Giant cell arteritis (GCA) can result in visual loss and other sequelae. An 81-year-old man presented with a one-week history of fever. He had bilateral temporal headache, jaw claudication, tenderness of the temporal arteries and a recent skin rash. A temporal artery biopsy showed typical GCA, but the symptoms were self-limiting. We continued close observation, without administering prednisolone treatment. Five months later, the symptoms did not recur, and prednisolone again was not administered. Our patient presented with an atypical course of GCA that created a clinical dilemma. The final diagnosis was self-limiting GCA.

Rash and fever are some of the most common chief complaints present in paediatric dermatology emergencies. The spectrum of differential diagnosis is broad, including many different infectious and some non-infectious agents. A systematic approach involving detailed history taking, careful clinical examination along with particular attention to epidemiological features are the most important factors to make a diagnosis. This article reviews the morphological patterns of various causes of fever with rash in children, including infectious as well as non-infectious causes, with special emphasis on the Indian scenario. We intend to highlight the clinical characteristics of each cause, which will not only help make a clinical diagnosis but also distinguish benign versus life-threatening causes of skin rash in febrile paediatric patients and provide early medical intervention.

A 40-year-old male with a history of human immunodeficiency virus (HIV) (CD4 absolute count 57 cells/uL) presented to the Emergency Department complaining of large, swollen abscesses on his face, right hand, and feet. He reported the outbreak of the lesions occurred four months ago and coincided with a week-long episode of diarrhea, rectal pain, and perirectal and inguinal lymphadenopathy. Physical exam was significant for a full-thickness fluid collection on the sole of the right foot, a plantar abscess on the left foot, an open, crusted ulcer on the left fifth finger, and several large, crusted lesions on the face. Of note, the patient was seen at a nearby hospital three months prior, underwent a biopsy that showed non-variola orthopoxvirus DNA via real-time polymerase chain reaction (PCR), and was diagnosed with monkeypox at that time. He was advised to pick up tecovirimat treatment from the Department of Health but stated it was unavailable when he arrived and never took it. On this admission, the lesion was again biopsied and detected non-variola orthopoxvirus DNA by real-time PCR. The patient was discharged on 600 mg tecovirimat orally twice daily for 14 days. At the 14-day follow-up, the patient\'s lesions had completely fallen off and were no longer painful.

UNASSIGNED: The precise management of hypersensitivity reactions to direct oral anticoagulants (DOACs) and the potential for cross-reactivity among different DOACs remain unclear. In such cases, switching between DOACs may be feasible and could be considered, but close monitoring for adverse effects is essential, tailored to individual patient responses and tolerability.
UNASSIGNED: Hypersensitivity reactions to DOACs, though considered rare, have been documented. This report describes the case of a 28-year-old male with a history of testicular cancer who was recently diagnosed with deep vein thrombosis. He was referred to an outpatient pharmacotherapy clinic due to suspected rivaroxaban-induced cutaneous reactions. Following a thorough evaluation, his anticoagulant therapy was switched from rivaroxaban to apixaban. This change was successfully implemented, and no hypersensitivity symptoms recurred during subsequent follow-up. This case demonstrates the importance of recognizing potential adverse reactions to DOACs and illustrates the feasibility of switching anticoagulants under close medical supervision to ensure patient safety and effective treatment.

Antibody-drug conjugates (ADCs) are an emerging class of anticancer agents that combine targeting antibodies with potent cytotoxic agents. Their molecular configuration allows for increased therapeutic efficacy and reduced adverse-effect profiles compared to monoclonal antibodies or cytotoxic chemotherapy alone. ADCs cause off-target toxicities through several mechanisms, including premature deconjugation of the cytotoxic agent in the serum and the presence of the targeted antigen on normal tissues. Given cutaneous adverse events comprise 31.3% of all-grade adverse events in clinical trials involving ADCs, dermatologists are increasingly called upon to manage the cutaneous toxicities caused by these drugs. In this review, we summarize known cutaneous toxicities of the ADCs that have been approved for use by the US Food and Drug Administration to date. Dermatologists can play a key role in recognizing cutaneous reactions associated with ADCs, contributing to guidelines for their management, and aiding during clinical trials to generate detailed morphologic and histopathologic descriptions of cutaneous toxicities caused by ADCs.

Tebentafusp is a gp100xCD3 bispecific ImmTAC designed to redirect polyclonal T cells against cells presenting the melanocyte lineage specific antigen gp100 on HLA-A*02:01. Skin-related adverse events, predominantly rash, are frequent and occur within a few hours after initial infusions, yet the mechanisms are unknown. Here we analysed clinical data from the randomised phase 3 trial (NCT03070392) of tebentafusp (n=252) versus investigator\'s choice (n=126). Translational analyses were performed on paired on-treatment skin samples from 19 patients collected in the phase 1 trial (NCT01211262). Our analyses showed that rash is a clinical manifestation of tebentafusp-induced recruitment of T cells to cutaneous melanocytes. Development of rash depended on baseline expression levels of gp100 and other melanin pathway genes in the skin. On treatment, melanocyte number was reduced and expression of melanocytic genes decreased, while gene expression related to immunity and cytokine signalling increased. When adjusted for baseline prognostic features, patients with rash within the first week of tebentafusp treatment had the same overall survival compared to patients without a rash in the phase 3 randomized trial IMCgp100-202 (HR 0.84; 95% CI 0.53-1.32). In summary, skin rash is an off-tumour, on-target effect of tebentafusp against gp100+ melanocytes, in line with the mechanism of action.

BACKGROUND: Membranous nephropathy (MN) is a common type of nephrotic syndrome (NS) in adults, accounting for about 20-30% of cases. Although secondary to specific factors, the coexistence of MN and mantle cell lymphoma (MCL) has been scarcely reported in clinical literature.
METHODS: A 59-year-old Chinese male was admitted to the hospital with a generalized pruritic rash with bilateral lower extremity edema, which did not improve significantly after symptomatic treatment. He had undergone renal biopsy, and the diagnosis was thought to be secondary MN (SMN), therefore, we did a lymph node biopsy on the patient and found that MN was complicated with MCL. Soon after, the patient was admitted to the hematology department for a BR chemotherapy regimen (composed of bendamustine 90 mg/m2 BSA (body surface area), rituximab 375 mg/m2 BSA and dexamethasone 5 mg), and during the post-treatment follow-up, both his symptoms and renal function improved.
CONCLUSIONS: The mechanism underlying the combination of SMN and MCL remains elusive and exceedingly rare, consequently often overlooked in clinical practice. This case serves to offer valuable clinical insights for diagnosis and treatment, while emphasizing the pivotal role of renal pathology in clinical assessment.

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BACKGROUND: Rash is one of common adverse drug reaction and which have been reported in typical and atypical antipsychotics. Reports of lurasidone induced skin reactions are sparse. In this study, we report a case of rash caused by lurasidone.
METHODS: A 63-year-old man with bipolar disorder (BD) who is treated by lurasidone. However, the patient presents a rash all over after lurasidone dose increasing from 40 mg/day to 60 mg/day. With the diagnosis of drug induced rash, lurasidone was discontinued, and the rash complete disappears within 2 weeks. In addition, all case reports about antipsychotics associated rash were reviewed by searching English and Chinese database including Pubmed, Embase, Cochrane Library, CNKI and Wanfang database. A total of 139 articles contained 172 patients were included in our study. The literature review and our case suggest that the cutaneous adverse events caused by antipsychotic drugs should not be ignored, particularly for the patient who was first use or at dose increasing of antipsychotic.
CONCLUSIONS: In conclusion, we report a case of lurasidone related rash and review rash caused by antipsychotics. Psychiatrists should be alert to the possibility of the rash caused by antipsychotics, especially the patient was first use of antipsychotics or the antipsychotic dose was increasing.

UNASSIGNED: Few studies have analysed oxaliplatin-induced adverse events (ADEs) in the immune system and skin and subcutaneous tissues through pharmacovigilance. We used this approach to analyse the risk of such ADEs when oxaliplatin combined with immune checkpoint inhibitors (ICIs).
UNASSIGNED: We evaluated the association between oxaliplatin and ADEs in the immune system and skin and subcutaneous tissues using the reporting odd ratio (ROR) for mining the ADE report signals in the FDA Adverse Event Reporting System database. Risk factors were analyzed using a binary logistic regression analysis using the sex and age of the patients.
UNASSIGNED: There were 40,474 reports of oxaliplatin as primary suspect drug or second suspect drug. The signal intensities of ADEs such as type II hypersensitivity, type I hypersensitivity, type III immune complex-mediated reaction, anaphylactoid shock and cytokine release syndrome were high in PTs classified by SOC as immune system disorders; in the PTs classified as skin and subcutaneous tissue disorders by SOC, the signal intensities of ADEs such as skin toxicity, skin reaction, rash maculo-papular and skin fissures were higher. In the risk assessment between the two groups, rash showed an increased risk in the oxaliplatin-ICI group, with an OR of 1.96. Nivolumab in combination with oxaliplatin had an OR of 2.196 and an adjusted OR of 2.231. Combined with pembrolizumab, OR was 2.762 and the adjusted OR was 2.678.
UNASSIGNED: Type II hypersensitivity shows a stronger pharmacovigilance signal. Oxaliplatin in combination with nivolumab or pembrolizumab has been shown to increase the risk of rash.