Drug Safety - Case Reports最新文献

A 32-year-old male developed recurrent ventricular tachycardia after taking mega doses of loperamide and famotidine in order to experience an opiate-like euphoric effect. He was taking up to 200 mg of loperamide and multiple doses of famotidine each day. He developed palpitations and syncope. Electrocardiography demonstrated ventricular tachycardia and QT interval prolongation (corrected QT interval was 597 ms). He was diagnosed with loperamide-induced QT prolongation resulting in incessant ventricular tachycardia. Loperamide was discontinued, and he was treated with electrolyte replacement, supportive care, and monitoring. After 5 days, his electrocardiogram (ECG) normalized and he had no more ventricular tachycardia. A Naranjo assessment score of 8 was obtained, indicating a probable relationship between QT prolongation and his use of loperamide. Large doses of loperamide can cause QT interval prolongation and life-threatening arrhythmias. These effects may be accentuated when histamine-2 receptor blockers are also abused.

Many chemicals used as medical treatments can cause chemical burns as an untoward side effect. One of such chemicals is potassium permanganate. It is a caustic chemical used as a disinfectant. The most common sites of burn by potassium permanganate are exposed sites like the face and hands. Chemical burns in the perianal and anal region are rare in clinical practice and even sparser in the pediatric age group. In this article, we report a case of perianal and anal chemical burn in an 18-month-old, male child, caused by potassium permanganate crystal applied wrongly for the treatment of pinworm infestation. As a chemical burn in this region can have serious complications, it is necessary to be vigilant when using such chemicals in these cases. Early and timely management in such cases leads to good outcomes. This is the first of such cases of chemical burn caused by potassium permanganate in the anal and perianal region.

We present a 35-year-old female patient who was started on rifampicin (900 mg orally once daily) and trimethoprim/sulfamethoxazole (TMP/SMX) (160/800 mg orally twice daily) after being diagnosed with brucellosis. Following defervescence and improvement in her general condition, fever recurred on the 12th day of treatment. A re-challenge drug test lead to causality assessment and treatment was switched to a combination of streptomycin (1 g intramuscularly) for 10 days and TMP/SMX (160/800 mg orally twice daily) for 4 weeks. Our patient is doing well after 12 months of follow-up.

A 54-year-old woman with type 2 diabetes mellitus, hypertension, and peripheral vascular disease developed life-threatening lactic acidosis during treatment with metformin for type 2 diabetes. The woman received metformin at 1000 mg orally twice a day for type 2 diabetes. She presented to our emergency department with a 3-day history of severe watery diarrhea, nausea, and vomiting. Her grandson whom she cared for had gastroenteritis several days prior to the onset of her symptoms. She was confused and hypotensive with a blood pressure of 70/39 mmHg. Her initial laboratory findings were remarkable with an arterial blood gas pH 6.57, HCO[Formula: see text] 2 mEq/L, anion gap 30 mmol/L, and lactate 16.3 mmol/L. She was diagnosed with severe lactic acidosis. Metformin was discontinued. Upon arrival in the emergency department, she became unresponsive and experienced a pulseless electrical activity cardiac arrest. After resuscitation, her severe acidemia persisted despite aggressive intervention with volume resuscitation and vasopressors, leading to the initiation of renal replacement therapy. After multiple dialysis treatments, her severe acidemia resolved. Serum metformin concentration from presentation ultimately returned to 42 mcg/mL (therapeutic concentration: 1-2 mcg/mL). She was discharged from the hospital on day 15 without any neurologic complications. A Naranjo assessment score of 8 was obtained, indicating a probable relationship between the patient's lactic acidosis and her use of the suspect drug.

We present two cases of paraplegic patients who developed secondary Raynaud's phenomenon. A 43-year-old man with paraplegia presented with dark purple discoloration and skin defects on his left second and third toes and complained of a cold sensation in both feet for a period of 1 year. He had been taking diuretics for 4 years. The capillary refilling time for both affected toes was delayed. His antihypertensive drug was changed to a calcium channel blocker under suspicion of Raynaud's phenomenon aggravated by hydrochlorothiazide, and the capillary refilling time normalized within 3 days. The toe skin defect was covered with a skin graft. A 51-year-old man with paraplegia presented with cyanotic color change and recurrent unstable wounds on his toes. He was also taking diuretics for hypertension. Suspecting secondary Raynaud's phenomenon aggravated by diuretics, we changed the diuretics to olmesartan medoxmil 20 mg and amlodipine besylate 2.5 mg per day. Subsequently, he has had no unstable wounds for 30 months. If hypertensive patients with paraplegia complain of skin discoloration in their extremities, Raynaud's phenomenon should be considered and the antihypertensive drug may need to be stopped in order to improve the wound-healing process.

After a registered drug is available on the market and used in everyday circumstances, hitherto unknown adverse drug reactions (ADRs) may occur. Furthermore, the patient can experience a previously unknown course of a known ADR. Voluntary reports by patients play an important role in gaining knowledge about ADRs in daily practice. The Netherlands Pharmacovigilance Centre Lareb received a report from a 55-year-old female-to-male transgender patient who experiences secondary polycythemia while using lifelong testosterone therapy. The onset age of the symptoms was 38 years. The symptoms appeared gradually and after approximately 1 year it was clear that the patient's hemoglobin and hematocrit had started to increase. A Naranjo assessment score of 6 was obtained, indicating a probable relationship between the patient's polycythemia and use of the suspect drug. Polycythemia is a known ADR in testosterone treatment, but little attention has been paid to the possible severity and complications of these symptoms as well as the impact on the patient's well-being.

A 52-year-old man developed interstitial pneumonitis during treatment with desvenlafaxine for major depressive disorder. The man received desvenlafaxine at 50 mg for symptoms of depression 4 years earlier. Six months after a dose increase to 100 mg, he developed bronchitic symptoms with mild, persistent dyspnea. Investigations revealed a restrictive pattern on pulmonary function testing, bilateral upper lobe reticular opacities with traction bronchiectasis on radiology imaging, and end-stage interstitial fibrosis with honeycomb changes consistent with chronic hypersensitivity pneumonitis on open lung biopsy. He was diagnosed with drug-induced interstitial pneumonitis. Desvenlafaxine was discontinued and the patient received prednisone and mycophenolate mofetil. The patient had subsequent stability in the progression of his pulmonary disease after 1 month. After 1 year of drug discontinuation and treatment, his disease process remained, but without major progression. A Naranjo assessment score of 4 was obtained, indicating a possible relationship between the patient's adverse drug reaction and his use of the suspect drug.

A 67-year-old man developed a suspected adverse drug reaction during treatment with topical 5-fluorouracil (5-FU) for multiple actinic keratosis of the face, neck, and forearms. The man received topical 5-FU at a dosage of 0.5% for the actinic keratoses. After 1 week, he developed extreme lethargy, fatigue, fever, and mouth erosions. Several days later, and after discontinuation of 5-FU, painful mucositis and systemic side effects occurred, meeting criteria for hospitalization because of dehydration and a 6.8 kg weight loss. Hematology/oncology was consulted, and a possible systemic 5-FU reaction, similar to reactions to intravenous chemotherapy seen with a dihydropyrimidine dehydrogenase deficiency was suggested. The patient was not taking any concurrent medications, and he refused dihydropyrimidine dehydrogenase deficiency testing.

Hiccups can be idiopathic, psychogenic and organic, with drugs being one of the most important causes of hiccups. Although the exact pathophysiological processes involved are still poorly understood, the neurotransmitters dopamine, serotonin, and γ-aminobutyric acid (GABA) have been documented to play a significant role in the generation of hiccups. We report on two patients with cellulitis who developed hiccups with the use of tramadol as an analgesic. The possible mechanisms and clinical implications of this rare adverse event are discussed. Both patients recovered from the hiccups with the use of baclofen tablets.

We present a rare case of generalized fixed drug eruption caused by fluconazole. A 45-year-old female patient was referred to our outpatient clinic because of suspicious drug eruptions that occurred 5 months earlier and resolved within a month. The patient had sequela of hyperpigmentation on her arms, legs, back, and abdomen after oral administration of the fourth dose of 150 mg of fluconazole once daily because of vaginal candidiasis. Patch tests with the culprit drug applied both on unaffected skin areas and over one of the lesions were negative. A lymphocyte transformation test was performed and in response to fluconazole, CD4⁺ T cells significantly proliferated. Because the patient needed a safe antifungal drug for her recurrent vaginal candidiasis symptoms, a single-blind placebo-controlled drug provocation test was performed with itraconazole and was negative. Accordingly, 200 mg of itraconazole once daily was given for 10 days safely.