Αρχειοθήκη ιστολογίου

Τετάρτη 2 Νοεμβρίου 2022

Xanthomatous erosive arthritis: A new disease entity?

alexandrossfakianakis shared this article with you from Inoreader
View on Web

Desmoid tumor occurrence in a patient with severe congenital neutropenia type 4: Case history and follow‐up

alexandrossfakianakis shared this article with you from Inoreader
View on Web

Acute In Vitro and In Vivo Effects of Dexamethasone in the Vocal Folds: a Pilot Study

alexandrossfakianakis shared this article with you from Inoreader
Acute In Vitro and In Vivo Effects of Dexamethasone in the Vocal Folds: a Pilot Study

Atrophy has been reported following dexamethasone injection into the vocal folds. Dexamethasone increased MuRF-1 gene expression in TA myoblasts. A single injection of dexamethasone, however, did not alter atrogene expression, TA morphology, or epithelial thickness in vivo.


Objectives/Hypothesis

Glucocorticoids (GC)s are commonly employed to treat vocal fold (VF) pathologies. However, VF atrophy has been associated with intracordal GC injections. Dexamethasone-induced skeletal muscle atrophy is well-documented in other tissues and believed to be mediated by increased muscle proteolysis via upregulation of Muscle Ring Finger (MuRF)-1 and Atrogin-1. Mechanisms of dexamethasone-mediated VF atrophy have not been described. This pilot study employed in vitro and in vivo models to investigate the effects of dexamethasone on VF epithelium, thyroarytenoid (TA) muscle, and TA-derived myoblasts. We hypothesized that dexamethasone will increase atrophy-associated gene expression in TA muscle and myoblasts and decrease TA muscle fiber size and epithelial thickness.

Study Design

In vitro, pre-clinical.

Methods

TA myoblasts were isolated from a female Sprague–Dawley rat and treated with 1 μM dexamethasone for 24-h. In vivo, 15 New Zealand white rabbits were randomly assigned to three treatment groups: (1) bilateral intracordal injection of 40 μL dexamethasone (10 mg/ml; n = 5), (2) volume-matched saline (n = 5), and (3) untreated controls (n = 5). Larynges were harvested 7-days post-injection. Across in vivo and in vitro experimentation, MuRF-1 and Atrogin-1 mRNA expression were measured via RT-qPCR. TA muscle fiber cross-sectional area (CSA) and epithelial thickness were also quantified in vivo.

Results

Dexamethasone increased MuRF-1 gene expression in TA myoblasts. Dexamethasone injection, however, did not alter atrophy-associated gene expression, TA CSA, or epithelial thickness in vivo.

Conclusion

Dexamethasone increased atrogene expression in TA myoblasts, providing foundational insight into GC induced atrophic gene transcription. Repeated dexamethasone injections may be required to elicit atrophy in vivo.

Level of Evidence

N/A Laryngoscope, 2022

View on Web

Spatial‐temporal dynamics and time series prediction of HFRS in mainland China: a long‐term retrospective study

alexandrossfakianakis shared this article with you from Inoreader

Abstract

Hemorrhagic fever with renal syndrome (HFRS) is highly endemic in mainland China. The current study aims to characterize the spatial-temporal dynamics of HFRS in mainland China during a long-term period (1950-2018). A total of 1,665,431 cases of HFRS were reported with an average annual incidence of 54.22 cases/100,000 individuals during 1950-2018. The joint regression model was used to define the global trend of the HFRS cases with an increasing-decreasing-slightly increasing-decreasing-slightly increasing trend during the 68 years. Then spatial correlation analysis and wavelet cluster analysis were used to identify four types of clusters of HFRS cases located in central and northeastern China. Lastly, the Prophet model predicts that 14,223 cases of HFRS will occur in mainland China during 2019-2038. Our findings will help reduce the knowledge gap on the transmission dynamics and distribution patterns of the HFRS in mainland China and facilitate to take rel evant preventive and control measures for the high-risk epidemic area.

This article is protected by copyright. All rights reserved.

View on Web

Comparison of clinical features and surgical outcomes between hypopnea‐ and apnea‐predominant obstructive sleep apnea

alexandrossfakianakis shared this article with you from Inoreader

Abstract

Objectives

This study is aimed to investigate the differences in the clinical features and surgical outcomes between hypopnea- and apnea-predominant obstructive sleep apnea (OSA).

Design

Cohort study

Setting

Single tertiary care center

Participants

This study included 190 patients with OSA who underwent multilevel upper airway surgery between September 2012 and September 2021. The patients were divided into two groups according to the proportion of each respiratory event: hypopnea-predominant (n = 102) and apnea-predominant (n = 88).

Main outcome measures

The primary outcome measure was the percentage improvement in the apnea-hypopnea index (AHI) from baseline AHI after surgery.

Results

The apnea-predominant group included more male patients and had higher AHI, respiratory disturbance index (RDI), and oxygen desaturation index (ODI) than the hypopnea-predominant group. Both groups showed significant improvements in AHI, apnea index, RDI, supine AHI, REM AHI, non-REM AHI, ODI, lowest O2 saturation, and Epworth Sleepiness Scale scores following the surgery. Notably, hypopnea index increased after surgery in the apnea-predominant OSA group. Although the improvement in the absolute value of AHI by surgery was significantly greater in the apnea-predominant group than in the hypopnea-predominant group, the two groups showed no significant difference in the percentage improvement in AHI from baseline AHI.

Conclusion

Patients with apnea-predominant OSA had more severe disease than those with hypopnea-predominant OSA; however, surgical outcomes, as evaluated by percentage AHI improvement, were comparable between the two groups. In addition, multilevel upper airway surgery may induce the transition from apnea to hypopnea in patients with apnea-predominant OSA.

View on Web

Hiperparatiroidismo: Todo lo que debes saber

alexandrossfakianakis shared this article with you from Inoreader

¿Qué es el hiperparatiroidismo?

Las glándulas paratiroideas, generalmente en número de 4 o 5, son pequeñas glándulas situadas en la parte posterior de la glándula tiroides. Son independientes del mismo pero muchas veces están incrustadas dentro del tejido tiroideo. Segregan la hormona paratiroidea (PTH), que junto con la vitamina D, es esencial para mantener el equilibrio fosforo-calcio de forma constante, y así tener una buena salud ósea y un buen funcionamiento del sistema nervioso y muscular.

El hiperparatiroidismo (HPT) se define como un exceso de secreción de la hormona paratiroidea (PTH). Es una patología frecuente, que afecta más a mujeres y su incidencia se incrementa con la edad a partir de la menopausia. La presencia en un paciente joven o de antecedentes familiares obliga a descartar una patología genética asociada.

Tipos de Hiperparatiroidismo

Existen dos tipos de hiperparatiroidismo:

1.Hiperparatiroidismo primario. Es debido a la hipersecreción autónoma de PTH por una glándula paratiroidea (adenoma paratiroideo), o varias glándulas (hiperplasia paratiroidea). Las lesiones son generalmente benignas. La presencia de un carcinoma paratiroideo es excepcional. La mayoría de las veces el HPT es esporádico, pero existen casos familiares de HPT aislados o asociados a otras patologías genéticas endocrinológicas (denominadas MEN), que coexisten con otras glándulas afectadas (hipófisis, suprarrenales, islotes pancreáticos u hormonas digestivas).

2.Hiperparatiroidismo secundario. Se produce por la respuesta secretoria de las glándulas paratiroideas a una disminución de la calcemia, lo que secundariamente provoca la hipersecreción de PTH para mantener la homeostasis de calcio-fósforo.

Las causas más frecuentes de HPT secundario son:

  • Deficiencia de Vitamina D cuya acción principal es favorecer la absorción del calcio intestinal. Se precisa una deficiencia severa de vitamina D para que se produzca un estímulo secundario de la hipersecreción de PTH por las glándulas paratiroideas. El déficit poblacional de vitamina D es cada vez más frecuente por baja exposición solar o por baja ingesta oral.
  • Hipocalcemia secundaria a baja ingesta de calcio o alteración de la absorción del mismo como consecuencia de cirugías abdominales con resecciones intestinales.
  • Insuficiencia renal crónica (IRC): La IRC se asocia a una disminución de la hidroxilación renal de Vit D, así como hipocalcemia y secundariamente a una elevación de los niveles de PTH para mantener el equilibrio calcio-fósforo. La insuficiencia renal crónica es la causa más frecuente de HPT secundario y causa a su vez del HPT terciario que provoca una hipercalcemia causada por la secreción de PTH excesiva y autónoma en un paciente con HPT secundario.

¿Cuáles son los síntomas del Hiperparatiroidismo?

La mayoría de las veces, el diagnóstico del HPT, se realiza de forma casual observando una hipercalcemia en una analítica de rutina y suele ser asintomático en los estadios iniciales. Como es una enfermedad de desarrollo lento, los síntomas dependen del daño orgánico que provoca la hipercalcemia (cólicos renales secundarios a litiasis cálcica, dolores articulares por daño óseo y síntomas derivados de la osteoporosis, incluso mayor incidencia de fracturas e hipertensión arterial).

¿Cómo se trata el Hiperparatiroidismo?

  • El HPT primario se trata generalmente con intervención quirúrgica del adenoma si es localizado con técnicas de imagen. La indicación de cirugía además de la localización se realiza en base a criterios clínicos como nivel de calcemia, presencia de osteoporosis y presencia de otras complicaciones. Cuando existe hiperplasia o las condiciones del paciente impiden la cirugía podemos recurrir a opciones de tratamiento médico.
  • En el HPT secundario requiere controlar la causa como la suplementación de Vitamina D cuando hay déficit, aporte de calcio cuando hay déficit o tratamiento específico en el paciente con IRC, que incluso puede llegar a cirugía de glándulas paratiroides cuando se produce un HPT terciario.

Si te ha gustado este artículo, quizá te interese leer:

La entrada Hiperparatiroidismo: Todo lo que debes saber se publicó primero en Cuida tu tiroides.

View on Web