Losartan/hydrochlorothiazide/omeprazole interaction
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Losartan/hydrochlorothiazide/omeprazole interaction Various toxicities: case report
An 88-year-old woman developed hypomagnesaemia, hypocalcaemia, disorientation, agitation, hypertonia, episodes of hallucinations, persecutory delusions and generalised rigidity following concomitant administration of omeprazole and losartan/hydrochlorothiazide [dosages, routes and indications and duration of treatment to reaction onsets not stated]. The woman, who had a history of right-sided capsulothalamic ischaemic stroke in April 2011, high BP, L1 osteoporotic wedging, dyslipidaemia, urinary incontinence and repeated urine infections (UTIs), presented to an emergency department with deterioration of performance status with agitation and disorientation. Few day prior to the presentation, she had experienced episodes of persecutory delusions and hallucinations which were treated with haloperidol. She also had generalised rigidity. She recently had UTI. Physical examination revealed agitation, disorientation and generalised rigidity in the limbs and trunk along with cogwheel rigidity in the upper limbs. Hyperextension in the feet and hands associated with hypertonia was also observed. Her BP was noted to be 150/100mm Hg, temperature was 36.6°C and baseline O2 saturation was 96%. Pulmonary and cardiac auscultation showed no relevant alterations, abdomen was observed to be soft, depressible without masses or megalies and peristalsis was maintained. Her medications 24 hours prior to admission included omeprazole and losartan/hydrochlorothiazide along with other concomitant medications including aspirin [ASA], clomethiazole, paracetamol, atorvastatin, escitalopram and cefuroxime. Laboratory investigations revealed systematic urine testing and sediment: blood++, leukocytes++, haemoglobin level of 11.1 g/dL and normal platelets and leucocytes. Other investigations were as follows: prothrombin time 73%, INR 1.23, glucose 104 mg/dL, CPK 2063, urea 84 mg/dL, magnesium (Mg) 0.4 mg/dL, corrected calcium 6.9 mg/dL, potassium 3.7 mEq/L, sodium 145 mEq/L, creatinine 1.86 mg/dL and CRP level 44 [not all units stated]. The woman’s treatment with losartan/hydrochlorothiazide and omeprazole was discontinued, and she started receiving parenteral substitution of calcium and magnesium deficits. She also started receiving unspecified empirical antibiotherapy for the UTI. After 24 hours, an improvement in the cognition and orientation was noticed, along with resolution of the episodes of delusions and hallucination. Examination revealed no hyperextension or generalised rigidity particularly in the hands. It was stated that hydrochlorothiazide may have contributed to the development of hypomagnesaemia, which was associated with the renal losses and omeprazole may have contributed to hypocalcaemia. During admission, omeprazole intake was suppressed which might have demonstrated progressive improvements in calcium and magnesium levels along with the associated hallucinations and generalised contraction of the hands and feet. An interaction between lo
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