Moxifloxacin

Abstract

toxic epidermal necrolysis (TEN) are serious dermatological conditions that cause severe mucocutaneous adverse S Moxifloxacin reactions, commonly to medications. The literature has reported several drug classes to cause the diseases including Stevens Johnson syndrome: case report antibiotics, antiepileptics . A 34-year-old man developed Stevens Johnson syndrome (SJS) during treatment with moxifloxacin for lower respiratory Siddika A, et al. Could there be a relation between Steven-Johnson syndrome and tract infection. ST-segment elevation myocardial infarction?. BMJ Case Reports 12: No. 11, Nov 2019. Available from: URL: http://doi.org/10.1136/bcr-2019-230331 United Arab The man presented to the emergency department due to Emirates 803440763 skin rashes all over the body. Prior to the presentation, he had a lower respiratory tract infection for 3 days for which he was prescribed moxifloxacin tablet [dosage and route not stated]. However, few hours following first dose of moxifloxacin, he started developing reddish spots all over the body. He continued to received moxifloxacin dose for the next 2 days. Subsequently, his rashes progressively worsened, started to ooze and became tender. His eyes became painful and reddish, and he developed oral lesions, cough with sputum, cracked lips and lethargy. During hospitalisation, his laboratory investigation revealed BP 140/98mm Hg, body temperature 38°C, pulse rate 105 beats/minutes and RR 18 breaths/minutes. Examination revealed target shaped skin lesions all over his body including genitals. Additionally, he had red eyes without any blurring of vision, erythematous oral mucosa with thrush and crusty lips that bleeds at times. The dermatologist diagnosed him with Stevens Johnson disease. The man was then treated with unspecified systemic steroids. On day 5 of hospitalisation, he suddenly developed typical central chest pain. A ECG revealed ST elevation in anterolateral chest leads. A significant elevation was noted in troponin and cardiac enzymes. He was then found to have anterior wall ST elevation myocardial infarction (STEMI). Thereafter, he underwent angiography, which revealed critical lesion in left anterior descending (LAD) artery with heavy load of thrombus. Thus, an angioplasty was performed. His inflammatory markers were found to be elevated including CRP (296 mg/L), procalcitonin (2.67 ng/mL) and ESR (43 mm/hour). His liver function tests (LFT) were deranged including AST (119 U/L), total bilirubin (1.6 mg/dL) and ALT (201 U/L). His lipid profile was also deranged including total cholesterol (179 mg/dL), LDL (153 mg/dL), HDL (27 mg/dL) and triglycerides (133 mg/dL). His fibrinogen and LDH was found to be 713 mg/dL and 55 U/L, respectively. A chest X-ray revealed some bilateral patchy consolidation. ECG revealed ST elevation in the anterolateral leads (V1–V3, lead I and aVL) with mild ST depression of 0.5mm in the inferior leads (leads II, III and aVF). Initially, his troponin was significantly raised to 337 ng/L, which further increased to 980 ng/L. Also, his creatine kinase MB was 50 U/L, which increased to 83 U/L. His complete blood count revealed elevated WBC count (13.38 × 109/L) and platelets count (650 × 109/L). After being diagnosed with STEMI, he was treated with aspirin, clopidogrel and enoxaparin [enoxaparin sodium] followed by unspecified anti-ischaemic medications. Therapy with unspecified steroids was discontinued. He developed ongoing mucocutaneous bleeding; although, thrombolysis was not considered. A coronary angiogram (CAG) was carried out for primary percutaneous coronary intervention. During CAG, a large intraluminal thrombus was noted in the ostium of the LAD artery, extending to proximal segment. Thus, direct stenting was carried out to the ostial and proximal LAD through drug eluding stent. However, the residual thrombus protruded inside the stent, thus it was aspirated and stent was postdilated. For mild residual clot, he received tirofiban, along with dual aspirin and ticagrelor. A transthoracic echocardiogram revealed fair left ventricular (LV) systolic function with estimated ejection fraction of 50%. ECG post-angioplasty revealed recovery of ST segment. It was noted that reactive thrombocytosis was an underlying pathophysiology of myocardial infraction. Additionally, SJS led to the development of reactive thrombocytosis through hyperviscosity syndrome. Thereafter, he remained stable and asymptomatic. All mucocutaneous lesions improved significantly. He was then discharged with various medications. Author comment: StevenJohnson syndrome (SJS) and 1