Investigation of effects of different treatment modalities on structural and functional vessel wall properties in patients with ankylosing spondylitis

Aim

Ankylosing spondylitis (AS) is a chronic systemic inflammatory disease that is associated with increased cardiovascular burden. The aim of this study was to investigate vascular structural and functional changes in patients with AS, with special emphasis on the effects of different treatment modalities, through evaluation of level of vascular stiffness (pulse wave velocity [PVW]) and carotid intima media thickness (IMT-C).

Methods

A total of 67 AS patients, and age, sex, body mass index (BMI) smoking status, lipid profiles and blood pressure-matched healthy control subjects (n = 34) were studied. Of these, 34 patients were on anti-TNF alpha and 33 on non steroid anti inflammatory drugs (NSAIDs). The IMT-C and PWV values of the right common carotid artery were measured by high-resolution ultrasound.

Results

The AS patients (n = 67) had significantly higher PWV values than the controls [9.0 ± 1.49 m/sec vs. 8.27 ± 0.90 m/sec, P = 0.004; 95% confidence interval (CI), −1.22 to −0.24]. Multiple stepwise linear regression analysis revealed that PWV could only be explained by systolic blood pressure (P < 0.05) and IMT (P < 0.05) in AS. Even though IMT-C in anti-TNF alpha treated group was higher compared to the NSAID treated group, it was not statistically significant (P = 0.5).

Conclusion

PWV was found to be higher in AS patients than in the control group, and there was no significant difference between the average PWV values of AS patients treated with anti -TNF alpha or NSAIDs.     

Long-term effects of cancer therapy on dental development: a case report

As the prognosis of malignant conditions in children improve by cancer therapy, long-term side effects due to antineoplastic treatment may be encountered. This case report demonstrates the long-term alterations on dental development in patient who had been treated for malignant condition. Alterations were observed during radiographic control 8 years after the therapy and included short, blunted, tapered and V-shaped root malformations as well as delayed and ectopic eruptions.     

Sociodemographic Characteristics,Risk Factors,and Prevalence of Comorbidity among Children and Adolescents with Intellectual Disability: A Cross-sectional Study

ABSTRACT

Introduction: Intellectual disability (ID) is characterized by limitations in cognitive and adaptive functioning. The aim of this study is to examine sociodemographic characteristics, perinatal and childhood risk factors, and prevalence of psychiatric and biomedical comorbidities in children with ID.

Methods: 260 patients with ID were included in the study (mean age: 8.42 ± 3.59, 61% male, 75% mild ID). The Ankara Developmental Screening Inventory, the Wechsler Intelligence Scale for Children–Revised, and the Porteus Maze Test were used to assess the intelligence of the participants. An additional questionnaire was used to investigate their sociodemographic characteristics and birth, developmental, and medical histories.

Results: Adverse perinatal/neonatal events (p < .001), biomedical comorbidities (p < .001) and seizure/convulsion history (p < .001) were strongly associated with the moderate-severe ID. The children with mild ID had more emotional-social deprivation (p = .022). Low socioeconomic situation, parental education, and teenage parenthood were risk factors for stimulus deficiency. While internalizing disorders were more common in those with mild ID and among girls, externalizing disorders were more common in those with moderate-severe ID and among boys.

Conclusion: Interventions to perinatal/neonatal events may reduce the rate of moderate-severe ID. Evaluation of psychiatric and medical comorbidities and elimination of emotional-social deprivation should be fundamental components of the services offered to children with ID.     

Stroke Mechanism in COVID-19 Infection: A Prospective Case-Control Study

BackgroundThe characteristics and pathophysiological mechanisms involved in acute ischemic stroke in patients with COVID-19 infection have not been fully clarified. We prospectively studied the phenotypic and etiological features of acute stroke occurring in COVID-19 infection.Patients & methodsWithin nine months starting from April-2020, the presence of COVID-19 infection was determined by thoracic CT and SARS-CoV-2 PCR in all acute stroke cases managed in a single tertiary center. Consecutive and prospective data on vascular risk factors/comorbidities, in-hospital quality metrics, discharge outcomes, etiological subclassification and blood markers of thrombosis / inflammation were compared in 44 COVID-19 positive cases (37 acute ischemic stroke, 5 TIA, 2 intracerebral hematoma) and 509 COVID-19 negative patients (355 ischemic, 105 TIA, 44 hematoma and 5 stroke mimic).ResultsCOVID-19 positive patients had more severe strokes, delayed hospital admission, longer hospital stay, higher mortality rates, but had similar vascular risk factors/comorbidities frequency, thrombolysis/thrombectomy utilization rates, metrics, and stroke etiological subtype. They had significantly higher CRP, fibrinogen, ferritin, leukocyte count and lower lymphocyte count. No difference was detected in aPTT, INR, D-dimer, platelet, hemoglobin, homocysteine levels and ANA, anti-dsDNA antibody and ENA panel positivity rates. Anti-phospholipid antibodies have been studied in 70% of COVID-19 positive and all cryptogenic patients, but were never found positive. Tests for coagulation factor levels and hereditary thrombophilia did not show major thrombophilia in any of the stroke patients with COVID-19.ConclusionWe documented that there is no significant difference in etiological spectrum in acute stroke patients with COVID-19 infection. In addition, cryptogenic stroke and antiphospholipid antibody positivity rates did not increase.     

Peripheral Treg count and it’s determinants in unsensitized and sensitized chronic kidney disease patients

Purpose

Sensitization to HLA antigens resulting in anti-HLA antibodies (panel reactive antibodies; PRA) is a major problem in chronic kidney disease (CKD) patients awaiting transplantation. Induction of anti-HLA antibodies normally occurs through blood transfusion, pregnancy and prior transplantation. However, some patients develop these antibodies for unknown immunological reasons. It is hypothesized that deviations in immune regulation may account for PRA positivity in these patients. We, therefore, investigated whether a quantitative deficiency in peripheral natural regulatory T cells (CD4⁺CD25^highFoxp3⁺; nTreg) plays a role in this phenomenon.

Methods

Peripheral blood mononuclear cells from 14 patients with positive (Class I and Class II; 10–100 %) and 25 patients with negative PRA, who had not previously been sensitized by blood transfusion, pregnancy and prior transplantation and who had not received any immunomodulatory treatment within the last year, were analyzed for absolute lymphocyte and nTreg numbers through flow cytometry. Samples from 10 healthy people were also used as control.

Results

Mean absolute nTreg numbers were determined to be severely reduced in CKD patients (12 ± 9; n = 39) compared with healthy individuals (53 ± 17; n = 10) (p = 0.008). However, absolute nTreg numbers were similar between PRA? (12 ± 11) and PRA+ (11 ± 8) groups. Interestingly, there was a moderate correlation between the nTreg numbers and HLADR2 genotype (n = 9, r = 0.508, p < 0.05).

Conclusion

This is the first study to demonstrate that the quantitative peripheral nTreg deficiency in CKD patients does not show a causal relationship with the presence of anti-HLA antibodies.     

Mutations in ANKS6 Cause a Nephronophthisis-Like Phenotype with ESRD

Nephronophthisis (NPHP) is one of the most common genetic causes of CKD; however, the underlying genetic abnormalities have been established in <50% of patients. We performed genome-wide analysis followed by targeted resequencing in a Turkish consanguineous multiplex family and identified a canonic splice site mutation in ANKS6 associated with an NPHP-like phenotype. Furthermore, we identified four additional ANKS6 variants in a cohort of 56 unrelated patients diagnosed with CKD due to nephronophthisis, chronic GN, interstitial nephritis, or unknown etiology. Immunohistochemistry in human embryonic kidney tissue demonstrated that the expression patterns of ANKS6 change substantially during development. Furthermore, we detected increased levels of both total and active β-catenin in precystic tubuli in Han:SPRD Cy/+ rats. Overall, these data indicate the importance of ANKS6 in human kidney development and suggest a mechanism by which mutations in ANKS6 may contribute to an NPHP-like phenotype in humans.     

Management of periprocedural anticoagulant therapy: a novel individualized approach—a transeusophageal echocardiographic study

Journal of Thrombosis and Thrombolysis - Patients with non-valvular atrial fibrillation who are under chronic oral anticoagulant therapy (OAC) treatment frequently require interruption of OAC...     

Evaluation of periodontal status and cytokine/chemokine profile of GCF in patients with severe congenital neutropenia

Severe congenital neutropenia (SCN) is a primary immunodeficiency characterized by defect in neutrophil count. Increased risk of infections in addition to periodontal problems, such as ulcerations of oral mucosa, gingival inflammation, and rapid loss of attachment are common in the course of the disease. The aim of the present study is to define the causal relationship between the severity of periodontal inflammation and severe congenital neutropenia through identification of cytokine profile in gingival crevicular fluid (GCF). A case–control study was performed in patients diagnosed with SCN and healthy controls. Demographic data, the molecular defect, laboratory work-up were gathered from the hospital registry. Periodontal indices were recorded and GCF samples were analyzed using multiplex analysis for the simultaneous measurements of the particular cytokines and chemokines. The present study included 14 patients and 22 control subjects. Both groups were comparable in terms of age and sex. Severity of gingival inflammation measured by the criteria of Löe was higher in the SCN cases (p < 0.05). Moreover, GCF levels of IFN-α, TNF-α, IL-10, IL-13, IL-15, IL-17, IL-2, IL-7, IL-33, IP-10, MIG, MIP-1β were significantly higher in the controls. Decreased cytokine secretion seems to correlate with the decrease in neutrophil counts. The severity of gingival inflammation in SCN patients may be due to the bacterial overgrowth and the change in the content of the oral flora due to the decreased neutrophil counts. Therefore, regular periodontal examinations, the motivation of oral hygiene as well as the compliance with therapy in SCN patients contribute to the periodontal health.