Interaction between warfarin and molnupiravir in a patient with coronavirus disease 2019 infection.

Molnupiravir is a novel antiviral agent for coronavirus disease 2019 (COVID-19) treatment. Warfarin is an oral anticoagulation agent with difficult management due to drug interactions. Here, we describe a case of international normalized ratio (INR) prolongation in a patient who administrated warfarin with molnupiravir for COVID-19. An increased INR at 3.80, enough to discontinue warfarin, was observed on the fifth day of molnupiravir therapy, although the warfarin dose and INR were stable at 4 mg/day and approximately 2.0 before the molnupiravir initiation, respectively. Factors that affect the INR, such as severe COVID-19, cytokine, diet, liver dysfunction, and the concomitant use of medications other than molnupiravir, were unlikely in this patient. This case suggests that healthcare physicians should be aware of the possibility of drug interaction between molnupiravir and warfarin.

Duloxetine-induced hyponatraemia in a patient with hypocortisolaemia.

Duloxetine-induced hyponatraemia is a known adverse effect that can lead to potentially life-threatening complications. In addition, hypocortisolaemia is associated with the development of hyponatraemia. Here, we report a case of severe hyponatraemia rapidly presenting after duloxetine treatment in a patient with hypocortisolaemia. A 75-year-old man administered hydrocortisone for the treatment of hypocortisolaemia induced by a Rathke's cleft cyst was admitted for anorexia 3 days after the initiation of duloxetine therapy. Laboratory findings showed severe hyponatraemia, hypo-osmolality, concentrated urine, and increased urine sodium. Because the syndrome of inappropriate antidiuretic hormone was diagnosed, duloxetine was ceased. Following admission to the hospital, endocrinological analyses revealed mild hypocortisolaemia, possibly due to low adherence to hydrocortisone replacement therapy. By the sixth day after admission, the patient's hyponatraemia, serum osmolality, and urine osmolality had improved. This case suggests that health-care physicians should be aware of the possibility of duloxetine-related hyponatraemia, particularly in patients with hypocortisolaemia.

A case of early detection of bisphosphonate-related osteonecrosis of the jaw.

Osteonecrosis of the jaws is an adverse reaction associated with the use of bisphosphonates. Although the diagnosis of bisphosphonate-related osteonecrosis of the jaw (BRONJ) is based on symptomatology, it is often detected late because the patients become symptomatic only after osteonecrosis is well established. We describe a case of early oral BRONJ detected by magnetic resonance imaging (MRI) accidentally. Head MRI revealed low signal of T1-weight images in left mandibula. Patient had been treated with minodronate for osteoporosis during 18 months. Based on the MRI findings and medication history, early stage BRONJ could be considered. Therefore minodronate was switched to teriparatide. Thereafter mandible pares-thesias, odontalgia and exposed bone were not observed. This case suggests that MRI is useful for the early detection of BRONJ.

Duloxetine-induced hyponatremia in an elderly patient treated with thiazide diuretics.

Hyponatremia is a known adverse effect of duloxetine, and it can lead to potentially life-threatening complications. Administration of thiazide diuretics also has been the cause of hyponatremia. We report a case of duloxetine-induced hyponatremia in an elderly patient treated with thiazide diuretics. An 86-year-old woman treated with the trichlormethiazide was admitted for vertebral compression fracture with disorientation and nausea on the 6(th) day of treatment with duloxetine. Laboratory findings revealed hyponatremia, hypo-osmolality, concentrated urine, and increased urine sodium. Syndrome of inappropriate antidiuretic hormone was considered, therefore, duloxetine, and trichlormethiazide was discontinued and treated with fluid restriction, furosemide and sodium chloride administered orally. Disorientation and nausea were improved after correction of hyponatremia. Health care practitioners should be aware of the possibility of duloxetine-induced hyponatremia, particularly in patients treated with thiazide diuretics.

Hyponatremia associated with paroxetine induced by sodium-restricted diet and hypotonic saline.

CASE DESCRIPTION: An 89-year-old woman taking paroxetine was admitted to our hospital for femoral neck fracture; her diet became sodium restricted due to hypertension. After admission, the femoral head replacement was performed and hypotonic saline was administered over 2 days. On the fifth day after the operation, severe hyponatremia was observed and treated with oral fluid restriction, furosemide, sodium chloride and paroxetine discontinuance. In a few days, serum sodium concentration returned to baseline level. CONCLUSIONS: Besides risk factors for SIADH, a sodium-restricted diet and infusions of hypotonic saline in the perioperative period should be considered risk factors for SIADH associated with paroxetine.

[The pharmacokinetics and safety of oxaliplatin in a hemodialysis patient treated with mFOLFOX6 therapy].

A postoperative rectum cancer patient with lung metastasis undergoing hemodialysis was treated with mFOLFOX6 therapy. The primary dose of oxaliplatin (L-OHP) ranged from 60 mg/m(2) to 85 mg/m(2), and adverse reactions and serum platinum concentration were monitored. The free platinum concentration (f-Pt), was eliminated efficiently using dialysis. The patient was tolerant of L-OHP doses of 60 mg/m(2) and 70 mg/m(2), but grade 2 neutropenia and grade 3 hemoglobin decrease developed with an L-OHP dose of 85 mg/m(2). The f-Pt after hemodialysis was higher than that before hemodialysis with a dose of 85 mg/m(2). But even with an 85 mg/m(2) dose, mFOLFOX6 therapy could be continued by extending the dosing interval. The monitoring of serum platinum concentrations, as well as therapeutic monitoring based on pharmacokinetics, contributes to safety management of cancer chemotherapy.

Severe QT interval prolongation associated with moxifloxacin: a case report.

INTRODUCTION: The QT interval prolongation is an adverse effect associated with moxifloxacin. This adverse effect can lead to potentially life-threatening arrhythmias such as Torsades de pointes. We describe a case of severe QT interval prolongation associated with moxifloxacin which may cause the development of Torsades de pointes. There have been no reported case of severe corrected QT interval prolongation caused by moxifloxacin in the patient of normal heart rate. CASE PRESENTATION: In an 85-year-old Japanese woman, oral moxifloxacin 400 mg daily was initiated for the forearm cellulitis. On the sixth day of oral moxifloxacin administration, monitor electrocardiogram showed prolongation of the corrected QT interval to 523 ms at a rate of 40 beats/min. Electrocardiogram before moxifloxacin therapy showed the corrected QT interval to 460 ms at a rate of 72 beats/min. On the sixth day after moxifloxacin discontinuance, monitor electrocardiogram showed the corrected QT interval to 432 ms at a rate of 70 beats/min. CONCLUSION: This case suggests that electrocardiogram monitoring during moxifloxacin therapy may be necessary in the patients even if they do not have high risk factors for QT interval prolongation.