Drug-induced hypersensitivity syndrome (DIHS) is a severe, potentially life-threatening adverse drug reaction marked by a prolonged latency period and frequent relapses, posing significant challenges for early clinical recognition.

To analyze the clinical characteristics, distribution of culprit drugs, laboratory abnormalities, and prognostic factors in patients with drug-induced hypersensitivity syndrome (DIHS), so as to provide evidence for early clinical identification and treatment.

Clinical data were collected from patients with DIHS who were hospitalized in the Department of Dermatology, the First Medical Center of PLA General Hospital from January 2015 to December 2025. Patients with a RegiSCAR score ＞5 were defined as confirmed cases. The demographic characteristics, culprit drugs, clinical manifestations, laboratory findings, treatment, and outcomes of the patients were analyzed.

A total of 34 patients diagnosed with DIHS were enrolled in this study, including 16 males and 18 females, with a mean age of (43.6±16.5) years. Most patients (76.5%) were aged between 30 and 55 years. The incubation period of the disease ranged from 2 to 60 days, with a median of 21 (IQR: 11 - 30) d. In terms of clinical manifestations, aside from skin rash, liver function impairment had an extremely high incidence (28 cases, 82.4%). The main causative sensitizing drugs included antibacterial agents (12 cases, 35.3%), traditional Chinese medicine (7 cases, 20.6%), anti-gout drugs (5 cases, 14.7%), and anti-epileptic drugs (4 cases, 11.8%), antipyretic and analgesic agents in 2 cases (5.9%),antidepressant medications in 2 cases (5.9%),additionally, 1 case was induced by an immunosuppressant and 1 case by a biological agent. Laboratory examinations revealed leukocytosis in 24 cases (70.6%) and eosinophilia in 17 cases (50.0%). Concomitant viral or pathogen infections were detected as follows: cytomegalovirus infection in 14 cases (41.2%), herpes simplex virus infection in 12 cases (35.3%), Epstein-Barr virus positive infection in 11 cases (32.4%), rubella virus positive infection in 9 cases (26.5%), Coxsackievirus positive in 1 case (2.9%), and mycoplasma pneumoniae positive in 4 cases (11.8%). All patients received glucocorticoid therapy, and nearly half (16 cases, 47.1%) received combined treatment with intravenous immunoglobulin. All 34 patients achieved short-term clinical remission after treatment, with an overall response rate of 100%; during long-term follow-up, 27 cases (79.4%) were cured and 7 cases (20.6%) experienced recurrence. The incubation period of the recurrence group was significantly longer than that of the non-recurrence group ([34.9±19.0] d vs [20.2±11.4] d, P=0.015).

DIHS cases in our center are characterized by a relatively long latency period. Antibacterials and traditional Chinese herbal medicines are the predominant culprit drugs, and liver function impairment is common. Early recognition, prompt withdrawal of the offending drug, and administration of systemic corticosteroids yield definite therapeutic efficacy. Viral infections may be associated with disease relapse, although the value of antiviral therapy remains to be validated.

Traumatic brain injury (TBI) is a major global cause of long-term disability, with mild-to-moderate cases often leading to persistent neurological deficits. Current pharmacological interventions are limited by the blood-brain barrier and systemic side effects.

This study aims to investigate the therapeutic potential of exosomes (Exos) derived from tumor necrosis factor ɑ (TNFα) preconditioned fibroblast-like mesenchymal stem cells (FMSCs) for moderate TBI and compare their efficacy with untreated exosomes.

A mouse TBI model was established by closed-capsule blast shock wave injury. A total of 68 male mice were randomly divided into four groups (17 mice in each group): Sham group, TBI group, TBI+Exos group and TBI+TNFα-Exos group. Frontal bone-derived FMSCs were preconditioned with TNFα for 48 h. Exos were isolated and purified using the OMEGA kit. Mice in the TBI, TBI+Exos and TBI+TNFα-Exos groups were subjected to TBI modeling, and intranasal administration was performed 1 h after modeling. Y-maze alternation test and nesting test were used to evaluate the recovery of behavioral function after Exos intervention. PKH67 fluorescence labeling was applied to observe the in vitro cellular uptake and intracerebral distribution of Exos. An inflammatory model of mouse microglial BV2 cells was induced by lipopolysaccharide (LPS), and cells were divided into Control group, LPS group, Exos group and TNFα-Exos group. qRT-PCR was adopted to detect the expression levels of pro-inflammatory factors TNFα, interleukin-1β (IL-1β) and interleukin-6 (IL-6) in vitro.

Behavioral tests showed that the spontaneous alternation rate of the Y-maze was markedly increased in the Exos and TNFɑ-Exos groups compared to the TBI model group (P＜0.05). Nesting ability was significantly reduced in the TBI group compared with the Sham group, while notable improvements were observed in the Exos and TNFɑ-Exos groups (P＜0.05). qRT-PCR results demonstrated that the expression levels of pro-inflammatory factors in microglia were significantly decreased in the Exos and TNFɑ-Exos groups compared with the LPS group (P＜0.05). Furthermore, the TNFα-Exos group showed better improvements in the above indicators than the Exos group, and the difference was statistically significant (P＜0.05).

TNFα-preconditioned MSC-derived Exos exhibit favorable neuroprotective potential for early intervention in mild-to-moderate traumatic brain injury. Compared with conventional Exos, TNFα-Exos show superior effects in downregulating pro-inflammatory factors and improving cognitive function, which provides experimental evidence for the early treatment of military blast-induced brain injury.