Oral pseudomembranous candidiasis and mucositis were assessed in 39 patients receiving a total dose of 39-70 Gy radiotherapy for head and neck cancer. Mucositis was scored using the Radiation Therapy Oncology Group criteria, and oral candidiasis was diagnosed on the basis of clinical evaluation and quantitative laboratory findings. Radiation-induced mucositis was observed in 9/39 patients. Only 3/39 patients discontinued radiotherapy due to acute severe mucosal effects. Candidiasis (colony-forming units 35 to > or = 60/lesion) associated with mucositis was diagnosed in 30/39 patients: the most frequent aetiology of the infection was Candida albicans (n = 23), followed by Candida glabrata (n = 3), Candida krusei (n = 2), Candida tropicalis (n = 1) and Candida kefyr (n = 1). Patients with confirmed oral pseudomembranous candidiasis were treated with either fluconazole 200 mg/day or itraconazole 200 mg/day for 2 weeks. Clinical improvement and concomitant negative Candida cultures (mycologic cure) were the criteria determining a response to antifungal treatment. Etest revealed very low voriconazole MICs (0.004-0.125 microg/ml) for all isolates, and fluconazole resistance for eight C. albicans strains (MIC > 64 microg/ml) and for the C. krusei isolates (MIC > 32 microg/ml). The same strains showed itraconazole susceptibility dose dependence (MIC 0.5 microg/ml). Despite the itraconazole susceptible dose dependent MIC readings, all patients with oral pseudomembranous candidiasis caused by these strains responded to antifungal treatment with 200 mg/day itraconazole. Oral mycologic surveillance of patients undergoing radiotherapy for head and neck malignancies and susceptibility testing of isolates may be indicated in cases with mucositis-associated confirmed oral pseudomembranous candidiasis to ensure prompt administration of targeted antifungal treatment. On the basis of the low MIC values found, clinical evaluation of voriconazole is indicated for management of oral pseudomembranous candidiasis refractory to other azoles.

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Objective Angiopoietin-like proteins (ANGPTL) 3, 4 and 8 are upcoming cardiovascular biomarkers. Experimental studies showed that thyroid hormones altered their levels. We assessed ANGPTL3, 4 and 8 as predictors of cardiovascular functions among naïve subclinical and naïve overt hypothyroidism (SCH and OH) and altered ANGPTL levels with levothyroxine replacement (LT4) and their association with improved cardiovascular risk factors and cardiovascular function. Design and methods The study was a prospective follow-up study that assessed ANGPTL3, 4 and 8 levels, vascular status (flow-mediated dilation% of brachial artery (FMD%), carotid intima-media thickness (CIMT), aortic stiffness index (ASI)), left ventricle (LV) parameters (ejection fraction (EF), myocardial performance index (MPI), and LV mass), well-known cardiovascular risk factors and homeostatic model for the assessment of insulin resistance, at two time points, that is, among naïve SCH, naïve OH, and healthy subjects groups; and at 6 months after achieving the euthyroid state with LT4 by calculating their increased or decreased delta changes (∆↑ or ∆↓) in longitudinal arm among LT4-hypothyroid groups. Results Significantly elevated levels of ANGPTL3, 4 and 8 among hypothyroid groups than the healthy subjects were reduced with LT4. Multivariate analysis revealed ANGPTLs as independent predictors of cardiovascular functions and the contributors for ANGPTL level included ANGPTL3 and 4 for impaired FMD%, and ANGPTL8 for LV mass among naïve SCH; ANGPTL3 for EF% and ANGPTL8 for CIMT in naïve OH; ∆↓ANGPTL3 for ∆↓ASI meanwhile ∆↑freeT4 for ∆↓ANGPTL3, ∆↓fasting glucose, ∆↓triglyceride, and ∆↓thyroid peroxidase antibody for ∆↓ANGPTL4 among LT4-SCH. ∆↓ANGPTL4 for ∆↓MPI and ∆↓LV mass, meanwhile ∆↓TSH and ∆↓triglyceride for ∆↓ANGPTL3, ∆↑free T3 and ∆↓HOMA-IR for ∆↓ANGPTL4, and systolic blood pressure and waist circumference for ∆↓ANGPTL8 among LT4-OH. Conclusion Elevated ANGPTL3, 4 and 8 levels are differentially independent predictors of endothelial and cardiac function and are reduced with LT4 in SCH and OH.

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Single nucleotide polymorphism (SNP) studies in the promoter region of tumor necrosis factor-alpha (TNF-α (238)) have suggested its role in increased insulin resistance and also in the progression from prediabetes to type 2 diabetes (T2DM). It has been reported that genetic variations in the promoter region regulate TNF-α production and transcription, and they influence susceptibility to inflammatory-related diseases. Impairment of normal functioning of the β-cells of pancreatic islets is one of the main causative factors for the suppression of insulin secretion. TNF-α is among the main stimuli that induce the inflammation in pancreatic islets which lead to the induction of apoptosis in β-cells of pancreatic islets. Transcription factor 7-like 2 (TCF7L2) gene has been found to be one of the most risky genes for prediabetes and progression toT2DM. However, the underlying mechanism of this is still unknown. This is a review article demonstrating the possible mechanisms of both TNF-α G/A 238 and TCF7L2 C/T gene polymorphisms in prediabetes and type 2 diabetes mellitus.