Sweet syndrome induced by FLT3 inhibitors: case report and literature review.

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.

Mercaptopurine-induced Sweet's syndrome.

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.

Sweet syndrome following the ChAdOx1-S vaccine.

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.

A case of filgrastim-induced neutrophilic dermatosis of the dorsal hands in a patient with Felty Syndrome.

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.

Neutrophilic dermatosis of the dorsal hands related to cocaine abuse

Abstract Neutrophilic dermatoses encompass a wide spectrum of diseases characterized by a dense infiltration mainly composed of neutrophils. Neutrophilic dermatosis of the dorsal hands is currently considered a localized variant of Sweet syndrome. Cocaine abuse has been related to a wide range of mucocutaneous manifestations, including neutrophilic dermatoses such as pyoderma gangrenosum. The authors of this study present a patient with neutrophilic dermatosis of the dorsal hands, in which cocaine abuse was identified as a probable trigger.

Sweet syndrome-like cutaneous drug reaction

Abstract: Cutaneous drug reactions are adverse reactions to medications that may present with different clinical features, ranging from localized to generalized lesions. In this report we describe a case of an unusual drug reaction, resembling the morphology of Sweet syndrome lesions. The patient had a psychiatric illness and was using thioridazine hydrochloride for one year. He developed infiltrated and grouped erythematous lesions on the elbows and knees three days after commencing multiple drugs (promethazine, haloperidol, mirtazapine and levomepromazine). After suspension of these four drugs and after the use of glucocorticoids, the patient had significant clinical improvement.

Quinupristin/Dalfopristin-induced Sweet's Syndrome

Quinupristin/Dalfopristin is a new combination of streptogramin antibiotics designed specifically to treat clinically significant infections due to Vancomycin-resistant Enterococcus Faecium. Sweet's syndrome is characterized by painful skin plaques, which is associated with dermal neutrophilic infiltration, fever and peripheral blood leukocytosis. Drug-induced Sweet's syndrome has a temporal relationship between drug ingestion, clinical presentation and the temporally-related resolution of lesions following drug withdrawal or on treatment with systemic corticosteroids. A 63-year-old woman received Quinupristin/Dalfopristin for acute pyelonephritis developed fever, arthralgia, vomiting, and painful erythematous skin plaques. A skin biopsy showed neutrophilic dermatosis, and there was rapid resolution of the symptoms and cutaneous lesions after discontinuation of Quinupristin/Dalfopristin, consistent with drug-induced Sweet's syndrome. To date, there has been no reported case of Sweet's syndrome associated with the use of Quinupristin/Dalfopristin.

Síndrome de Sweet em paciente com HIV/AIDS / Sweet's Syndrome in a HIV/Aids patient

Relata-se um caso clínico de uma paciente, 50 anos, portadora de HIV/Aids, que desenvolveu lesöes cutâneas dolorosas de forma aguda, em placas eritematosas, com superfície irregular e bem delimitada, diagnosticada como síndrome de Sweet. A analíse histopatológica revelou edema de derme papilar e infiltrado inflamatório neutrofílico difuso. Poucos casos säo descritos na literatura sobre esta condiçäo em paciente com HIV/Aids.

Sweet's syndrome during the treatment of acute promyelocytic leukemia with all-trans retinoic acid

All-trans retinoic acid (ATRA) is the standard induction treatment for acute promyelocytic leukemia (APL). Quite many ATRA-related side effects, including retinoic acid syndrome, were reported. So far, it has rarely been reported that Sweet's syndrome, characterized by fever, neutrophilia, painful erythematous cutaneous plaques, dense dermal infiltrates of mature neutrophils and rapid response to steroid therapy, is associated with ATRA. In the case that Sweet's syndrome associated with ATRA is found, physicians will have to face a great challenge over the possibility of infectious conditions. We present here a case of Sweet's syndrome associated with ATRA. A 35-year-old female with APL developed fever, painful erythematous cutaneous plaques on both cheeks, right wrist and both shins during induction chemotherapy with ATRA. A skin biopsy revealed a dense dermal infiltrate, consisting of mature neutrophils without vasculitis or cutaneous immunoglobulin deposits, which is compatible with Sweet's syndrome. Oral prednisone was administered and the lesions started to improve within 48 hours

Síndrome de sweet y factor estimulante de colonias de granulocitos (G-CSF). Descripción de un caso con esta posible relación / Sweet's syndrome and granulocyte colony-stimulating factor (G-CSF). A case report with this probable relationship

En la patogenia del síndrome de Sweet se han involucrado diversos desencadenantes, entre los que se ha hecho referencia al papel desempeñado por algunas citocinas como los factores de crecimiento hematológicos. Describimos el caso de una paciente de 75 años diagnosticada de linfoma no Hodgking centrofolicular que desarrolló un síndrome de Sweet después de ser tratada con factor estimulante de colonias de granulocitos (G-CSF) para corregir una neutropenia febril postquimioterapia. Se discuten los aspectos etiopatogénicos y clínicos del síndrome de Sweet en relación con el G-CSF, resaltando la escasa frecuencia con la que se ha descrito dicha asociación. En el caso presentado destacamos además varios aspectos que consideramos de interés: a) la localización exclusiva en manos, sin presentar lesiones en otras zonas; b) la aparición de las lesiones 9 días después del inicio del tratamiento con el G-CSF (y 5 días después de su suspensión), y c) su aparición en una paciente diagnosticada previamente de un linfoma no Hodgkin (AU)