactive protein, and fever frequently seen in patients with HTLV-I-induced adult T-cell leukemia/lymphoma.
Intravascular lymphomatosis (IVL) was favoured by the presence of low grade fever and raised serum C reactive protein, CSF pleocytosis, raised lymphoma markers (serum LDH, soluble IL-2 receptor), and steroid responsiveness.
The duration of fever and maximum serum C-reactive protein (CRP) levels also were significantly increased in the GT+TT group (P = .012 and .036, respectively), whereas plasma PAF-AH activity was significantly lower (P <.0001).
The patient finally had a partial clinical response (reduction in fever and irritability) and complete laboratory response (improved C-reactive protein and serum amyloid A levels) to humanized anti-IL-6 receptor antibody (MRA), but died from congestive heart failure and interstitial pneumonia 2 months after initiation of therapy.
Demographic characteristics and clinical results were similar except for longer fever duration before admission, longer fever continuation following antibiotic treatment and higher C-reactive protein values noted in the ALN group.
Patients with associated osteomyelitis were more likely to be bacteremic (P = 0.001), have fever >2 days (P = 0.03), and to have C-reactive protein (CRP) > or = 10 mg/dL (P = 0.01).
A set of initial clinical criteria have been drawn up which it is recommended should be fulfilled before a patient is tested: at least three recurrent bouts, age at disease onset < 20 years and elevated levels of C-reactive protein, especially in individuals with urticaria and moderate fever.
Specifically, correlations between SNPs and different levels of PDT-V efficacy have been detected by examining the gene variants influencing (i) thrombo-coagulative pathways, i.e. methylenetetrahydrofolate reductase (MTHFR) 677C>T (rs1801133), factor V (F5) 1691G>A (rs6025), prothrombin (F2) 20210G>A (rs1799963), and factor XIII-A (F13A1) 185G>T (rs5985); (ii) complement activation and/or inflammatory processes, i.e. complement factor H (CFH) 1277T>C (rs1061170), high-temperature requirement factor A1 (HTRA1) promoter -512G>A (rs11200638), and two variants of the C-reactive protein (CRP) gene (rs2808635 and rs876538); and (iii) production and bioavailability of vascular endothelial growth factor (VEGFA -2578C>A [rs699947] and rs2146323).
In addition, patients infected with PVL-positive MSSA strains had fever for a significantly longer duration and tended to have higher C-reactive protein levels than patients with PVL-negative MSSA infections.
Eleven cases (65%) had elevated-C reactive protein levels and fever protraction as well as images of bronchitis or pneumonia on chest radiographs approximately 1 week after onset.
Children with virus-positive exacerbations were more likely to require hospitalisation (59% vs 32.5% (p=0.02)) and have fever (OR 3.1, 95% CI 1.2 to 11.1), hypoxia (OR 25.5, 95% CI 2.0 to 322.6), chest signs (OR 3.3, 95% CI 1.1 to 10.2) and raised CRP (OR 4.7, 95% CI 1.7 to 13.1) when compared with virus-negative exacerbations.
Significantly prolonged duration of fever (>5 days), higher leukocyte counts, higher neutrophil counts, and higher C-reactive protein levels were in the adenoviral infected group (n = 53, P < 0.001), compared with the non-adenoviral infected group (n = 107).
It was found that a history of relapse, a refractory state of underlying disease, and high C-reactive protein concentrations at the beginning of fever were significant risk factors for mortality after developing sepsis.
This pilot study enrolled children with fever without source and compared PD-L1 expression on myeloid cells to C-reactive protein, erythrocyte sedimentation rate, leukocyte counts, S100A12, S100A8, S100A9, calprotectin, and procalcitonin.
ESR (P=0.001), CRP (P=0.001), fibrinogen (P=0.009), lymphopenia (P<0.001), neutrophilia (P<0.001), ferritin (P<0.001), leukocytosis (P=0.003), duration of fever before PET/CT (<3 months) were found to be statistically significant for positive contribution of PET/CT results to the diagnosis.
Seventy-four percentage of children had fever (20/27), and the mean values of white blood cell count and C-reactive protein level were 14.6 ± 4.5 × 10/L and 23.8 ± 24.1 mg/L, respectively.
There were more systemic findings, including fever (P = .01), poor intake (P = .01), elevated white blood cell count (P < .01), and elevated C-reactive protein level (P < .01), in children with isolated pulmonary disease than in children with extrapulmonary disease.
All SID victims had complained of mild fever and insomnia for a few days preceding death, which required infectious laboratory investigations marked with an elevated white blood cell count (WBC) and C-reactive protein (CRP).
Diagnostic criteria include the traditional clinical signs, in addition to the following biomarkers: elevated C-reactive protein in the absence of elevated procalcitonin, vitamin D, CD64, mean corpuscular volume, and other nonspecific inflammatory mediators in the absence of an infectious explanation for fever.