ABSTRACT
BACKGROUND: Vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) which were approved for emergency use have been administered on a large scale globally to contain the pandemic coronavirus disease 2019 (COVID-19) and to save lives. Vaccine safety is one of the issues under surveillance and a possible correlation between vaccines and thyroid function has been reported. However, reports of the impact of coronavirus vaccines on those with Graves' disease (GD) are rare. CASE SUMMARY: This paper presents two patients with underlying GD in remission, both developed thyrotoxicosis and one developed thyroid storm following the adenovirus-vectored vaccine (Oxford-AstraZeneca, United Kingdom). The objective of this article is to raise awareness regarding a possible association between COVID-19 vaccination and the onset of thyroid dysfunction in patients with underlying GD in remission. CONCLUSION: Receiving either the mRNA or an adenovirus-vectored vaccine for SARS-CoV-2 could be safe under effective treatment. Vaccine induced thyroid dysfunction has been reported, but the pathophysiology still not well understood. Further investigation is required to evaluate the possible predisposing factors for developing thyrotoxicosis especially in patients with underlying GD. However, early awareness of thyroid dysfunction following vaccination could avoid a life-threatening event.
Subject(s)
Diverticulitis , Mediastinal Emphysema , Pneumopericardium , Pneumoperitoneum , Retropneumoperitoneum , Female , Humans , Aged , Mediastinal Emphysema/diagnostic imaging , Mediastinal Emphysema/etiology , Retropneumoperitoneum/diagnostic imaging , Retropneumoperitoneum/etiology , Pneumopericardium/diagnostic imaging , Pneumopericardium/etiology , Pneumoperitoneum/diagnostic imaging , Pneumoperitoneum/etiologyABSTRACT
BACKGROUND: It is widely accepted that tumor necrosis factor-α (TNF-α) plays an important role in the pathogenesis of emphysema. This study aimed at investigating the protective effects of anti-TNF-α antibody, infliximab, in the development of emphysema induced by passive smoking in rats. METHODS: Thirty-nine rats were randomly divided into a normal control group (group 1), an emphysema group (group 2), and an infliximab-intervention group (group 3). Rat models of emphysema were established by exposure to cigarette smoking daily for 74 days. After 1 month, the infliximab intervention group was treated with infliximab via subcutaneous injection. The levels of TNF-α, IL-8 and vascular endothelial growth factor (VEGF) in bronchoalveolar lavage fluid (BALF) were measured with enzyme linked immunosorbent assay (ELISA). The number and classification of cells in the BALF were measured. Lung tissue sections stained by hematoxylin and eosin (HE) were observed, and mean linear intercept (MLI) and mean alveolar numbers (MAN) were measured. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods were used to examine the percentage of positive cells and distribution of apoptotic cells. RESULTS: The levels of TNF-α and IL-8 in BALF were higher in group 2 than in group 1 and group 3. The MLI was greater in group 2 than that in group 1 and group 3 while MAN was decreased. The concentration of VEGF in BALF of group 2 was significantly decreased as compared with group 1. The total cells and neutrophils number was significantly increased in group 2 as compared with group 1 and group 3, so was the percentage of neutrophils. The number of TUNEL positive cells in the alveolar septa was significantly increased in group 2 as compared with group 1 and group 3. CONCLUSION: Infliximab protects against cigarette smoking-induced emphysema by reducing airway inflammation, attenuating alveolar septa cell apoptosis and improving pathological changes.
