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UNASSIGNED: Blood eosinophilia is often associated with various dermatoses, such as atopic eczema, urticaria, drug eruption, bullous pemphigoid, and hypereosinophilic syndrome (HES). Differential diagnosis is very challenging due to the similarities of clinical and pathological characteristics.
UNASSIGNED: To investigate and analyze the clinical characteristics of dermatoses associated with blood eosinophilia (DABE) to further optimize disease management.
UNASSIGNED: We conducted a retrospective analysis on 397 DABE patients with blood absolute eosinophil count (AEC) greater than or equal to 0.5×109/L. Clinical characteristics, laboratory values, treatment course, and associated diagnoses were evaluated. All DABE patients were grouped based on the severity of eosinophilia as mild group (0.5 ≤ AEC×109/L < 1.5), moderate group (1.5 ≤ AEC×109/L < 3), and severe group (AEC×109/L ≥ 3).
UNASSIGNED: Our study revealed three distinct patterns: (1) Mild eosinophilia associated with localized skin lesions, atopic history, mildly elevated total serum IgE level, diagnosed with eczema/dermatitis, and frequent antihistamines use. (2) Moderate eosinophilia has the characteristics of both mild group and severe group. (3) The severe eosinophilia group had a high proportion of elderly people without atopic history, but with acute onset, generalized skin lesions, and high level of lactate dehydrogenase, and the majority of them were diagnosed with systemic diseases (HES or tumor).
UNASSIGNED: We summarize the clinical rules of dermatoses associated with blood eosinophilia, hoping to facilitate the diagnosis and treatment for patients.

Graves\' disease (GD) and drug eruption are closely associated and frequently observed in the clinical setting. However, it remains unclear whether a causal relationship exists between these two conditions. The aim of the study is to investigate whether GD is causal to drug eruptions using two-sample Mendelian randomization.
We launched a two-sample MR to investigate whether GD is causal to drug eruption using Genome-wide association study (GWAS) summary data from Biobank Japan and FinnGen. Genetic variants were used as instrumental variables to avoid confounding bias. Statistical methods including inverse variance weighted (IVW), weighted median, MR-Egger, and MR-PRESSO were conducted to identify the robustness of the causal effect.
Genetically predicted GD may increase the risk of drug eruption by 30.3% (OR=1.303, 95% CI 1.119-1.516, p<0.001) in the Asian population. In European populations, GD may increase the generalized drug eruption by 15.9% (OR=1.159, 95%CI 0.982-1.367, p=0.080).
We found GD is potentially causal to drug eruption. This finding expanded the view of the frequently observed co-existence of GD and adverse drug reactions involving the skin. The mechanism remains for further investigation.

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.

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.

BACKGROUND: The clinical manifestations of drug eruption are complex and diverse, which can lead to missed diagnosis or misdiagnosis. The clinical manifestations of drug eruption caused by compound honeysuckle have not been reported.
METHODS: A 20-year-old man was admitted to our department of dermatology due to erythema and papules on the chest and abdomen with pruritus for 3 d. The next day after taking compound honeysuckle granules, the patient suddenly developed a rash and intense itching on his chest and abdomen. Physical examination revealed diffuse red needle-cap size macules and papules with well-defined borders on the chest and abdomen, and discoloration after finger pressure. No abnormality was observed in other areas of the skin. Back skin scratch was positive. White blood cells, eosinophil count and eosinophil ratio were higher than normal. Histopathological examination of the skin lesions on the left abdomen revealed intercellular edema, blurred focal basal cell layers, and focal lymphocyte infiltration in the superficial dermis and perivascular areas. Immunohistochemistry showed CD3+ , CD4+ and CD8+ T lymphocytes. The diagnosis was drug eruption with special manifestations induced by compound honeysuckle. The skin lesions completely subsided without pruritus after 2 wk of antihistamine and hormone therapy. Follow-up for > 1 mo showed no recurrence.
CONCLUSIONS: Chinese patent medicine compound honeysuckle granules can induce allergic reaction and rare skin damage.

Acute generalized exanthematous pustulosis is a severe, usually drug-related reaction, characterized by an acute onset of mainly small non-follicular pustules on an erythematous base. Most cases of acute generalized exanthematous pustulosis (AGEP) clear quickly with a systemic corticosteroid, but severe or recalcitrant cases may need other systemic therapies. In this case, a man in his 40 s with a history of psoriasis consulted a physician about widespread erythema, pustules, target lesions, and fever after the administration of a quadruple antituberculosis drug. Routine laboratory testing revealed elevated white blood cell count and C-reactive protein. The histopathology showed subcorneal pustules, spongiosis as well as lymphocyte and eosinophils infiltration in the dermis. The patient was diagnosed with definitive AGEP according to the diagnostic score from the EuroSCAR study. Cutaneous lesions especially pustules and erythema multiforme-like lesions on the upper arms and palms are crucial for distinguishing AGEP from Generalized pustular psoriasis. The patient was treated with secukinumab as a result of his failure to respond to topical corticosteroids and constrain of systemic steroids. Remission with secukinumab therapy was safe without increased risks of infections. This case indicates that secukinumab is a potential therapy that can rapidly improve the clinical symptoms of AGEP.

OBJECTIVE: Enzalutamide is the most frequently prescribed compound for treating metastatic castration-resistant prostate cancer (mCRPC). Common adverse drug events of enzalutamide are febrile neutropenia, hot flashes, hypertension, and fatigue.
METHODS: We present a case of a patient with mCRPC who received enzalutamide and developed Stevens-Johnson syndrome (SJS). The culprit drug was confirmed using the Naranjo Adverse Drug Reaction Probability Scale. Clinical characteristics and management principles were analyzed in combination with literature reports.
RESULTS: SJS occurred within two weeks of enzalutamide therapy. Supportive care such as steroid treatment led to a complete resolution of skin lesions and improved clinical symptoms after three weeks.
CONCLUSIONS: Most cutaneous adverse events occur early during enzalutamide therapy, and close observation should be given within two weeks of starting treatment.

BACKGROUND: To explore the clinical manifestations, diagnosis, and treatment of patients with acquired immunodeficiency syndrome (AIDS) complicated with drug-induced erythroderma.
METHODS: The clinical data of 12 AIDS patients with drug-induced erythroderma in our hospital were retrospectively analyzed. The general information, offending medications, complications, modified severity-of-illness score for toxic epidermal necrolysis (SCORTEN) scores, and disease outcome spectrums were analyzed.
RESULTS: Drug-induced erythroderma was mostly caused by antiviral drugs, antituberculosis drugs, antibiotics, traditional Chinese medicine, and immune checkpoint inhibitors. The spectrum of sensitizing drugs was broad, the clinical situation was complex, and infections were common. The affected areas were greater than 40% body surface area in all patients. The modified SCOTERN score averaged 3.01±0.99. All patients were treated with glucocorticoids, and nine patients were treated with intravenous immunoglobulin (IVIG) pulse therapy at the same time. The average time to effectiveness was 7.08±2.23 days, and the average hospital stay was 17.92±8.46 days. Eleven patients were cured, and one patient died of secondary multiple infections, who had a modified SCORTEN score of 5 points. The mortality rate in this study was 8.3%.
CONCLUSIONS: The clinical situation of AIDS patients with drug-induced erythroderma in hospitalized patients is complex and the co-infection rate is high. The use of modified SCORTEN score may objectively and accurately assess the conditions, and the use of glucocorticoid combined with IVIG therapy may improve the prognosis.

Severe drug eruption (SDE), a common skin disease, becomes dangerous when it occurs in patients with human immunodeficiency virus (HIV). However, the molecular mechanisms are poorly understood. Forty patients including HIV+ SDE+ (n = 15), HIV- SDE+ (n = 15) and HIV+ SDE- (n = 10) subjects were enrolled in our study. All HIV+ patients were at acquired immune deficiency syndrome (AIDS) stage. Serum levels of TNF-α, IFN-γ, IL-4, IL-13, IL-6, CXCL9, and CCL17 were quantified by ELISA. Epstein-Barr virus (EBV) and cytomegalovirus (CMV) loads were quantified by RT-qPCR. CD4, CD8, Th1, Th2, TNF-α-CD8, and IFN-γ-CD8 T cell populations were measured by flow cytometry. Levels of biochemical indexes in HIV+ SDE+ patients were significantly different from in HIV- SDE+ patients (P < .05). EBV and CMV viral loads were significantly higher in HIV+ SDE+ patients, but not in HIV- SDE+ patients (P < .05). Inflammatory cytokines TNF-α and IFN-γ were significantly elevated in HIV+ SDE+ patients (P < .05). Th2/Th1 populations and TNF-α secreting or IFN-γ secreting CD8+ T cells, were significantly up-regulated in HIV+ SDE+ patients compared to HIV- SDE+ patients (P < .05). Conversely, the CD4/CD8 ratio was significantly down-regulated in HIV+ SDE+ patients compared to HIV- SDE+ patients (P < .05). HIV infection confers distinct clinical phenotypes and immune inflammatory mechanisms in SDE. Sustained EBV and CMV activation, unbalanced Th2/Th1 and overactive CD8+ T cells mediating a pro-inflammatory response could act as distinct mechanisms in the aggravation of SDE in HIV+ SDE+ patients.