Does tonsil hypertrophy occur as a result of colonization of actinomycosis?

To determine the relationship between the presence of actinomyces in adenoid/tonsillar tissue and hypertrophy, and to investigate seasonal changes in frequency of actinomycosis in adenoidectomy/tonsillectomy materials. In this retrospective study, the data of 175 patients who underwent adenoidectomy/tonsillectomy between January 2016 December 2018 were examined. After the exclusion of patients with immunosuppression, malignancy or without adequate medical data,158 patients were included to the study. Age, sex, adenoid/tonsil diameter and date of appointment were recorded. In our study, Actinomycosis was found in 44(28%) of 158 patients. Whilst there was no significant relationship between the presence of actinomycetes colonization and sex or date of appointment, increasing age was positively correlated with actinomycetes colonization. No relationship between actinomycetes colonization and hypertrophy was found. Besides, actinomycosis was found to be more prevalent in right and bilateral tonsillar tissues. Actinomyces can be found in adenoid/tonsils independent of hypertrophy and sex, and it shows a positive correlation with increasing age. It tends to be found in the right tonsil or bilateral tonsils more frequently. [Med-Science 2019; 8(4.000): 971-4

Intracoronary epinephrine in the treatment of refractory no-reflow after primary percutaneous coronary intervention: a retrospective study.

BACKGROUND: Despite the advances in medical and interventional treatment modalities, some patients develop epicardial coronary artery reperfusion but not myocardial reperfusion after primary percutaneous coronary intervention (PCI), known as no-reflow. The goal of this study was to evaluate the safety and efficacy of intracoronary epinephrine in reversing refractory no-reflow during primary PCI. METHODS: A total of 248 consecutive STEMI patients who had undergone primary PCI were retrospectively evaluated. Among those, 12 patients which received intracoronary epinephrine to treat a refractory no-reflow phenomenon were evaluated. Refractory no-reflow was defined as persistent TIMI flow grade (TFG) ≤2 despite intracoronary administration of at least one other pharmacologic intervention. TFG, TIMI frame count (TFC), and TIMI myocardial perfusion grade (TMPG) were recorded before and after intracoronary epinephrine administration. RESULTS: A mean of 333 ± 123 mcg of intracoronary epinephrine was administered. No-reflow was successfully reversed with complete restoration of TIMI 3 flow in 9 of 12 patients (75%). TFG improved from 1.33 ± 0.49 prior to epinephrine to 2.66 ± 0.65 after the treatment (p < 0.001). There was an improvement in coronary flow of at least one TFG in 11 (93%) patients, two TFG in 5 (42%) cases. TFC decreased from 56 ± 10 at the time of no-reflow to 19 ± 11 (p < 0.001). A reduction of TMPG from 0.83 ± 0.71 to 2.58 ± 0.66 was detected after epinephrine bolus (p < 0.001). Epinephrine administration was well tolerated without serious adverse hemodynamic or chronotropic effects. Intracoronary epinephrine resulted in significant but tolerable increase in heart rate (68 ± 13 to 95 ± 16 beats/min; p < 0.001) and systolic blood pressure (94 ± 18 to 140 ± 20; p < 0.001). Hypotension associated with no-reflow developed in 5 (42%) patients. During the procedure, intra-aortic balloon pump counterpulsation was required in two (17%) patients, transvenous pacing in 2 (17%) cases, and both intra-aortic balloon counterpulsation and transvenous pacing in one (8%) patients. One patient (8%) died despite all therapeutic measures. CONCLUSION: Intracoronary epinephrine may become an effective alternative in patients suffering refractory no-reflow following primary PCI

The CYP2C19*2 and CYP2C19*17 Polymorphisms play a Vital Role in Clopidogrel Responsiveness after Percutaneous Coronary Intervention: A Pharmacogenomics Study

Clopidogrel inhibits platelet activation and aggregation by blocking the P2Y12 receptor. Dual antiplatelet therapy with clopidogrel and aspirin is recommended treatment by current guidelines for patients undergoing percutaneous interventions. Recurrent ischaemic cardiac events after this treatment showed lack of clopidogrel responsiveness. We aimed to investigate the most noticeable variants in the genes involved in clopidogrel pharmacokinetics and pharmacodynamics. A total of 347 Turkish patients who underwent percutaneous coronary interventions with stent implantation were included in our study. Platelet reactivity (PRU) and % inhibition were measured with VerifyNow P2Y12 assay in blood samples collected from patients who took a standard dose of clopidogrel (75 mg/day) for at least 7 days. The variants in the CYP2C19, CYP3A4, CYP2B6, ABCB1, ITGB3 and PON1 genes were genotyped using the Sequenom MassARRAY system. When grouped, the patients with PRU values >208 as non-responsiveness to clopidogrel therapy; 104 (30%) patients were non-responders and 243 (70%) patients were responders. A significant association was found between the CYP2C19*2 (G636A) polymorphism and non-responsiveness to clopidogrel therapy (p < 0.001). An allele frequency of this single nucleotide polymorphism was high in non-responders; its odds ratio was 2.92 compared with G allele (p < 0.001). PRU values of CT genotypes were lower (p = 0.029) and % inhibition values of CT genotypes were higher (p = 0.008) compared with CC genotypes for the CYP2C19*17 (C806T) polymorphism. None of the other genetic variants were found to be statistically associated with non-responsiveness to clopidogrel and antiplatelet activity. Our findings suggest that the CYP2C19*2 polymorphism is associated with non-responsiveness to clopidogrel therapy and the CYP2C19*17 polymorphism enhances antiplatelet activity of clopidogrel. Depending on haplotypes of these two polymorphisms, clopidogrel-treated patients can be protected or not from stent thrombosis and ischaemic events

Mortality analysis of COVID-19 infection in chronic kidney disease, haemodialysis and renal transplant patients compared with patients without kidney disease: A nationwide analysis from Turkey

© The Author(s) 2020.Background. Chronic kidney disease (CKD) and immunosuppression, such as in renal transplantation (RT), stand as one of the established potential risk factors for severe coronavirus disease 2019 (COVID-19). Case morbidity and mortality rates for any type of infection have always been much higher in CKD, haemodialysis (HD) and RT patients than in the general population. A large study comparing COVID-19 outcome in moderate to advanced CKD (Stages 3-5), HD and RT patients with a control group of patients is still lacking. Methods. We conducted a multicentre, retrospective, observational study, involving hospitalized adult patients with COVID-19 from 47 centres in Turkey. Patients with CKD Stages 3-5, chronic HD and RT were compared with patients who had COVID-19 but no kidney disease. Demographics, comorbidities, medications, laboratory tests, COVID-19 treatments and outcome [in-hospital mortality and combined in-hospital outcome mortality or admission to the intensive care unit (ICU)] were compared. Results. A total of 1210 patients were included [median age, 61 (quartile 1-quartile 3 48-71) years, female 551 (45.5%)] composed of four groups: Control (n = 450), HD (n = 390), RT (n = 81) and CKD (n = 289). The ICU admission rate was 266/ 1210 (22.0%). A total of 172/1210 (14.2%) patients died. The ICU admission and in-hospital mortality rates in the CKD group [114/289 (39.4%); 95% confidence interval (CI) 33.9-45.2; and 82/289 (28.4%); 95% CI 23.9-34.5)] were significantly higher than the other groups: HD = 99/390 (25.4%; 95% CI 21.3-29.9; P<0.001) and 63/390 (16.2%; 95% CI 13.0-20.4; P<0.001); RT = 17/81 (21.0%; 95% CI 13.2-30.8; P = 0.002) and 9/81 (11.1%; 95% CI 5.7-19.5; P = 0.001); and control = 36/450 (8.0%; 95% CI 5.8-10.8; P<0.001) and 18/450 (4%; 95% CI 2.5-6.2; P<0.001). Adjusted mortality and adjusted combined outcomes in CKD group and HD groups were significantly higher than the control group [hazard ratio (HR) (95% CI) CKD: 2.88 (1.52- 5.44); P = 0.001; 2.44 (1.35-4.40); P = 0.003; HD: 2.32 (1.21- 4.46); P = 0.011; 2.25 (1.23-4.12); P = 0.008), respectively], but these were not significantly different in the RT from in the control group [HR (95% CI) 1.89 (0.76-4.72); P = 0.169; 1.87 (0.81-4.28); P = 0.138, respectively]. Conclusions. Hospitalized COVID-19 patients with CKDs, including Stages 3-5 CKD, HD and RT, have significantly higher mortality than patients without kidney disease. Stages 3-5 CKD patients have an in-hospital mortality rate as much as HD patients, which may be in part because of similar age and comorbidity burden. We were unable to assess if RT patients were or were not at increased risk for in-hospital mortality because of the relatively small sample size of the RT patients in this study