Asthma

Benralizumab used to treat near-fatal asthma


Benralizumab has been used to treat an acute asthma attack in a patient with a serious adverse reaction to steroids, respiratory physicians in the UK report.

The anti-IL5ra monoclonal antibody is licensed in the UK for the prevention of asthma attacks only.

The team of doctors from the Nuffield Department of Clinical Medicine, Oxford, detailed the case of a 52-year old man with asthma who had experienced central serous retinopathy after a course of dexamethasone, resulting in complete vision loss which took him four months to recover from.

His asthma was usually well controlled on budesonide/formoterol 200/6µg two puffs twice a day with a best expiratory flow rate (PEFR) of 450L/min at 87% of predicted PEFR (520L/min).

Upon presenting to emergency with symptoms consistent with a near fatal asthma attack the patient was treated with hourly short acting beta-2 agonists, short acting muscarinic receptor antagonists and oxygen.

The patient was also given IV magnesium, aminophylline and oral montelukast and carbocysteine.

The patients symptoms improved slightly but deteriorated when aminophylline was reduced.

The doctors noted that the patient continued to have an elevated PBEC, with a peak at 840 cells/uL on the 16th day of admission when his sputum eosinophil count was 44% and inhaled nitric oxide was 28 ppb.

“We postulated that the persistent eosinophilic inflammation was the likely driver for his incomplete recovery and proposed an alternative method of eosinophil suppression,”the authors  wrote in their case study published in the American Journal of Respiratory and Critical Care Medicine.

Within six hours of initiating benralizumab the patient achieved a clinically significant improvement in breathlessness, wheeze and cough.

Within 19 hours of treatment there was marked improvement of post-bronchodilator lung function with a PEFR increase from 270L/min to 370 L/min and a FEV1 from 1.34L to 2.26L.

He was discharged from hospital two days later.

“The prompt clinical improvement supports our hypothesis that T-helper 2 eosinophil-mediated inflammation was the primary driver of symptoms and raises the possibility that rapid onset biological treatment targeting this pathway may be a future non-corticosteroid treatment of eosinophilic acute attacks,” they added.

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