Compound-honeysuckle-induced drug eruption with special manifestations:A case report

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.CASE SUMMARY 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 welldefined 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.CONCLUSION Chinese patent medicine compound honeysuckle granules can induce allergic reaction and rare skin damage.

Delayed hypersensitivity reaction resulting in maculopapular-type eruption due to entecavir in the treatment of chronic hepatitis B

Several clinical trials have demonstrated the potent antiviral efficacy of entecavir (ETV), and this relatively new nucleoside analogue drug has rapidly become a frequently prescribed therapy for chronic hepatitis B (CHB) worldwide. While the studies have also shown a good overall safety profile for ETV, adverse drug reactions (ADRs) in patients with advanced cirrhosis have been reported and represent a broad spectrum of drug-induced injuries, including lactic acidosis, myalgia, neuropathy, azotemia, hypophosphatemia, muscular weakness, and pancreatitis, as well as immune-mediated responses (i.e., allergic reactions). Cutaneous ADRs associated with ETV are very rare, with only two case reports in the publicly available literature; both of these cases were classified as unspecified hypersensitivity allergic (type I) ADR, but neither were reported as pathologically proven or as evaluated by cytokine release analysis. Here, we report the case of a 45-year-old woman who presented with a generalized maculopapular rash after one week of ETV treatment for lamivudine-resistant CHB. The patient reported having experienced a similar skin eruption during a previous three-month regimen of ETV, for which she had self-discontinued the medication. Histopathological analysis of a skin biopsy showed acanthotic epidermis with focal parakeratosis and a perivascular lymphocytic infiltrate admixed with interstitial eosinophils in the papillary and reticular dermis, consistent with a diagnosis of drug sensitivity. A lymphocyte stimulation test showed significantly enhanced IL-4, indicating a classification of type IVb delayed hypersensitivity. The patient was switched to an adefovir-lamivudine combination regimen and the skin eruption resolved two weeks after the ETV withdrawal. This case represents the first pathologically and immunologically evidenced ETV-induced delayed type hypersensitivity skin reaction reported to date. Physicians should be aware of the potential, although rare, for cutaneous ADRs associated with ETV treatment.

Drug-induced erythroderma in patients with acquired immunodeficiency syndrome

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.

Two cases of childhood absence epilepsy who showed seizure disappearance after ethosuximide drug eruption

Background Recent studies suggest potential roles of immune response in the pathophysiology of epilepsy.Anti-seizure medications(ASMs)are known to have side effects of drug eruption caused by immune responses.A few reports in adults have demonstrated disappearance of seizures after an ASM drug eruption episode.In this paper,we described 2 cases of childhood absence epilepsy(CAE)who showed seizure disappearance after ethosuximide(ESM)drug eruption,suggesting the possibility that the epilepsy disappears due to immune responses to ASM.Case presentation Case 1 was an 8-year-old girl diagnosed with CAE.She was treated with valproate acid(VPA)initially,and then ESM was administered as an additional treatment.Her epileptic seizure disappeared 4 days after initiation of ESM.However,drug eruption appeared 1 week after the administration of ESM.Even after discontinuation of ESM administration,she maintains no seizure after the drug eruption.Case 2 was a 5-year-old boy diagnosed as CAE.He was treated with VPA initially,and ESM was administered additionally.Drug eruption appeared 1 month after the administration of ESM.Even after ESM was terminated,he maintained seizure freedom after the appearance of eruption.Conclusions Epileptic seizures may have been suppressed due to the immune responses caused by ASM eruption.Further studies are needed to elucidate the pathophysiologic effects of drug eruption on epilepsy through immune responses.

Severe cutaneous adverse drug reactions： a review on epidemiology, etiology, clinical manifestation and pathogenesis

Purpose To review the current progress in epidemiology, etiology, clinical manifestation, and pathophysiology of severe cutaneous adverse drug reactions （SCADRs）. Data sources Data were acquired by using Blackwell-Synergy, PubMed, original articles published in the main Chinese journals and related medical textbooks materials. Study selection and data extraction Throughout the literature review 49 articles were selected. Results SCADRs cases are rare, however, the implication is life threatening with significant mortality rates. Epidemiology studies have shown various incidences from different regions, gender, age, race and concurrent illness. There are typical signs and symptoms for each type of SCADRs, but this is not always so. Drugs associated with inducing SCADRs are anticonvulsants, antibiotics, NSAIDs and antirheumatic drugs. In some countries, especially in Asia, traditional drugs are often the cause of SCADRs. Genetic polymorphisms and viral infections are predisposition factors of SCADRs. Patients with certain genetic alleles and underlying diseases are vulnerable to SCADRs. The exact pathogenesis of SCADRs is not well defined. Nonetheless, recent study showed that reactive metabolites and immunological processes have a significant role in SCADRs. Conclusions The different SCADRs reactions are attributed by different intrinsic factors, such as genetic polymorphisms, gender, age and race as well as extrinsic factors, such as underlying diseases. Different regions and culprit drugs also play a role in the various types of SCADRs.