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Azithromycin, an azolide antibiotic with structural and functional similarities to macrolides, possesses distinct features such as its effects persisting for seven days, an extended half-life by administering it once daily for three days, and strong antimicrobial activity. Notably, vomiting and diarrhea are recognized as the primary adverse events related to azithromycin. In this particular case, we present a unique case describing a purpuric-type drug eruption associated with azithromycin, which represents an uncommon cutaneous manifestation. A 64-year-old female developed a purpuric eruption on her trunk and lower extremities seven days after receiving daily intravenous azithromycin for upper bronchitis. A previous occurrence of punctate purpuric eruption following azithromycin administration was documented in her medical history. The diagnosis of azithromycin-induced skin eruption was confirmed based on the clinical progression and the recurrence of the eruption upon re-administration of the drug. In response to this diagnosis, the patient underwent treatment involving the discontinuation of azithromycin and the application of topical betamethasone butyrate propionate ointment. Remarkably, her eruption significantly improved within two weeks, although residual pigmentation persisted post-treatment. Additionally, we offer a comprehensive review of the literature, examining cases of drug eruptions related to azithromycin.

Onychomycosis is the most prevalent nail disease and is frequently encountered in clinical practice. Despite having multiple therapeutic options, of which systemic antifungals are the most effective, treatment is not always mandatory in all patients. Especially when considering systemic treatment, the risk of adverse reactions may outweigh the potential benefits of treatment. In this case report, we present a clinical case of a 49-year-old male patient with a blank past medical history who experienced a severe drug eruption from terbinafine prescribed for mild onychomycosis that required discontinuation of terbinafine, additional evaluation, and treatment of this adverse reaction.

A new quinolone antibiotic called garenoxacin was developed in Japan. Garenoxacin is known to produce cutaneous adverse effects, particularly fixed drug eruption in Japan, despite several reports of cutaneous adverse events in English-language literature. However, English-language literature has not yet reported that fixed drug eruption is a common clinical manifestation of garenoxacin-induced drug eruption. In this article, we present a case of multiple fixed drug eruptions and review the literature on case reports of drug eruptions caused by garenoxacin.

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A 76-year-old male developed a maculopapular rash on his trunk and extremities. The rash appeared 2 months after Finasteride administration for his prostatic hyperplasia. Clinical suspicion was of drug exanthema due to Finasteride. The clinical and histologic data were compatible with pharmacologic eruption by Finasteride.

Drug reaction with eosinophilia and systemic symptoms (DRESS syndrome) or drug-induced hypersensitivity syndrome (DIHS) is a severe skin reaction associated with general symptoms and mortality reaching up to 10% of cases. DRESS/DIHS is one of the few dermatological emergencies which need to be taken into consideration when dealing with a patient with acute exanthema and systemic symptoms like: fever, lymphadenopathy, muscle pain, hepatosplenomegaly, abnormal blood count results and systemic inflammation. The aim of this article is to summarize the literature finding regarding this dermatological emergency and present the case of a 42-year-old male suffering from DRESS syndrome as a consequence of sulfasalazine intake due to an inflammatory bowel disease, who was effectively treated with oral prednisolone and immediate drug withdrawal.

Stevens-Johnson syndrome is a type of severe drug eruption, which is characterized by rapid onset and rapid progress. If not treated in time, it can develop into toxic epidermal necrolysis, even life-threatening. Common sensitizing drugs include sulfa, carbamazepine, etc. In China, reports and studies of carbamazepine causing Stevens-Johnson syndrome mainly focus on the HLA-B * 1502 gene, and there are no reports of HLA-A * 3101 gene positive. We reported a patient who got Stevens-Johnson syndrome with HLA-A * 3101 gene positive caused by carbamazepine. She took carbamazepine for trigeminal neuralgia and had never taken the drug before. After 2 weeks, papules and edematous target-like erythema gradually appeared on the trunk and limbs, surface blisters and scabs, and the oral, eyes, and vulvar mucosa appeared erosion, accompanied by fever and pain, with an area of about 3% exfoliation. She was diagnosed with Stevens-Johnson syndrome and admitted to Peking University Third Hospital on March 24, 2020. After admission, in order to identify the sensitizing drugs, We performed a genetic test on her for carbamazepine-related drugs. The results showed that the HLA-A * 3101 gene was positive, and the HLA-B * 1502 and HLA-B * 5801 genes were negative. In terms of treatment, the patient was systematically given a single intravenous infusion of 300 mg of infliximab, and symptomatic treatment and care of the oral, eye, and vulvar mucosa. After 6 days, the rash on the trunk and limbs subsided, and the mucosa returned to normal and was discharged from the hospital. Retrieving domestic and foreign literature, it is not uncommon to report that carbamazepine causes drug eruption, including severe drug eruption, and there are obvious ethnic differences in the pathogenicity of HLA genotyping. In China and Asia, stu-dies on carbamazepine causing Stevens-Johnson syndrome emphasized that the adverse reactions were strongly related to the HLA-B * 1502 gene. However, there is a strong correlation with HLA-A * 3101 gene in people suffering from the disease in Europe and Japan. In this case report, the HLA-B * 1502 gene was negative and the HLA-A * 3101 gene was positive. This is the first domestic report that carba-mazepine causes HLA-A * 3101 positive for Stevens-Johnson syndrome. This report reminds that HLA-A * 3101 gene testing should be taken seriously besides HLA-B * 1502 gene.

Phenylephrine is a sympathomimetic, which means it acts analogous to adrenaline. Phenylephrine can be taken orally to treat nasal congestion symptoms. It is also frequently mixed with other medicines in products meant to relieve cough and cold symptoms. Given the widespread usage of phenylephrine, related drug eruptions appear to be uncommon.
Here we discuss a case of a 19-year-old female patient who reported to our hospital with blebs on the skin throughout her legs and torso. The drug eruption or adverse drug response was linked with itching, had a slow beginning, and progressed. Her medical history indicated that she had been taking phenylephrine 10 mg orally twice a day. On the sixth day, she experienced an adverse medication response caused by the medicine phenylephrine. Phenylephrine was stopped immediately and the other medications, such as levocetirizine, montelukast, and nasal spray, were continued. The patient was told not to use phenylephrine, either alone or in combination with FDCs. There are no other complaints. As a result, the patient was diagnosed with phenylephrine- induced eruption.
We present this case to highlight the importance of inspiring a pharmacovigilance mindset among all clinicians providing care as a routine alert drug, phenylephrine-induced drug eruption.

Stevens-Johnson syndrome (SJS) typically involves a skin rash, mucositis, and conjunctivitis. Previous reports of SJS without skin manifestations affect children and are usually associated with Mycoplasma pneumoniae infection. We present a rare case of oral and ocular SJS without skin lesions in a healthy adult after exposure to azithromycin without mycoplasma pneumonia infection.