Objectives Coronavirus 2019 disease (COVID‐19) lead to one of the pandemics of the last century. We aimed to predict poor prognosis among severe patients to lead early intervention. Methods The data of 534 hospitalized patients were assessed retrospectively. Risk factors and laboratory tests that might enable the prediction of prognosis defined as being transferred to the intensive care unit and/or exitus have been investigated. Results At the admission, 398 of 534 patients (74.5%) were mild‐moderate ill. It was determined that the male gender, advanced age, and comorbidity were risk factors for severity. To estimate the severity of the disease, receiver operating characteristic analysis revealed that the areas under the curve which were determined based on the optimal cut off values that were calculated for the variables of values of neutrophil to lymphocyte ratio (NLR > 3.69), C‐reactive protein (CRP > 46 mg/L), troponin I ( > 5.3 ng/L), lactate dehydrogenase (LDH > 325 U/L), ferritin ( > 303 ug/L), d‐dimer ( > 574 μg/L), neutrophil NE ( > 4.99 × 109/L), lymphocyte (LE < 1.04 × 109/L), SO2 ( < %92) were 0.762, 0.757,0.742, 0.705, 0.698, 0.694,0.688, 0.678, and 0.66, respectively. To predict mortality, AUC of values for optimal cutoff troponin I ( > 7.4 ng/L), age ( > 62), SO2 ( < %89), urea ( > 40 mg/dL), procalcitonin ( > 0.21 ug/L), CKMB ( > 2.6 ng/L) were 0.715, 0.685, 0.644, 0.632, 0.627, and 0.617, respectively. Conclusions The clinical progress could be severe if the baseline values of NLR, CRP, troponin I, LDH, are above, and LE is below the specified cut‐off point. We found that the troponin I, elder age, and SO2 values could predict mortality.

Toscana virus (TOSV), West Nile virus (WNV) and tickborne encephalitis virus (TBEV) are among major viral pathogens causing febrile disease and meningitis/encephalitis. The impact of these viruses was investigated at a referral centre in Ankara Province, Central Anatolia in 2012, where previous reports suggested virus circulation but with scarce information on clinical cases and vector activity. Serum and/or cerebrospinal fluid samples from 94 individuals were evaluated, in addition to field-collected arthropod specimens that included 767 sandflies and 239 mosquitoes. Viral nucleic acids in clinical samples and arthropods were sought via specific and generic nested/real-time PCRs, and antibody responses in clinical samples were investigated via commercial indirect immunofluorescence tests (IIFTs) and virus neutralization. A WNV antigen assay was also employed for mosquitoes. WNV neuroinvasive disease has been identified in a 63-year-old male via RNA detection, and the WNV strain was characterized as lineage 1. TOSV infections were diagnosed in six individuals (6.3%) via RNA or IgM detection. Partial sequences in a 23-year-old female, presented with fever and transient pancytopenia, were characterized as TOSV genotype A. Febrile disease with arthralgia and/or peripheral cranial nerve involvement was noted in cases with TOSV infections. Previous WNV and TOSV exposures have been observed in 5.3% and 2.1% of the subjects, respectively. No confirmed TBEV exposure could be identified. Morphological identification of the field-collected mosquitoes revealed Culex pipiens sensu lato (74.4%), Anopheles maculipennis (20.9%), An. claviger (2.1%) and others. Sandfly species were determined as Phlebotomus papatasi (36.2%), P. halepensis (27.3%), P. major s. l. (19.3%), P. sergenti (8.9%), P. perfiliewi (4.4%), P. simici (2.6%) and others. Viral infections in arthropods could not be demonstrated. TOSV genotype A and WNV lineage 1 activity have been demonstrated as well as serologically proven exposure in patients. Presence of sandfly and mosquito species capable of virus transmission has also been revealed.

Objective: The tendency to reduce thyroid stimulating hormone (TSH) referral cut-off values in congenital hypothyroidism (CH) neonatal screening programs has resulted in an increase in the incidence of CH, but also the referral of infants with mild transient elevation of TSH. Therefore, there is a need to develop markers for differentiation of transient elevated TSH and permanent CH as early as safely possible to avoid unnecessary treatment. The aim was to evaluate sixth-month L-thyroxine (LT4) dose as a predictive marker for differentiation of transient elevated TSH and permanent CH. Methods: Data of patients who had been followed after referral from the neonatal screening programme between the year 2010 and 2019 in a tertiary pediatric endocrine centre were examined retrospectively. Results: There were 226 cases referred, of whom 186 (82.3%) had eutopic thyroid gland, and 40 (17.7%) had dysgenetic gland. In patients with a dysgentic gland there was a non-significant tendency to have lower diagnostic free thyroxine concentration but significantly higher TSH compared with those with eutopic gland (p=0.44 and p=0.023, respectively). Patients with thyroid dysgenesis required higher initial and six month LT4 doses compared with those with eutopic glands (p=0.001). Receiver operator curve analysis showed the optimum cut-off value for LT4 at six months for transient vs. permanent CH was 2 μg/kg/day (sensitivity 77% and specificity 55%), regardless of etiology. Similarly, in patients with eutopic glands the optimum cut-off value for LT4 dose at six months for permanent vs. transient patients was 2 μg/kg/day (sensitivity 72% and specificity 54%). Conclusion: Results suggest that LT4 requirement at six months of therapy may be a good marker for predicting transient TSH elevation in patients with eutopic thyroid gland, thus facilitating the decision to halt LT4 therapy.

West Nile virus (WNV) is a mosquito-borne Flavivirus (family Flaviviridae), maintained in an enzootic cycle between birds as amplifying hosts and mosquito vectors. While WNV exposure in humans frequently remain subclinical, a febrile illness called West Nile fever occurs in about 20% and neuroinvasive disease in less than 1% of the affected individuals. For the last two decades, WNV has caused outbreaks of severe neuroinvasive disease in humans and horses in Europe, the Mediterranean Basin and emerged in the American continent. Although, previous serosurveillance reports have revealed human WNV exposure in various regions in Turkey; well-characterized clinical cases have only been reported after 2009-2010. In this report, a case of WNV encephalitis caused by a Lineage 1 virus strain and identified in Ankara province, Central Anatolia, Turkey, was presented. An 87 year-old woman with a history of hypertension and a recent febrile episode was admitted to Hacettepe University Hospital in late May 2012, with altered consciousness, myoclonic jerks in facial muscles and left extremity. Hyponatremia and increased alanine and aspartate aminotransferase levels were noted in blood analyses. Initial electroencephalogram (EEG) demonstrated diffuse slow waves. Areas of restricted diffusion in right dorsal thalamus was observed in cranial magnetic resonance imaging (MRI). Despite supportive therapy, the patient's neurological condition worsened. Follow-up EEG displayed paroxysmal lateralizing epileptiform discharges (PLEDs) in the right hemisphere and T2-hyperintense lesions in the right temporoparietal cortex, insula and thalamus with components of cytotoxic and vasogenic edema were observed in MRI. A cerebrospinal fluid (CSF)-serum pair was evaluated to identify potential causes of encephalitis. CSF biochemical and microscopic findings were within normal limits except for decreased glucose levels. Bacterial, mycobacterial and fungal cultures, antigen assays and polymerase chain reaction (PCR) employed for Herpes simplex virus types 1 and 2 were negative. Commercial and in house assays for WNV, tick-borne encephalitis virus, Toscana virus (TOSV) antibodies revealed TOSV IgG in serum. Previously described nested PCRs targeting WNV envelope glycoprotein and phlebovirus consensus sequences demonstrated WNV positive results in serum and CSF, which were further characterized via cycle sequencing of amplicons as WNV Lineage 1 Clade 1a. Four serum samples obtained within 23 days after the diagnosis were negative for viral RNA and specific antibodies via commercial assays and WNV plaque reduction neutralization assay. During follow-up with supportive therapy and anti-epileptics, the patient's general and neurological condition improved mildly and control EEG and MRI demonstrated regression of previous lesions. However, the patient passed away on the 10th week of hospital admission due to nosocomial infections. These findings confirmed the inital data which indicated the circulation of WNV Lineage 1 strains in Central Anatolia, Turkey...

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