Acute severe asthma with thyroid crisis and myasthenia: a case report and literature review.

BACKGROUND AND AIMS: Acute severe asthma, thyroid crisis and acute myasthenia are all medical emergencies that rarely coexistent. Here, we report a young man with severe asthma attack, necessitate invasive mechanical ventilation at the onset, followed by thyroid crisis, rhabdomyolysis, acute kidney injury, thrombocytopenia and progressive myasthenia. The aim of this study is to better understand the relationships among severe asthma, autoimmune thyroiditis and myasthenia. METHODS: The case was presented and former literatures were reviewed. RESULTS: This is the first case report of a young patient presented with severe asthma and autoimmune thyroiditis, followed by thyroid storm, multiple organ dysfunction and myasthenia. Neither conventional treatment for asthma or thyroid storm was effective separately. The patient's clinical condition did not improve until after plasmapheresis. CONCLUSION: Here, we highlighted both the importance of early recognition of thyroid storm and prompt therapies, which likely attenuated organ dysfunction and enabled this patient to recover from the life-threatening attack. Asthmatic patients should be closely controlled when suspected of thyroid disorders, especially those with high levels of anti-thyroid antibodies irrespective of thyroid hormones concentrations.

Investigation of the measurement of murine airway hyperresponsiveness and the therapeutic effects of budesonide on ovalbumin sensitized and challenged mice.

BACKGROUND: Airway hyperresponsiveness (AHR) is one of the most important characteristics of asthma. This study investigated the parameters, by which assess the airway responsiveness under tidal ventilation. METHODS: Female BALB/c mice were sensitized and challenged with ovalbumin (OVA) (group A), and part of them were treated with budesonide aerosol (group B). All the mice were anaesthetized and mechanically ventilated. The values of tidal volume (Vt), airway pressure (PA), airway flow (F), expiratory lung resistance (RL) and dynamic compliance of the thorax and lung (CT-L) were recorded by the AniRes2003 animal lung function system. In addition, the expiratory volume in the first 0.1 second after the start of expiration (EV0.1) was obtained according to the flow-volume (F-V) curve. The maximal or minimal values of EV0.1, RL and CT-L were documented after each dose of methacholine (MCH) and compared with values from negative control group (group C). RESULTS: (1) When the dose of MCH reached 100 ng/g or 200 ng/g, the decrease of Vt in group A was much more significant than group C (P = 0.001, < 0.001 respectively), but not so between groups B and group C (P = 0.974, 0.362 respectively). (2) With the dose of 25, 50, 100 or 200 ng/g MCH, the decrease in percentage of EV0.1 in group A was much higher than group C (P = 0.012, 0.025, 0.001, 0.003 respectively), while that in group B showed no significant difference as compared with group C (P = 0.507, 0.896, 0.972, 0.785). (3) RL and CT-L: with the dose of 200 ng/g MCH, there was a statistically significant increase of RL in group A compared to group B or group C (P < 0.001, < 0.001 respectively), but no significant difference between groups B and C (P = 0.266). With doses of 100 ng/g and 200 ng/g MCH, there was a statistically significant decrease of CT-L in group A compared to group B (P = 0.001, = 0.001) and group C (P < 0.001, < 0.001 respectively), but no significant difference between groups B and C (P = 0.775, 0.310). (4) Histopathology: there were eosinophilic predominant peribronchial and perivascular inflammatory influx in murine lungs after OVA sensitizing and challenging, which could be counteracted by inhalation of budesonide in group B. CONCLUSIONS: The decline in EV0.1 in response to MCH challenge correlated with simultaneous changes in Vt, RL and CT-L, but more sensitively than all the other parameters. The decline in EV0.1 and inflammation in murine lung could be significantly alleviated by inhalation of nebulized budesonide solution, which indicated that EV0.1 to MCH is a valid measure of AHR in mice.

[Dynamic changes in airway hyperresponsiveness as a result of allergen and therapeutic effects of budesonide in rats].

OBJECTIVE: To investigate the dynamic changes in airway hyperresponsiveness (AHR) in allergen-induced asthma in rats and the effects of budesonide. METHODS: Among 36 BALB/c female mice, 6 were randomized as negative control group (group C), the remaining mice were challenged with ovalbumin (OVA) to reproduce asthma. Kinetics of airway AHR of OVA-induced asthmatic mice was carried out as follows: on day 15, 18, 21 and 25 (A1, A2, A3, A4 groups), 6 mice were randomly chosen and sacrificed after measurement of airway AHR to investigate tidal volume (V(T)), airway resistance of expiring phase (R(A)), compliance of thorax and lung (C(T-L)) with different doses of methacholine chloride (MCH). In group B 6 mice were randomly chosen and treated with 1 mg budesonide aerosol once per day from day 15 to 17, then sacrificed on day 18. Their physiological and pathological changes were determined similarly to those of A2 group. RESULTS: (1) The increase of R(A) in group A1, A2 and A3 were significantly higher than that in group C when MCH reached the dose of 200 ng/g. (2) The decrease of C(T-L) in group A1 and A2 was significant with 100 ng/g and 200 ng/g MCH. (3) The value of V(T) markedly decreased in group A2 with 100 ng/g MCH and in all asthma model groups with 200 ng/g MCH than that in group C. (4) There was an eosinophil-dominant inflammatory infiltration in the asthma lungs, and the degree of infiltration peaked on day 15, and then alleviated afterwards. (5) With the dose of 200 ng/g MCH, the increase of R(A) in group B was significantly alleviated when compared with that in group A2, but there was no significant difference between group B and C. With the dose of 100 and 200 ng/g MCH, the decrease of C(T-L) in group B was significantly less marked compared with that in group A2 but there was no significant difference between group B and group C; the decrease of V(T) in group B was significantly lessened in degree when compared with that in group A2, while there was no statistical difference between group B and group C. The infiltration of inflammatory cells was obviously alleviated and the repair of airway epithelium was better in budesonide group. CONCLUSION: (1) Airway hyperresponsiveness increases greatly in mice challenged and sensitized with OVA, and it lasts for about 7 days and then declines afterwards. (2) Budesonide aerosol could effectively alleviate the eosinophil dominant inflammatory response and decrease AHR in the murine asthma model.