Background To compare the utility of ESR, CRP and platelets for the diagnosis of GCA. Method A clinical diagnosis of GCA was determined by case-note review of 270 individuals (68% female, mean age 72 years) referred to a central pathology service for a temporal artery biopsy between 2011 and 2014. The highest levels of ESR, CRP and platelets (within 2 weeks of diagnosis) were documented. Evaluation of ESR, CRP and platelets for the diagnosis of GCA were compared using Receiver Operating Characteristic Area Under the Curve (ROC-AUC), and sensitivity/specificity at optimum cut-off values. Results GCA was clinically diagnosed in 139 (67%) patients, with 81 TAB positive. The AUC estimates for ESR, CRP and platelets were comparable (0.65 vs 0.72 vs 0.72, p = 0.08). The estimated optimal cut-off levels were confirmed at 50 mm/hour for ESR, and determined as 20 mg/L for CRP and 300 × 10 9 /L for platelets. Sensitivity estimates for these three tests were comparable ( p = 0.45) and ranged between 66% for ESR and 71% for platelets. Specificity estimates were also comparable ( p = 0.11) and ranged between 57% for ESR and 68% for CRP. There was only moderate agreement between the three positive tests (agreement 67%, kappa: 0.34), and when considered collectively, CRP and platelet positive tests were independent predictors of GCA ( p <  0.001), but the ESR was not ( p = 0.76). Conclusion ESR, CRP and platelets are moderate, equivalent diagnostic tests for GCA, but may yield disparate results in individual patients. A combination of CRP and platelet tests may provide the best diagnostic utility for GCA.

Strongyloides hyperinfection syndrome is rarely described in immunocompetent individuals. We present a case of fatal Strongyloides hyperinfection syndrome, and a literature review identifying nine other cases occurring in immunocompetent individuals, highlighting the challenges of diagnosis and treatment in this setting. While overall mortality is lower compared to immunocompromised patients, fatal outcomes still occur. A high index of suspicion is required for early diagnosis and treatment.

BACKGROUND: In hypertrophic cardiomyopathy (HCM), myocyte disarray and microvascular disease (MVD) have been implicated in adverse events, and recent evidence suggests that these may occur early. As novel therapy provides promise for disease modification, detection of phenotype development is an emerging priority. To evaluate their utility as early and disease-specific biomarkers, we measured myocardial microstructure and MVD in 3 HCM groups—overt, either genotype-positive (G+LVH+) or genotype-negative (G−LVH+), and subclinical (G+LVH−) HCM—exploring relationships with electrical changes and genetic substrate. METHODS: This was a multicenter collaboration to study 206 subjects: 101 patients with overt HCM (51 G+LVH+ and 50 G−LVH+), 77 patients with G+LVH−, and 28 matched healthy volunteers. All underwent 12-lead ECG, quantitative perfusion cardiac magnetic resonance imaging (measuring myocardial blood flow, myocardial perfusion reserve, and perfusion defects), and cardiac diffusion tensor imaging measuring fractional anisotropy (lower values expected with more disarray), mean diffusivity (reflecting myocyte packing/interstitial expansion), and second eigenvector angle (measuring sheetlet orientation). RESULTS: Compared with healthy volunteers, patients with overt HCM had evidence of altered microstructure (lower fractional anisotropy, higher mean diffusivity, and higher second eigenvector angle; all P <0.001) and MVD (lower stress myocardial blood flow and myocardial perfusion reserve; both P <0.001). Patients with G−LVH+ were similar to those with G+LVH+ but had elevated second eigenvector angle ( P <0.001 after adjustment for left ventricular hypertrophy and fibrosis). In overt disease, perfusion defects were found in all G+ but not all G− patients (100% [51/51] versus 82% [41/50]; P =0.001). Patients with G+LVH− compared with healthy volunteers similarly had altered microstructure, although to a lesser extent (all diffusion tensor imaging parameters; P <0.001), and MVD (reduced stress myocardial blood flow [ P =0.015] with perfusion defects in 28% versus 0 healthy volunteers [ P =0.002]). Disarray and MVD were independently associated with pathological electrocardiographic abnormalities in both overt and subclinical disease after adjustment for fibrosis and left ventricular hypertrophy (overt: fractional anisotropy: odds ratio for an abnormal ECG, 3.3, P =0.01; stress myocardial blood flow: odds ratio, 2.8, P =0.015; subclinical: fractional anisotropy odds ratio, 4.0, P =0.001; myocardial perfusion reserve odds ratio, 2.2, P =0.049). CONCLUSIONS: Microstructural alteration and MVD occur in overt HCM and are different in G+ and G− patients. Both also occur in the absence of hypertrophy in sarcomeric mutation carriers, in whom changes are associated with electrocardiographic abnormalities. Measurable changes in myocardial microstructure and microvascular function are early-phenotype biomarkers in the emerging era of disease-modifying therapy.