Drug-Induced Sweet‘s Syndrome

Kim

Knee Surg Sports Traumatol Arthrosc

et al. 2017

Sweet's syndrome (SS) or acute febrile neutrophilic dermatosis is an uncommon condition. It is characterized by fever, polymorphonuclear leukocytosis, painful erythematous cutaneous plaques, and dense dermal infiltrate of neutrophils without vasculitis at the site of skin lesions. Lesions in SS might enlarge and coalesce with increasing dermal oedema, resulting in pseudo-vesicular appearance mimicking joint infections. Here, a rare case of SS mimicking acute haematogenous periprosthetic infection in a 74-year-old woman with a history of total knee arthroplasty is reported. This report aims to elaborate clinical various manifestations of SS in a patient with a history of total knee arthroplasty. In addition, this report describes how to discriminate inflammation between SS and periprosthetic joint infection. Level of evidence V.

“…It affects middle-aged woman. Skin lesions usually appear 5-7 days after the first administration of the offending drug [14]. The fever will subside at 1-3 days after drug cessation.…”

Section: Discussionmentioning

confidence: 99%

Sweet’s syndrome: a clinical entity need to discriminate against acute haematogenous periprosthetic joint infection

Kim

Knee Surg Sports Traumatol Arthrosc

et al. 2017

“…Drug-induced SS was first reported in 1986, attributed to trimethoprim-sulfamethoxazole [ 23 ]. Although several hundred cases of SS have been reported in the literature, reviews report that drug-induced SS can make up anywhere from 1 to 27% of cases [ 15 , 24 ]. Currently, the most common instigating drug is G-CSF, although cases secondary to non-steroidal anti-inflammatory drugs, antivirals, antibacterials, and several other drug groups have also been reported [ 13 ].…”

Section: Sweet’s Syndromementioning

confidence: 99%

“…Initial symptoms of SS typically present several days after upper respiratory tract infection of acute gastroenteritis [ 28 ]. Case reports of drug-related SS demonstrate disease onset anywhere from 5 to 10 days of therapy onset with a general consensus of SS onset within 2 weeks of inciting drug exposure [ 19 , 24 ]. Cutaneous manifestations can be preceded by several days to weeks of isolated fever and can occur concurrently during the entire course of dermatosis.…”

Section: Sweet’s Syndromementioning

confidence: 99%

Neutrophilic Dermatosis and Management Strategies for the Inpatient Dermatologist

et al. 2022

Purpose of Review Neutrophilic dermatoses are a heterogeneous group of disorders with significant overlap in associated conditions, clinical presentation, and histopathologic features. This review provides a structural overview of neutrophilic dermatoses that may present in the inpatient setting along with diagnostic work-up and management strategies. Recent Findings Sweet’s syndrome has been found in patients with coronavirus disease 2019 (COVID-19). Pyoderma gangrenosum (PG) has been shown to be equally associated with ulcerative colitis and Crohn’s disease. A clinical trial shows that cyclosporine is equally effective as prednisone in treating PG. Neutrophilic eccrine hidradenitis has been found in the setting of newer antineoplastic medications, such as BRAF inhibitors, as well as in the setting of malignancy without chemotherapy exposure. Summary Neutrophilic dermatoses are a rare and complex group of dermatoses with varying and overlapping clinical presentations. Physicians should be aware of the growing list of associated diseases in order to build a better differential diagnosis or to potentially investigate for co-existing disease.

“…This inevitably could result in adverse reactions in particular with long-time use [4]. Due to their widespread distribution within the body, these drugs may even cause some side effects on bone marrow [5,6], blood [7], skin [8], and other tissues [9]. Consequently, to meet the clinical requirements, some therapies such as repair of the intestinal mucosal barrier, balancing the gut microbiota, or specific and targeted distribution are usually considered as the strategy for new courses of treatment.…”

Section: Introductionmentioning

confidence: 99%

Study on the Anti-Ulcerative Colitis Effect of Pseudo-Ginsenoside RT4 Based on Gut Microbiota, Pharmacokinetics, and Tissue Distribution

Yu,

Wang,

et al. 2024

IJMS

The purpose of this study was to explore the therapeutic effect of the oral administration of pseudo-ginsenoside RT4 (RT4) on ulcerative colitis (UC), and to determine the rate of absorption and distribution of RT4 in mice with UC. Balb/c mice were induced using dextran sulfate sodium salts (DSS) to establish the UC model, and 10, 20, or 40 mg/kg of RT4 was subsequently administered via gavage. The clinical symptoms, inflammatory response, intestinal barrier, content of total short-chain fatty acids (SCFAs), and gut microbiota were investigated. Caco-2 cells were induced to establish the epithelial barrier damage model using LPS, and an intervention was performed using 4, 8, and 16 µg/mL of RT4. The inflammatory factors, transient electrical resistance (TEER), and tight-junction protein expression were determined. Finally, pharmacokinetic and tissue distribution studies following the intragastric administration of RT4 in UC mice were performed. According to the results in mice, RT4 decreased the disease activity index (DAI) score, restored the colon length, reduced the levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β), and boosted the levels of immunosuppressive cytokine IL-10, increased the content of SCFAs, improved the colonic histopathology, maintained the ultrastructure of colonic mucosal epithelial cells, and corrected disturbances in the intestinal microbiota. Based on the results in caco-2 cells, RT4 reduced the levels of TNF-α, IL-6, and IL-1β; protected integrity of monolayers; and increased tight-junction protein expression. Additionally, the main pharmacokinetic parameters (Cmax, Tmax, t1/2, Vd, CL, AUC) were obtained, the absolute bioavailability was calculated as 18.90% ± 2.70%, and the main distribution tissues were the small intestine and colon. In conclusion, RT4, with the features of slow elimination and directional distribution, could alleviate UC by inhibiting inflammatory factors, repairing the intestinal mucosal barrier, boosting the dominant intestinal microflora, and modulating the expression of SCFAs.