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Abstract Background: The course of chronic spontaneous urticaria (CSU) can be influenced by infections, depression, and stress. Objectives: Our aim was to investigate the impact of the COVID-19 pandemic on the course of refractory CSU together with patient adherence to omalizumab and treatment adjustments. Methods: Urticaria Activity Score (UAS7) was used to assess disease activity. Fear of COVID-19 Scale (FC-19s), and Depression Anxiety Stress Scale (DASS-21s) were performed to assess mental health status. All scales were performed during the Quarantine Period (QP) and Return to the Normal Period (RTNP). UAS7 Before Pandemic (BP) was recorded from the patients medical records. Results: The authors evaluated 104 omalizumab-receiving CSU patients. UAS7 scores during QP were significantly higher than those in RTNP and BP (p < 0.01). DASS-21 and FC-19 scores were significantly higher during QP compared to RTNP (p < 0.01). Nineteen (18.2%) patients ceased omalizumab, 9 patients prolonged the intervals between subsequent doses during the pandemic. UAS7 scores in QP were significantly higher in patients who ceased omalizumab than in those who continued (p < 0.001). Among patients who continued omalizumab, 22.4% had an increase in urticaria activity and higher FC-19 scores in comparison with those with stable disease activity (p = 0.008). Study limitations: The small sample size of patients with prolonged intervals of omalizumab and the lack of mental health evaluation with the same tools prior to the study. Conclusions: Fear induced by COVID-19 can determine an increase in disease activity. Therefore, patients on omalizumab should continue their treatment and prolonged interval without omalizumab can be considered in patients with good urticaria control.
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SUMMARY OBJECTIVE: Acute appendicitis is one of the most common surgical causes of an acute abdomen among patients admitted to the emergency room due to abdominal pain. The clinical diagnosis of acute appendicitis is usually difficult and is made by evaluating the clinical, laboratory, and radiological findings together. The aim of this study was to investigate the diagnostic potential of signal peptide-CUB-EGF-like domain-containing protein 1 as a biomarker for acute appendicitis. METHODS: A total of 67 adult patients without any comorbidities who presented to the emergency department with abdominal pain and were clinically diagnosed with acute appendicitis were included in the case group. The patients included in the study were classified into the negative appendectomy group and the acute appendicitis group according to their histopathological final diagnosis. In addition, 48 healthy volunteers without comorbidities were included in the control group. Signal peptide-CUB-EGF-like domain-containing protein 1 levels of patients and the control group were measured. RESULTS: According to postoperative histopathological examinations of the patients, 7 (10.4%) patients were diagnosed with negative appendectomy, and 60 (89.6%) patients were diagnosed with acute appendicitis. Signal peptide-CUB-EGF-like domain-containing protein 1 levels were higher in the patients with acute appendicitis than in negative appendectomy patients (p=0.012). Signal peptide-CUB-EGF-like domain-containing protein 1 levels were also higher in the case group compared to the control group (p=0.001). CONCLUSION: The admission signal peptide-CUB-EGF-like domain-containing protein 1 level was significantly higher in adults with acute appendicitis. The SCUBE1 level is a novel but promising biomarker that aids in the diagnosis of acute appendicitis.
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JUSTIFICATIVA E OBJETIVOS: Este estudo investigou os efeitos analgésicos e nociceptivos da adição de dexmedetomidina à bupivacaína em anestesia do neuroeixo usando os testes de retirada da cauda (tail-flick [TF]) e da placa quente (hot-plate [HP]) e microscopia de luz para as alterações histopatológicas de nervos espinhais e raízes nervosas. MÉTODOS: Quarenta ratos Sprague-Dawley anestesiados, machos, foram cateterizados intratecalmente. Os valores basais dos testes TF e HP foram medidos antes e depois do cateterismo. Trinta e seis ratos cateterizados com sucesso foram distribuídos em quatro grupos. O Grupo B recebeu 10 µg de bupivacaína, o Grupo BD3 recebeu 10 µg de bupivacaína + 3 µg de dexmedetomidina, o Grupo BD10 recebeu 10 µg de bupivacaína + 10 µg de dexmedetomidina e o Grupo Controle recebeu 10 µL de líquido cefalorraquidiano artificial. Os testes TF e HP foram feitos entre cinco e 300 minutos a partir da administração das drogas. Vinte e quatro horas após a administração, os ratos foram sacrificados e retiradas as medulas espinhais e raízes nervosas para investigação patológica. RESULTADOS: Os valores basais dos testes TF e HP não foram estatisticamente diferentes entre os grupos (6,8 ± 0,15 s). As latências de TF e HP no Grupo Controle não apresentaram alteração significativa durante o estudo. Os resultados dos testes TF e HP mostraram que a adição de 3 e 10 µg de dexmedetomidina causou um aumento dose-dependente na duração e amplitude do efeito analgésico e nociceptivo de bupivacaína (TF: 37,52 ± 1,08%, 57,86 ± 1,16%, respectivamente; HP: 44,24 ± 1,15%, 68,43 ± 1,24%, respectivamente). CONCLUSÕES: Não houve alterações histopatológicas aparentes em pelo menos 24 horas após a administração intratecal da dose única de dexmedetomidina (3 µg e 10 µg). Dexmedetomidina adicionado à bupivacaína para raquianestesia melhora a analgesia e prolonga a duração do bloqueio.
BACKGROUND AND OBJECTIVES: This study investigates analgesic and nociceptive effects of adding dexmedetomidine to bupivacaine neuraxial anesthesia through Tail-flick (TF) and Hot-plate (HP) tests and the pathohistological changes on spinal nerves and nerve roots through light microscopy. METHODS: Forty anesthetized, male Sprague-Dawley rats were intrathecally catheterized. Basal values of TF and HP tests were measured before and after catheterization. Thirty-six successfully catheterized rats were assigned to four groups. Group B received 10 µg bupivacaine, Group BD3 received 10 µg bupivacaine + 3 µg dexmedetomidine, Group BD10 received 10 µg bupivacaine + 10 µg dexmedetomidine and Control group received 10 µL volume of artificial cerebrospinal fluid. TF and HP tests were performed between the 5th and 300th minutes of drug administration. Twenty-four hours after administration of drugs, rats were sacrificed and spinal cord and nerve roots were removed for pathological investigation. RESULTS: Baseline values of the TF and HP tests were not statistically different among the groups (6.8 ± 0.15 s). TF and HP latencies in the Control group did not change significantly during the study. TF and HP test results showed that adding 3 and 10 µg dexmedetomidine caused a dosedependent increase in duration and amplitude of analgesic and nociceptive effect of bupivacaine (TF: 37.52 ± 1.08%, 57.86 ± 1.16% respectively, HP: 44.24 ± 1.15%, 68.43 ± 1.24% respectively). CONCLUSIONS: There were no apparent pathohistological changes at least 24 hours after the intrathecal administration of a single dose of dexmedetomidine 3 µg and 10 µg. Dexmedetomidine added to bupivacaine for spinal block improves analgesia and prolongs block duration.
JUSTIFICATIVAS Y OBJETIVOS: Este estudio investigó los efectos analgésicos y nociceptivos de la adición de dexmedetomidina a la bupivacaína en anestesia del neuro eje, usando los test de retirada de la cola (tail-flick [TF]) y de la placa caliente (hot-plate [HP]) y microscopía de luz para las alteraciones histopatológicas de nervios espinales y raíces nerviosas. MÉTODOS: Cuarenta ratones anestesiados, Sprague-Dawley machos, fueron cateterizados intratecalmente. Los valores basales de los testes TF y HP fueron medidos antes y después del cateterismo. Treinta y seis ratones cateterizados con éxito fueron distribuidos en cuatro grupos. El Grupo B recibió 10 µg de bupivacaína, el Grupo BD3 recibió 10 µg de bupivacaína + 3 µg de dexmedetomidina, el Grupo BD10 recibió 10 µg de bupivacaína + 10 µg de dexmedetomidina y el Grupo Control recibió 10 µL de líquido cefalorraquídeo artificial. Los test TF y HP se hicieron entre cinco y 300 minutos a partir de la administración de los fármacos. Veinte y cuatro horas después de la administración, los ratones fueron sacrificados y se les retiraron las médulas espinales y las raíces nerviosas para investigación patológica. RESULTADOS: Los valores basales de los test TF y HP no fueron estadísticamente diferentes entre los grupos (6,8 ± 0,15 s). Las latencias de TF y HP en el Grupo Control no tenían ninguna alteración significativa durante el estudio. Los resultados de los test TF y HP mostraron que la adición de 3 y 10 µg de dexmedetomidina causó un aumento dosis dependiente en la duración y en la amplitud del efecto analgésico y nociceptivo de bupivacaína (TF: 37,52 ± 1,08%, 57,86 ± 1,16%, respectivamente; HP: 44,24 ± 1,15%, 68,43 ± 1,24%, respectivamente). CONCLUSIONES: No hubo alteraciones histopatológicas aparentes en por lo menos 24 horas después de la administración intratecal de la dosis única de dexmedetomidina (3 µg y 10 µg). Dexmedetomidina añadido a la bupivacaína para raquianestesia mejora y prolonga la duración del bloqueo.