Immunogenicity and safety of the CoronaVac vaccine in patients undergoing treatment for breast and lung cancer.

OBJECTIVE: To compare seroconversion for SARS-CoV-2 receptor-binding domain (RBD) specific IgG positivity against two doses of the CoronaVac vaccine in breast and lung cancer patients receiving systemic therapy, to determine the factors affecting seropositivity, and to observe long-term results up to a secondary booster vaccine. RESULTS: The analysis included 201 cancer patients (99 breasts, 102 lungs; median age: 59 years (range: 28-92), 42.3 % men) and 97 controls (median age: 62 years (range: 24-87), 38.1 % men). The seropositivity rate for RBD IgG after 2 doses of vaccine in the cancer group was 81.6 % (n=164) and 93.8 % (n=91) in the control group (p=0.005). The median IgG titer of cancer patients was significantly lower than in the control group (338 (IQR, 95-933) AU/mL vs 676 (IQR, 389-1270) AU/mL; p<0.001). Multivariate analysis of all the patients determined that having cancer (OR: 0.303, 95%CI: 0.123-0.750, p=0.010) and being over 60 years of age (OR: 0.447, 95%CI: 0.218-0.917, p=0.028) was associated with a reduced vaccine response. A subgroup analysis of cancer patients revealed that seroconversion was lower in men than in women (75.3 % vs 86.2 %, p=0.049) and lower in ≥60 patients than in <60 patients (75.9 % vs 89.4 %, p=0.014). DISCUSSION AND CONCLUSION: Cancer patients receiving an active systemic therapy with two doses of the CoronaVac vaccine had a lower antibody response than the non-cancer population, and deaths due to COVID-19 may occur in these patients despite the vaccine. Therefore, extensive protective measures should be taken to protect against COVID-19 in cancer patients aged 60 years and older, who have received two doses of the CoronaVac vaccine (Tab. 4, Fig. 4, Ref. 27).

Serum Calprotectin Level as an Inflammatory Marker in Newly Diagnosed Hypertensive Patients.

BACKGROUND: Hypertension is one of the leading causes of cardiovascular mortality. Although the pathogenetic process involved is not yet fully understood, the disease involves endothelial damage and inflammation. Calprotectin is an inflammatory marker that rises in parallel with disease activity in conditions such as systemic inflammatory diseases, infection, and atherosclerosis. The purpose of this study was to evaluate inflammation through serum calprotectin levels in newly diagnosed primary hypertension patients. METHODS: Forty-nine newly diagnosed hypertensive patients and 38 healthy adults were included in the study. Patients' office blood pressure values, biochemical findings, and demographic characteristics were recorded. Serum calprotectin levels were measured using ELISA. Parameters affecting serum calprotectin levels and determinants of hypertension were evaluated. RESULTS: Serum calprotectin levels were 242.8 (72.4-524) ng/mL in the control group and 112.6 (67.4-389.8) ng/mL in the hypertensive patient group, the difference being statistically significant (p=0.001). There was no correlation between serum calprotectin levels and other parameters (blood pressure values, age, gender, serum creatinine, uric acid, and calcium levels) in the hypertensive group. A lower serum calprotectin level was found to be independently related to hypertension (ß = -0.009, p=0.005). Serum calprotectin at a cutoff level of 128.6 ng/mL differentiated hypertensives from healthy controls with a sensitivity of 69.4% and specificity of 68.4% (AUC = 0.767). CONCLUSIONS: The results of this study were the opposite of our hypothesis that a higher calprotectin level may reflect subclinical endothelial damage in newly diagnosed hypertensive patients. Further comparative studies involving patients at different stages of hypertension may contribute to clarifying the relationship between calprotectin and hypertension. We conclude that molecular studies seem essential for understanding the place of calprotectin in hypertension-associated inflammation, a complex process.

Investigation of the peripheral inflammation (neutrophil-lymphocyte ratio) in two neurodegenerative diseases of the central nervous system.

INTRODUCTION: Alzheimer's disease (AD), and idiopathic Parkinson's disease (IPD) are the neurodegenerative diseases of the central nervous system (CNS). Cognitive impairment is on the forefront in AD. However, IPD is a movement disorder. Inflammation was suggested to have an effect in the pathophysiology of these two diseases. Neutrophil-lymphocyte ratio (NLR) was shown to be a possible marker showing the peripheral inflammation. We aimed to investigate the NLR of patiens with the diagnosis of AD, and IPD, and individuals with no neurodegenerative disease. MATERIALS AND METHODS: A total of 100 patients with the diagnosis of IPD, and 94 with diagnosis of AD, and 61 healthy controls were included into the study. All the demographic, clinical, and laboratory data were retrospectively obtained from the hospital automated database system. RESULTS: The NLR in the IPD group was found statistically significantly higher compared with the control group and the AD group (p < 0.001, p = 0.04, respectively). The age-adjusted values were statistically analyzed because of age difference. No statistically significant difference was detected between AD and control groups in terms of NLR (p = 0.6). The age-adjusted NLR value in the Parkinson's group was found significantly higher compared to the control group (p = 0.02) and Alzheimer's group (p = 0.03). DISCUSSION: Chronic inflammation has an important role in the emergence and progression of the chronic neurodegenerative diseases of the CNS. Our results show that the inflammation in the peripheral blood in IPD was more significant compared with the inflammation in AD.

MicroRNA 21 and microRNA 155 levels in resistant hypertension, and their relationships with aldosterone.

AIM: MicroRNAs (miRNAs) are non-coding RNA molecules that serve as regulators following gene expression transcription. While studies have investigated the role of miRNAs in the pathogenesis of essential hypertension (HT), very few have considered their place in the pathogenesis of resistant hypertension (RH). The purpose of this study was to investigate levels of miRNA 21 and miRNA 155 in RH and their relationships with aldosterone. METHOD: Thirty-two normotensive patients, 30 newly diagnosed HT patients, and 20 RH patients were included in the study. Patients' demographic data were recorded, and office blood pressure measurement and 24-h ambulatory blood pressure monitoring (24-h ABPM) were performed. Blood specimens were collected for miRNA 21, miRNA 155 and aldosterone measurement. MiRNA 21 and miRNA 155 levels in the control and patient groups and their relations with other demographic and biochemical parameters were then subjected to analysis. RESULTS: No difference was determined in miRNA 155 levels between the groups, but miRNA 21 and aldosterone levels were significantly higher in the RH group (p < 0.001 and <0.05, respectively). At correlation analysis, miRNA 21 exhibited positive correlation with aldosterone, age, office SBP, 24-h ABPM all-day SBP. A 9.6 copy/uL level for miRNA 21 predicted presence or absence of RH with 95% sensitivity and 71% specificity (AUC:0.823, 95% CI (0.72-0.92). CONCLUSION: The study results revealed significantly higher miRNA 21 and aldosterone in RH patients than in healthy individuals and newly diagnosed hypertensives.

Relationship between Microfibrillar-Associated Protein 4 Levels and Subclinical Myocardial Damage in Chronic Kidney Disease.

INTRODUCTION: Chronic kidney disease (CKD) is a widespread health problem, in which mortality is most frequently due to cardiovascular diseases. Microfibrillar-associated protein 4 (MFAP4) is an extracellular matrix protein. MFAP4 is involved in several biological processes, particularly the maintenance of vascular integrity and extracellular matrix remodeling. Our review of the literature revealed no data concerning MFAP4 levels in CKD and its relationship with myocardial functions. OBJECTIVE: The purpose of this study was therefore to investigate MFAP4 levels in CKD, parameters affecting these, and the relationship with myocardial functions. MATERIALS AND METHODS: Seventy-nine CKD patients and 30 healthy controls were included in the study. Routine biochemical tests and echocardiography were performed once demographic data had been recorded. Blood specimens were collected for MFAP4 analysis, and the results were subjected to statistical analysis. RESULTS: MFAP4 levels were significantly higher in the patient group than in the control group (p< 0.001). Doppler parameters revealed more frequent LV diastolic impairment in the patient group. Tissue Doppler systolic velocity and global longitudinal strain were significantly impaired, revealing the subclinical LV systolic dysfunction in CKD patients. MFAP4 elevation in the patient group was positively correlated with aortic root (AR), global circumferential strain (GCS), and GCS rate. CONCLUSION: Our results showed MFAP4 elevation in CKD for the first time in the literature, and that this elevation may be related to GCS and AR dilation. We think that, once supported by further studies, MFAP4 may constitute a marker in the evaluation of myocardial functions in CKD.

Soluble endothelial protein C is associated with blood pressure variability and salt consumption but not mean blood pressure in patients with newly diagnosed primary hypertension.

BACKGROUND: Hypertension is a widespread disease involving frequent thrombotic complications. Blood pressure variability (BPV) has recently been shown to be associated with end-organ damage and cardiovascular events. However, the pathogenesis of the relation between BPV and cardiovascular events has not yet been explained. Soluble endothelial protein C (sEPCR) exhibits a procoagulant effect by reducing the anticoagulant and anti-inflammatory effects of protein C and activated protein C. The purpose of this study was to evaluate sEPCR levels in hypertensive individuals and the parameters affecting that level, particularly BPV. METHODS: Fifty-one newly diagnosed hypertensive subjects and 31 healthy individuals were included in the study. Twenty-four-hour ambulatory blood pressure monitoring (ABPM) was performed after office control, and simultaneous 24-h urine was collected. BPV was calculated with average real variability (ARV) from ABPM data. Blood specimens were collected under appropriate conditions for sEPCR levels and biochemical tests. sEPCR levels were compared between the patient and healthy groups, after which parameters affecting sEPCR elevation in the hypertensive group were evaluated. RESULTS: sEPCR levels were significantly high in the hypertensive group (p < 0.05). At multivariate regression analysis in the hypertensive group, sEPCR was determined to be independently associated with 24-h systolic ARV (ß = 0.572, p < 0.05) and 24-h urine Na (ß = 0.428, p < 0.05). CONCLUSION: In our study, sEPCR was high in hypertensive individuals, and this elevation was related to ARV and urine Na excretion independently of mean blood pressure.

A rare cause of fever in an adult: a case of familial Mediterranean fever.

BACKGROUND: Familial Mediterranean fever (FMF) is a hereditary autoinflammatory disease characterized by recurrent fever attacks and serositis. Nonspecific manifestations of the FMF can mimic many common acquired disorders such as infections and acute abdomen. This can delay recognition for many years and lead to comprehensive assessments and even unnecessary surgeries. Untreated FMF may lead to serious complications such as end-stage renal disease and malabsorption due to amyloid deposits in the kidneys and the digestive system. Colchicine has been used successfully to treat FMF since the 1970s. CASE PRESENTATION: A 30-year-old male was admitted to our hospital with the complaints of fever, nausea, vomiting, and generalized myalgia and weakness for 15 days. The day after hospitalization, the patient had abdominal pain. Approximately a month before, the patient was treated for a diagnosis of urinary tract infection, with similar complaints. MEFV gene mutation analysis revealed homozygosity for the R202Q mutation. FMF was considered in the patient due to the presence of recurrent febrile serositis attacks and R202Q homozygous mutation in the FMF gene analyses. Colchicine was started 3×0.5 mg/day by consulting rheumatology on day 8 of admission. After the colchicine treatment, the patient's complaints markedly improved and the inflammatory markers returned to normal levels. At his follow-up visit at 6 months, the patient remained asymptomatic. CONCLUSION: We present a case of adult-onset FMF accompanied by peritonitis as a disease among the rare causes of fever in an adult who was treated with colchicine. Based on this case, we suggest that FMF should be kept in mind in the differential diagnosis of patients with periodic fever syndromes.

Relationship Among Pulmonary Hypertension, Autoimmunity, Thyroid Hormones and Dyspnea in Patients With Hyperthyroidism.

OBJECTIVE: Previous studies have reported conflicting results regarding the mechanisms underlying the pathophysiology of pulmonary hypertension (PHT) in patients with hyperthyroidism. Therefore, in this study, we investigated the association between PHT and thyroid-stimulating hormone (TSH) receptor antibody, thyroid peroxidase antibody, thyroglobulin antibody, TSH, fT3, fT4 and dyspnea during daily activities in a large population of patients with hyperthyroidism. METHODS: A total of 129 consecutive patients with hyperthyroidism, 37 with hypothyroidism and 38 euthyroid controls were enrolled in this study. The modified medical research council scale was used for the assessment of dyspnea in daily activities. All the patients and euthyroid controls underwent transthoracic echocardiography for the assessment of PHT. RESULTS: Mild PHT was present in 35%, 36%, 13.5% and 5% of the patients with Graves׳ disease, toxic multinodular goiter, hypothyroidism and euthyroid controls, respectively. Pulmonary vascular resistance (PVR) was higher in hyperthyroid patients with PHT than in those without PHT. Moreover, a significant positive correlation was found between modified medical research council scale and pulmonary artery systolic pressure as well as PVR in patients with hyperthyroidism. No association was found between PHT and serum TSH receptor antibody, thyroid peroxidase antibody, thyroglobulin antibody, TSH, fT3 and fT4 levels. CONCLUSIONS: Mild PHT is present in a significant proportion of patients with hyperthyroidism, regardless of etiology. PVR appears to be the main cause of PHT in patients with hyperthyroidism, and neither autoimmunity nor thyroid hormones are associated with PHT in these patients. Mild dyspnea during daily activities in patients with hyperthyroidism may be related to PHT; however, severe dyspnea requires further evaluation.

The association of vitamin D with inflammatory cytokines in diabetic peripheral neuropathy.

[Purpose] The effects of vitamin D on the circulating levels of IL-17 and IL-13 were investigated in patients with diabetic peripheral neuropathy, patients with diabetes mellitus type 2 without neuropathy, and healthy controls. [Subjects and Methods] A single-blind controlled clinical study was performed, including70 type 2 diabetic patients with or without diabetic peripheral neuropathy and 33 healthy volunteer controls. The 25(OH)D levels were evaluated using ultra-performance liquid chromatography, and IL-17 and IL-13 levels were assessed using enzyme-linked immunosorbent assays. [Results] The 25(OH) vitamin D concentration was lower in diabetic peripheral neuropathy patients than in diabetes mellitus patients without neuropathy and healthy controls. Similarly, 25(OH)D levels were lower in diabetes mellitus patients than healthy controls. IL-17 and IL-13 levels were higher in diabetes mellitus patients than in controls. Additionally, IL-13 levels were higher in diabetic peripheral neuropathy patients than in diabetes mellitus patients without neuropathy. These differences were statistically significant. There was a significant positive correlation between 25(OH)D and IL-13,and a negative correlation between 25(OH)D andIL-17 in the diabetic and diabetic neuropathy groups. [Conclusion] Vitamin D is a potential modifiable risk factor for diabetic peripheral neuropathy and may regulate inflammatory mediators, e.g., IL-17 and IL-13.