COVID-19 in familial Mediterranean fever: Clinical course and complications related to primary disease.

OBJECTIVES: To evaluate the impact of familial Mediterranean fever (FMF) features on the clinical course and outcomes of coronavirus disease 2019 (COVID-19) and clinical course of FMF after COVID-19. METHODS: Consecutive FMF patients with COVID-19 were enrolled from three referral hospitals. Clinical features of FMF and detailed COVID-19 information were obtained from patient interviews and medical records. RESULTS: Seventy-three FMF patients were included in the study. 94.5% of patients had clinical symptoms of COVID-19. We found 24.7% hospitalization, 12.3% respiratory support, 4.1% intensive care unit admission, 6.8% complication, and 1.4% mortality rate in patients. The risk factors of hospitalization for respiratory support were male gender [OR: 7.167 (95% CI: 1.368-37.535)], greater age [OR: 1.067 (95% CI: 1.016-1.121)], and non-adherence to colchicine treatment before the infection [OR: 7.5 (95% CI: 1.348-41.722)]. One-third of patients had reported attacks after COVID-19. The patterns of triggered attacks were fever, peritonitis, pleuritis, transient arthritis, chronic knee mono-arthritis, and protracted febrile myalgia. CONCLUSIONS: FMF characteristics were not associated with worse outcomes of COVID-19. Colchicine non-adherence was the risk factor of hospitalization for oxygen support. The rate of FMF attacks after COVID-19 is prominently increased, with some of them being protracted and destructive.

Coexistence of 3q29 microdeletion syndrome and Takayasu arteritis: A case report.

Takayasu arteritis (TAK) is a rare type of large and medial vessel systemic vasculitis. A variety of factors are thought to play a role in the occurrence and development of TAK such as human leukocyte antigen-B52, autoimmunity, inflammation and environmental factors. 3q29 microdeletion syndrome is also a very rare inherited disease, which includes intellectual disability, growth retardation and neuropsychiatric disorders. Here, we present a case with concomitant TAK and 3q29 microdeletion syndrome. A 22-year-old woman presented to the emergency department with sudden bilateral vision loss and severe headache. During physical examination, the patient was noted to have a difference in blood pressure between extremities. Computed tomography angiography revealed vascular wall inflammation in the abdominal aorta. Based on clinical and radiographical findings, a diagnosis of TAK was made. Concurrently, the patient was found to have short stature and intellectual disability. A possible genetic etiology was sought out. Chromosome analysis showed a 1.5 Mb heterozygous deletion on chromosome 3 and a diagnosis of 3q29 microdeletion was made. Additional imaging also revealed a split cord in medulla spinalis along with hemivertebrae and fusion anomalies, neither of which were reported in TAK or 3q29 microdeletion cases in the literature.

Global and region-specific post-transcriptional and post-translational modifications of bisphenol A in human prostate cancer cells.

Bisphenol A (BPA), as synthetic monomer used in the production of polycarbonate plastic and epoxy resins, has endocrine disruptor properties and high risk on human health. Epigenetic alterations could act an important role in BPA-induced toxicity, but its mechanism has not been fully understood. We investigated the effects of BPA on gene expression of chromatin modifying enzymes, promoter methylation of tumor suppressor genes and histone modifications in human prostate carcinoma cells (PC-3). IC50 value of BPA was determined as 217 and 190 µM in PC-3 cells by MTT and NRU tests, respectively. We revealed an increase in global levels of 5-methylcytocine and 5-hydroxymethylcytocine at 10 µM of BPA for 96 h. We observed a significant increase on promoter DNA methylation and decrease on gene expression of p16 gene while no change was observed for Cyclin D2 and Rassf1. Significant changes were observed in global histone modifications (H3K9ac, H3K9me3, H3K27me3, and H4K20me3) in PC-3 cells. According to these results, we investigated wide-range epigenetic modifications using PCR arrays. After 96 h BPA exposure, chromatin modifying enzymes including KDM5B and NSD1 were significantly downregulated. Also, promoter methylation of tumor suppressor genes including BCR, GSTP1, LOX, MGMT, NEUROG1, PDLIM4, PTGS2, PYCARD, TIMP3, TSC2 and ZMYDN10 altered significantly. ChIP results showed that H3K9ac, H3K9me3 and H3K27me3 modifications on p16 gene showed significant increases after 1 and 10 µM of BPA exposure. In conclusion, epigenetic signatures such as DNA methylation and histone modifications could be proposed as molecular biomarkers of BPA-induced prostate cancer progression.