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Sweet's syndrome (or acute febrile dermatosis) is a neutrophilic dermatosis with a characteristic presentation encompassing specific clinical (fever and erythemato-violaceous oedematous papules, plaques and nodules), laboratory (neutrophilia and increased inflammatory markers), and histological (dermal neutrophilic infiltrate without vasculitis) features. Its pathophysiology is poorly understood but there seems to be an auto-inflammatory component related to mutations in inflammasome genes. It has been subdivided into its classic form, malignancy-associated, and drug-induced, according to its aetiology. The condition usually responds rapidly to steroid therapy, but recurrences are common. This report presents an extremely rare case of hydroxychloroquine-induced Sweet's syndrome, plus a review of the literature, which encompasses 3 previous cases of Sweet's syndrome induced by hydroxychloroquine and 1 induced by chloroquine. Despite being relatively easy to diagnose, aetiological investigation poses challenges to the clinician, especially in the elderly population, as several confounding factors might be present. Further studies are necessary to shed light on the pathophysiology behind this entity, to further facilitate diagnostic workup and treatment strategies.

Sweet syndrome, also known as acute febrile neutrophilic dermatosis, is a rare inflammatory skin condition associated with the sudden onset of high-grade fever, painful rashes usually on the upper body, leukocytosis and neutrophilia. Approximately 21% of patients with Sweet syndrome have a concurrent malignancy, 80% of which are linked to haematological diseases, especially myelodysplastic syndrome and acute myeloid leukaemia. This is a case report of a woman in her 50s who was recently diagnosed with acute myeloid leukaemia and was started on decitabine 20 mg/m 2 (40 mg). She complained of fever, multiple hyperpigmented nodules over her limbs with pus, swelling with erythema over the right eye and erosion over the tongue 2 days after her first round of chemotherapy. The condition was diagnosed as Sweet syndrome owing to the presence of fever, leukocytosis, elevated erythrocyte sedimentation rate and neutrophil-dense infiltrates on skin biopsy. The patient was symptomatically treated, and decitabine was dechallenged. The patient started recovering after 4 days and was discharged. On follow-up, chemotherapy with other agents were not reinitiated because of the adverse reaction which ultimately led to the patient's death., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2024. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Acute febrile neutrophilic dermatosis, also commonly referred to as Sweet syndrome, is often associated with tumors, infections, immune disorders and medications. FLT3 inhibitor-induced Sweet syndrome is a rare complication., Methods and Results: We report a patient with relapsed and refractory acute monocytic leukemia harboring high-frequency FLT3-ITD and DNMT3a mutations. The FLT3 inhibitor gilteritinib was administered for reinduction therapy after failure of chemotherapy with a combination of venetoclax, decitabine, aclarubicin, cytarabine and granulocyte colony-stimulating factor. The leukemia patient achieved remission after 1 month of treatment. However, Sweet syndrome induced by gilteritinib, which was confirmed by skin biopsy, developed during induction therapy. Similar cases of Sweet syndrome following FLT3 inhibitor therapy for acute myeloid leukemia were reviewed., Conclusion: Attention should be given to this rare complication when FLT3 inhibitors are used for acute myeloid leukemia therapy, and appropriate treatments need to be administered in a timely manner.

Background: Sweet syndrome (SS) is a rare dermatological adverse reaction caused by granulocyte colony-stimulating factor (G-CSF), but the characteristics of G-CSF-induced SS are unclear. This study aims to elucidate the characteristics of G-CSF-induced SS and offer guidance for its prevention and management., Methods: We collected relevant case reports of G-CSF-induced SS by searching pertinent databases until June 30, 2024, and synthesized the data for retrospective analysis., Results: A total of fifty patients were analyzed, with a median age of 44 years (1.7-77). The onset of SS occurred between 2 and 90 days post-administration, with a median onset time of 7 days. The predominant cutaneous manifestations included papules/plaques (74.0%), nodules (32.0%), and vesicles/bullae (24.0%). Fever presented in 74.0% of cases, while extra-cutaneous symptoms appeared in 32% of patients. Skin biopsy revealed key findings such as dermal diffuse neutrophil infiltration (97.8%), leukocytoclasis (19.1%), and dermal papillary edema (27.7%). Following both the cessation of G-CSF and systemic corticosteroids treatment, patients showed symptomatic improvement at a median interval of 7 days (2-70)., Conclusion: Clinicians should remain vigilant for the risk of SS during G-CSF administration. Skin biopsy plays a crucial role in confirming SS diagnosis. G-CSF-induced SS exhibits a favorable response to corticosteroids, and re-administration of G-CSF should be avoided due to the risk of symptom recurrence., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Histiocytoid Sweet's syndrome (HSS) is a variant of Sweet's syndrome (SS) that clinically resembles SS but differs histologically by infiltrates, predominantly composed of immature cells of the myeloid lineage. Medications such as proteasome inhibitors have been reported to cause HSS but there has been little discussion on the underlying mechanism. Here we report two cases of HSS associated with a proteasome inhibitor. Both patients were on ixazomib for the treatment of multiple myeloma and presented with acute erythematous plaques on the upper half of the body. Pathological findings were consistent with HSS. Similarities between proteasome inhibitor-induced HSS and Nakajo-Nishimura syndrome, an inherited inflammatory disease, can be identified both clinically and histologically, suggesting a potential explanation of the mechanism behind proteasome inhibitor-associated HSS., (© 2024 Japanese Dermatological Association.)

Aims: Sweet's syndrome is an acute febrile neutrophilic dermatosis first described in 1964 by Robert Douglas Sweet. The pathophysiological mechanism is not fully established; however, several cases of Sweet's syndrome have been reported following drug administration., Methods: To investigate the existence of pharmacovigilance signals between drugs and the occurrence of Sweet's syndrome, we performed a case/non-case study on reports of 'acute febrile neutrophilic dermatosis' registered in the French pharmacovigilance database. Reporting odds ratio (ROR) with its 95% confidence interval were calculated., Results: Amongthe 994 789 reports recorded in the database, 136 were Sweet's syndrome, of which 50.7% were men and the median age was 59 years (range 15-91). A total of 224 drugs were mentioned as suspects: 21.0% were antibacterials, 19.2% were antineoplastics and 12.1% were immunosuppressants. Median time to onset from drug initiation to the development of Sweet's syndrome was 15 days (range 1-1095). The highest RORs were observed with bortezomib (74.04 [40.8-134.2]), azacitidine (72.14 [29.4-176.9]), perfilgrastim (67.05 [21.2-211.6]), azathioprine (55.46 [34.8-88.4]) and bendamustine (35.84 [11.4-112.8])., Conclusions: Pharmacovigilance signals have been observed between the occurrence of Sweet's syndrome and colony-stimulating factors, immunosuppressants, antineoplastics and antibiotics. Clinicians should be aware of the potential associations with these drugs and should be encouraged to report any case of drug-induced Sweet's syndrome., (© 2023 The Authors. British Journal of Clinical Pharmacology published by John Wiley & Sons Ltd on behalf of British Pharmacological Society.)

Abstract: Sweet syndrome is a rare, etiologically unknown dermatosis that can be idiopathic or associated with certain clinical conditions. Among these conditions are infections, autoimmune diseases, inflammatory bowel diseases, vaccinations, the use of medications, and neoplasias. Hematological neoplasias, particularly acute myeloid leukemia, are the most commonly described; however, the condition may also be related to solid tumors, being those of the genitourinary tract the most associated with the syndrome. Drug-induced Sweet syndrome has also been reported; however, it is rarely seen. We report a case of 59 years old male patient with a diagnosis of carcinoma urinary bladder, who developed skin eruption after infusion of the first cycle of chemotherapy (gemcitabine and cisplatin) and resolved after treatment with steroids. The diagnosis of Sweet syndrome was confirmed only after skin biopsy, cultures and laboratory investigations. Malignancy as the cause of skin eruptions was eliminated by the fact that it occurred only after infusion of chemotherapy and the tumor was still there in the bladder, and skin eruptions did not occur after stopping steroids., (Copyright © 2023 Copyright: © 2023 Journal of Cancer Research and Therapeutics.)

Sweet's syndrome is an acute febrile neutrophilic dermatosis. Drug-induced Sweet's syndrome typically occurs soon after drug administration, with rapid resolution of symptoms with cessation of the offending agent. We report a man in his early 40s who presented with fever and widespread erythematous rash on a background of recently diagnosed mild stricturing ileal Crohn's disease. He was commenced on 6-mercaptopurine 12 days before presentation. Skin biopsy demonstrated diffuse infiltration of neutrophils in the upper dermis, dermal oedema, eosinophils and fibrin deposition. Symptoms rapidly improved with cessation of 6-mercaptopurine without requiring systemic corticosteroids., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2024. No commercial re-use. See rights and permissions. Published by BMJ.)

We report a case of vaccine-induced Sweet syndrome in a female patient in her 50s presenting with fevers and a scattered red patchy rash on the lower limbs. Seven days prior, she had received the first dose of AstraZeneca ChAdOx1-S vaccine. A skin biopsy confirmed Sweet syndrome. She did not respond to high doses of prednisolone and required methotrexate therapy to induce remission. This is one of the first reports of Sweet syndrome caused by the ChAdOx1-S vaccine and provides further evidence for vaccine-induced dermatosis. This case demonstrates that methotrexate can induce remission in cases of Sweet syndrome resistant to corticosteroids. This report also describes an approach to the differential diagnosis of patients presenting with a rash, fever and malaise., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2024. No commercial re-use. See rights and permissions. Published by BMJ.)

Neutrophilic dermatosis of the dorsal hands (NDDH) is a variant of Sweet syndrome that presents with erythematous bullae, papules/plaques, or pustules on the dorsal hands. It is most commonly associated with hematologic and solid organ malignancies, though cases of NDDH associated with inflammatory bowel disease, rheumatologic disorders, and medication exposure have also been described in the literature. Felty syndrome is a rare complication of long-standing rheumatoid arthritis characterized by neuropathy, splenomegaly, and neutropenia. Granulocyte colony stimulating factors (e.g., filgrastim) can be utilized to rescue the neutropenia observed in Felty syndrome, but this treatment may subsequently cause Sweet syndrome. Herein, we present a 64-year-old man with Felty syndrome and a complex medical history who presented with sudden onset, painful blisters located on the dorsal and palmar aspects of his bilateral hands. Given the patient's past medical history, a broad differential diagnosis, including disseminated fungal and viral infection was initially considered. A punch biopsy of the skin lesion disclosed neutrophilic dermatosis, which together with laboratory data satisfied the von den Driesch criteria for Sweet syndrome. As the lesions were localized exclusively on the patient's hands, the qualification of NDDH was also endorsed.

Sweet syndrome is a rare complication of azathioprine treatment with unelucidated clinical features. The purpose of this study was to investigate the clinical characteristics of azathioprine-induced Sweet syndrome (AISS) and provide a reference for diagnosis, treatment and prognosis. We collected relevant case reports of AISS by searching Chinese and English databases from 1960 to December 31, 2022, extracted the data and carried out a retrospective analysis. The median age of the 44 patients was 50 (range 9-89) years, and they included 32 males (72.7%). Fever (86.4%) and arthralgia (31.8%) were the most common clinical symptoms. The skin lesions were mainly pustules (54.5%), papules (40.9%), plaques (40.9%) and nodules (31.8%), which were mainly distributed on the extremities (54.5%), face (38.6%) and hands (36.4%). Laboratory examination revealed neutropenia (65.9%) as well as elevated C-reactive protein (63.6%) and erythrocyte sedimentation (40.9%) rates. Histopathology of the lesioned skin showed neutrophil infiltration (93.2%) and dermal edema (38.6%). Symptom relief was achieved at a median time of 7 days (range 2-28 days) after azathioprine discontinuation in all patients. Nine patients (20.5%) had skin lesions that recurred within 24 h after taking azathioprine again. Clinicians and pharmacists should grasp the regularity and characteristics of AISS and should not recommend the readministration of azathioprine, to avoid the recurrence of Sweet syndrome., (© 2023. The Author(s), under exclusive licence to Springer Nature Switzerland AG.)

Since COVID-19 became a global pandemic in 2020, the development and application of SARS-CoV-2 vaccines has become an important task to prevent the spread of the epidemic. In addition to the safety and efficacy of COVID-19 vaccines, the adverse reactions caused by vaccines in a small number of people also deserve our attention. We aimed to discuss and analyze the possible causes of Sweet syndrome caused by the COVID-19 vaccine by integrating the effective information from 16 patients and combining it with the latest views on the innate immune mechanism. We searched the PubMed and Embase databases for published patient reports on the occurrence or recurrence of Sweet syndrome after COVID-19 vaccination. We summarized the basic information of the patients, the type of vaccination, the presence of underlying diseases, and the clinical manifestations, clinical treatment and prognosis of the patients. The results were reported in narrative methods and were sorted into tables. We initially identified 53 studies. 16 articles were included through full-text screening. Based on the table we compiled, we generally concluded that the first dose of any type of COVID-19 vaccine was more likely to cause Sweet syndrome than subsequent doses. Sweet syndrome may occur after COVID-19 vaccination. Clinicians should consider Sweet syndrome in addition to common adverse reactions such as anaphylaxis and infection when a patient presents with acute fever accompanied by nodular erythema, pustules, and edematous plaques after COVID-19 vaccination.

Sweet syndrome (SS), also known as acute febrile neutrophilic dermatosis, is characterized by the abrupt appearance of edematous and erythematous papules, plaques, or nodules on the skin that have a distinct histopathologic appearance. Several subtypes of SS exist, including classic (also referred to as idiopathic) and drug induced. Although multiple medications have been implicated as causative agents, we present a rare case of SS caused by dupilumab, a monoclonal antibody therapy, used in the treatment of severe eosinophilic asthma and other conditions. Clinicians should be aware of this potential adverse reaction, as prompt recognition and treatment are essential.

Abstract: Antitumor necrosis factor therapies have shown to produce a broad range of cutaneous eruptions. We report the case of a patient under adalimumab biosimilar treatment for a punctate inner choroidopathy who developed a cutaneous eruption on sun-exposed areas that showed a diffuse dermal neutrophilic infiltrate consistent with a Sweet-like neutrophilic dermatosis and some features of autoimmunity., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)

Competing Interests: Competing interests: None declared.

We describe a strikingly robust presentation of trimethoprim-sulfamethoxazole (TMP-SMX)-induced pustular Sweet syndrome and discuss how to distinguish it from iododerma and other neutrophil-rich conditions. A review of the literature indicates that TMP-SMX-induced Sweet syndrome (SS) may have higher rates of neutrophilia and greater ocular, mucosal, and musculoskeletal involvement compared to SS from other drugs. Recognizing these features and identifying the offending agent are critical for correctly diagnosing TMP-SMX-induced SS in a timely manner., (© 2022 The Authors. Australasian Journal of Dermatology published by John Wiley & Sons Australia, Ltd on behalf of Australasian College of Dermatologists.)

Competing Interests: Competing interests: None declared.

Abstract: Histiocytoid Sweet syndrome (HSS) is an uncommon histologic variant of Sweet syndrome (SS). HSS can be distinguished from the classic SS with an infiltrate of histiocyte-like immature myeloid cells rather than dense neutrophilic infiltration, although the clinical features are similar. Previous studies have shown that the risk of hematologic malignancy is significantly higher in HSS compared with classic SS. To lesser extent, HSS is also associated with infections, inflammatory diseases, and drugs, particularly with antineoplastic agents as well. Here, we report a case of 2 patients with an abrupt onset of erythematous, tender plaques accompanied by fever, with that revealed similar histopathologic and immunohistochemical features, whom had a history of antibiotic use. Clinicopathologic correlation led to diagnosis of drug-induced HSS, associated with the use of levofloxacin and amoxicillin-clavulanate, respectively. Both patients were then successfully treated with systemic corticosteroid therapy, and neither of them had recurrence during the period of 24-month follow-up., Competing Interests: The authors declare no conflicts of interest, (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)

Sweet syndrome, or acute febrile neutrophilic dermatosis, is a skin condition consisting of erythematous papules and plaques in association with fever, neutrophilia, and a neutrophilic infiltrate that typically involves the papillary dermis. Although development is most commonly idiopathic, medications are also frequently associated with the eruption, notably, the granulocyte colony-stimulating factor (G-CSF), filgrastim. Pegylated G-CSF, despite similar activity, is not commonly reported, with only four published cases. We present a case of drug-induced sweet syndrome with unique histologic features (deep inflammatory infiltrate) in association with the usage of pegfilgrastim in the treatment of invasive ductal carcinoma of the breast. J Drugs Dermatol. 2022;21(4):422-424. doi:10.36849/JDD.4794.

Sweet's syndrome (acute febrile neutrophilic dermatosis) is a rare disorder of unclear aetiology characterised by painful cutaneous lesions, sometimes accompanied by systemic symptoms. It has been associated with several autoimmune conditions, drugs, malignancies and infections, though many cases are idiopathic. We describe a case of Sweet's syndrome in a 49-year-old man with pre-existing psoriasis following recent initiation of risankizumab therapy. There are very few reported cases of Sweet's syndrome in association with psoriasis and no existing reports in association with an IL-23 inhibiting medication. Further investigation of the potentially overlapping immunologic pathways implicated in cutaneous reactions to biologic agents and autoimmune conditions such as psoriasis may yield insights into the pathogenesis of such conditions and guide advancements in the rapidly evolving field of targeted biologic therapies., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2022. No commercial re-use. See rights and permissions. Published by BMJ.)

Tumor necrosis factor (TNF) α inhibitors are widely used to treat inflammatory bowel disease (IBD); however, some patients have unexpected inflammatory episodes during anti-TNF therapy. The objective of our research was to highlight a paradoxical case of anti-TNF-agent-induced Sweet syndrome compared with Sweet syndrome treated by anti-TNF agents. We describe a 62-year-old male with a history of ulcerative colitis presenting with multiple polymorphic indurated skin macules and plaques after 2 months of adalimumab therapy. Neutrophilic dermatosis was diagnosed based on the clinical presentation and skin biopsy and may have resulted from extraintestinal manifestations of a flare-up of IBD or been induced by adalimumab therapy. We conclude that when facing this dilemma, adalimumab should be discontinued, and the dose of prednisolone should be increased before determining the definitive cause. Based on drug hypersensitivity syndrome (DHS) risk assessment in the 10-D assessment system, this case was classified as grade 1 (no risk). Finally, we review the molecular and cellular mechanisms connecting cytokine dysregulation to Sweet syndrome.

Vaccination for COVID19 infection is in full swing all around the world and while the vaccines are considered overall safe, many cutaneous and extracutaneous adverse effects have been reported after their use. Local injection-site reactions are the commonest adverse effect described with the use of these vaccines. We describe a case of Sweet syndrome in an elderly female after the first dose of Oxford-AstraZeneca COVID-19 vaccine (AZD1222)., (© 2021 Wiley Periodicals LLC.)

Sweet syndrome (SS), also referred as acute febrile neutrophilic dermatosis, is an inflammatory process characterised by the abrupt appearance of erythematous papules or nodules with predominant neutrophilic infiltration in the dermis. Fever and neutrophilia are common presenting features. However, extracellular manifestations, including ocular and musculoskeletal, may occur. SS is divided into three subtypes: classical (or idiopathic), malignancy associated and drug induced. Medication-induced subtype accounts for up to 26% of cases. In recent years, emerging evidence has showed that SS may also occur in neutropenic patients who underwent induction for acute myeloid leukemia (AML). The identification of FMS-like tyrosine kinase 3 (FLT3) gene mutation in approximately 30% of patients with AML has promoted the targeted therapy with FLT3-internal tandem duplication (ITD) inhibitors. Midostaurin, a recently Food and Drug Administration-approved medication for FLT3-ITD-positive AML, was reported once as cause for SS. We report a midostaurin-induced SS with neutropenia in a patient following induction chemotherapy of AML., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2021. No commercial re-use. See rights and permissions. Published by BMJ.)

Introduction: Sweet Syndrome, also known as acute febrile neutrophilic dermatosis, is a rare inflammatory disease characterized by the sudden emergence of painful, edematous, and erythematous papules, plaques, or nodules on the skin, which usually fully responsive to systemic corticosteroids. Skin lesions are often accompanied by fever and leukocytosis. Here we present a case of Sweet Syndrome caused by pemetrexed in metastatic lung adenocarcinoma., Case Report: A 52-year-old patient with metastatic lung adenocarcinoma received multiple lines of chemotherapy. The patient presented with extensive skin lesions after performing of pemetrexed chemotherapy. He had a fever and elevations in blood levels of C-reactive protein (CRP), sedimentation, leucocytes, and neutrophils. Neutrophil predominant perivascular and interstitial dermatitis, focal micropustule formation, and severe neutrophilic dermatosis were reported in skin biopsy. Topical steroid and oral antihistamine treatment were started as initial treatment. Discussion and conclusions: Cutaneous side effects related to pemetrexed are often reported as 'skin rash,' which is a non-specific term. Therefore, the diagnosis of Sweet Syndrome must be confirmed by skin biopsy. It is essential to exclude the presence of an infection and medication history. Recovery in drug-induced Sweet Syndrome occurs after the drug that caused it was discontinued. Systemic corticosteroids are the first-line treatment for most cases.

Azathioprine hypersensitivity syndrome is a rare but potentially severe side effect of azathioprine use. It has a variable and non-specific presentation making it difficult to distinguish from sepsis or disease relapse. High clinical suspicion is therefore required for recognition and prompt cessation of azathioprine for symptom resolution. Herewith two cases of severe azathioprine hypersensitivity syndrome are described, one in association with Sweet syndrome. Both presented with vague symptoms 2 weeks after commencing azathioprine for antineutrophil cytoplasmic antibody vasculitis. The differentials of sepsis and disease relapse were considered prior to cessation of azathioprine which resulted in a dramatic improvement in both cases. These cases highlight the diagnostic challenge azathioprine hypersensitivity syndrome presents. It should be suspected when there is a temporal relationship to drug initiation, with absence of infection or serological evidence of disease relapse., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2021. No commercial re-use. See rights and permissions. Published by BMJ.)

Tyrosine kinase inhibitors are a class of targeted anticancer drugs that inhibit cancer cell proliferation by inactivating proteins involved in signal transduction cascades. Various cutaneous adverse events have been observed after tyrosine kinase inhibitor administration, including Sweet syndrome. We queried the PubMed database to identify 14 cases of Sweet syndrome thought to be secondary to tyrosine kinase inhibitors. Tyrosine kinase inhibitor-induced Sweet syndrome had a median of 2 months latency following drug administration. All cases but one had morphologic features classic for Sweet syndrome (erythematous and tender papules, plaques, or nodules). All cases also had classic histopathologic findings (dermal neutrophilic infiltrate without vasculitis or necrosis). Using diagnostic criteria for drug-induced Sweet syndrome and the Naranjo Drug Reaction Probability Scale for a drug-induced cutaneous eruption, we found that six cases favored a drug-induced etiology over malignancy, two cases favored a malignancy-associated Sweet syndrome, and the remaining eight met drug-induced Sweet syndrome criteria but had low Naranjo scores. Nine cases resulted in medication discontinuation, while five cases continued anticancer therapy and were treated only with corticosteroids with quick resolution of skin lesions. Dermatologists should be aware of this adverse cutaneous reaction to tyrosine kinase inhibitors and should treat on a case-by-case basis, though limited evidence in this review suggests that oncologic therapy may safely be continued with prompt corticosteroid treatment., (© 2020 Wiley Periodicals LLC.)