Search

Background: AERD (aspirin-exacerbated respiratory disease) is the combination of asthma, chronic rhinosinusitis/nasal polyposis (CRSwNP) and acute respiratory reactions after intake of NSAIDs (cyclooxygenase-1-inhibitors). It is characterized by chronic eosinophilic airway inflammation which is exacerbated by NSAIDs. Despite guideline-based treatment for asthma and CRSwNP and avoidance of NSAIDs, the disease is often progressive. Long-term aspirin treatment after desensitization can be effective., Case Description: A 60-year old man with a history of polyposis nasi and pansinusitis was admitted for sinus surgery. Prior to the surgery he developed hypoxemic failure after taking diclofenac. He was diagnosed with acute asthma exacerbation due to diclofenac. After treatment with oxygen, nebulized bronchodilators and prednisolone he recovered within one day. AERD was diagnosed based on patient's comorbidity and sensitivity to diclofenac., Conclusion: Patients with rhinosinusitis, nasal polyps or asthma have a high risk of NSAID hypersensitivity. Therefore routinely treatment with NSAIDs should be avoided in these patients.

Background: The occurrence of acute ischaemia or myocardial infarction in a patient experiencing an allergic reaction is known as allergic acute coronary syndrome or Kounis syndrome., Case Description: A 63-year-old male had a postoperative anaphylactic reaction to an intravenous dose of diclofenac. Myocardial ischaemia occurred during treatment of the anaphylaxis, caused by spasm of the right coronary artery followed by occlusion of the left anterior descending artery (the ramus interventricularis anterior). Despite percutaneous coronary intervention, he suffered an infarct of the anterior myocardium, resulting in reduced left ventricular function., Conclusion: In patients with Kounis syndrome therapy should focus on both the allergy and the acute coronary syndrome. Early recognition and intervention have a great effect on prognosis.

In 2013 the European Medicines Agency declared that diclofenac is contraindicated in patients with arterial thrombotic complications, based on a meta-analysis of randomised controlled trials on the adverse reactions of NSAIDs. The same decision was taken for coxibs some years earlier. The Dutch authorities (CBG/MEB) informed physicians and pharmacists about this decision without taking into account whether these patients were using prophylactic acetylsalicylic acid or not. It has been shown that NSAIDs with high COX-1 affinity like ibuprofen and naproxen cause a pharmacodynamic interaction with the inhibition of thromboxane synthesis by acetylsalicylic acid. This interaction does not occur with relatively COX-2-selective NSAIDs such as coxibs and diclofenac. Therefore, in patients who use acetylsalicylic acid for thromboprophylaxis, contraindicating coxibs or diclofenac is not justified, on the contrary: they are preferable.

A 77-year-old male was diagnosed with immunohaemolytic anaemia. He presented with fever, jaundice and oliguric renal insufficiency. He had been taking diclofenac for three days. Additional examinations and tests revealed a Coombs-positive haemolytic anaemia and thrombopenia. The micro-card gel-agglutination test demonstrated antibodies against diclofenac metabolites. After discontinuation of diclofenac and short-term treatment with prednisone and haemodialysis for two days, the patient made an almost full recovery. Haemolytic anaemia caused by diclofenac is rare. It can be caused by autoantibodies against erythrocytes and complement-fixing antibodies that bind to erythrocytes only in the presence of diclofenac or its metabolites. A timely diagnosis-supported by the appropriate laboratory tests--is of critical importance in this rare but extremely serious complication of the use of diclofenac. The treatment consists of withdrawal of diclofenac and supportive measures, possibly in combination with immunosuppressants.

Unlabelled: We report a case who developed a small bowel ulceration in a long segment of distal duodenum and proximal jejunum, a few days after he had taken high doses of diclofenac. After a month, it was complicated by a stenosis of the same segment. Nonsteroidal antiinflammatory drugs have recently been recognised as a possible etiologic factor of small bowel ulcerations. Clinical findings are aspecific. Complications of small bowel ulcerations are: obstruction, perforation or bleeding. Those have to be treated by surgery. We proposed a physiopathologic model and correlated it with histological findings., Conclusion: careful prescription of those drugs has to be pursued and one should think about a small bowel ulceration in a patient with an abdominal syndrome, who takes non-steroidal antiinflammatory drugs.