A 50-year-old woman living with untreated HIV and injection drug use presented with right shoulder pain. The shoulder exam and computed tomography (CT) scan were concerning for septic arthritis. She was started on empiric vancomycin and cefepime and underwent right shoulder debridement and humeral head resection. Bone cultures grew methicillin sensitive Staphylococcus aureus (MSSA); empiric broad-spectrum antibiotics were changed to cefazolin. The patient subsequently developed severe anemia refractory to blood transfusions approximately 6 days later. Further evaluation disclosed hemolytic anemia attributable to cefazolin. Antibiotic therapy was switched from cefazolin to daptomycin, and the patient was started on prednisone. She had sustained improvement in hemoglobin values above 6 g/dL without requiring further transfusions prior to hospital discharge. Drug-induced immune hemolytic anemia from cefazolin is rare but has been reported primarily in the perioperative setting. Here, we present a case following initiation of treatment for septic arthritis.

Andexanet alfa is a recombinant, modified factor Xa (FXa) molecule that is used for the reversal of the anticoagulant effect of oral anti-FXa anticoagulants in patients with major haemorrhage. Here, we present a case of an 85-year-old man taking rivaroxaban for atrial fibrillation, who presented with an acute, upper gastrointestinal bleed. He was stabilised with red cell transfusion and then received a 400 mg bolus of andexanet alfa. Within minutes of this, he developed chest tightness, shortness of breath, ischaemic electrocardiographic changes and then cardiac arrest from which he could not be resuscitated. The onset of symptoms was clearly temporally related to andexanet alfa administration and the differential diagnosis includes anaphylaxis with Kounis syndrome, or myocardial infarction. Although infusion site reactions have been reported and are relatively common, this is to date the first case of a fatal drug reaction andexanet alfa. This knowledge can be factored into physicians\' risk-benefit decisions when treating patients with oral anti-FXa anticoagulant-associated major haemorrhage.

Allopurinol lowers urate production through the inhibition of xanthine oxidase. It is oxidatively hydroxylated to oxypurinol and is the most prescribed medication for gout treatment. Although it has a beneficial effect in the treatment of this common disease, like many medications, it is also known for having numerous adverse effects. Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), diseases that exist on a spectrum, are two of the most dangerous adverse effects associated with allopurinol use. These immune-mediated disease processes involve almost every organ system. They are essential to recognize as early as possible, as they could potentially be deadly, requiring cessation of the medication with initial signs of rash or other early manifestations of SJS/TEN. One major consideration in the increased risk of allopurinol-mediated or modulated SJS/TEN is the need to have a lower dose in the setting of renal disease. The purpose of this review is not only to examine the involvement of allopurinol in SJS/TEN but also to provide detailed information about the drug, allopurinol, and general features and characteristics of SJS/TEN and other associated drug reactions.

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Drug reaction with eosinophilia and systemic symptoms (DRESS)/drug-induced hypersensitivity syndrome (DIHS) is a life-threatening, multi-organ adverse drug reaction with a mortality rate of approximately 10 %-20 %. The most common culprit drugs are anticonvulsants, some antibiotics such as dapsone and minocycline, salazosulfapyridine, allopurinol and some antiretroviral molecules such as abacavir and nevirapine. Only one case of DRESS induced by sildenafil has been reported in the literature. Here we report a new case.

Hydroxychloroquine (HCQ) is a commonly used medication for its immunosuppressive and dermatologic effects. It has known ocular side effects, which include retinopathy, corneal deposits, and choroidal thinning. Herein, we report the first known case of HCQ-induced hyperpigmentation of the sclera. A 75-year-old female presented after 10 months of gradual progression of painless blue-gray discoloration of the bilateral sclera, fingernails, and lower extremities secondary to oral HCQ therapy. Cessation of the drug led to a partial reversal of the hyperpigmentation at 5 months, further supporting HCQ as the causative agent. Hyperpigmentation reactions can be distressing to patients and lead to decreased medication adherence; given the widespread use of HCQ, it is important to increase awareness of this potential drug reaction.

This study aims to characterize the timeline and clinical features of onset, progression, and management of drug-induced epidermal necrolysis in pediatric patients. Sixteen pediatric patients were retrospectively identified and selected if under age 18 years at admission with one identified culprit drug exposure. Culprit drugs were antiepileptics (12/16, 75%) and antibiotics (4/16, 25%). Notably, anti-epileptic drugs (AED) had delayed onset and reported dose escalations that precipitated symptom onset; thus, patients prescribed AED with or without planned dose escalations should be monitored for prodromal symptoms longer than the typical onset window.

A subtype of cutaneous lupus erythematosus known as lupus erythematosus tumidus (LET) is characterized by sun-exposed areas that typically display urticaria-like papules and plaques. For LET, systemic therapy with antimalarials - particularly hydroxychloroquine (HCQ) - is the first line of treatment. Even though the safety profile of these medications appears to be high, there have been very few reports of side effects in the literature, including hemolytic anemia, retinal toxicity, maculopapular rash, gastrointestinal disturbance, and blue-gray discoloration of the skin or mucous membranes. Here, we report a unique instance of a 46-year-old LET smoker who, following HCQ treatment, developed a generalized myopathy.

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