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Fixed drug eruption (FDE) is an adverse drug reaction characterized by recurrent circumscribed lesions at the same location upon re-exposure to the culprit medication, resulting in distinct postinflammatory hyperpigmentation. Histopathologically, FDE demonstrates a predominantly lymphocytic interface or lichenoid infiltrate with basal cell vacuolar changes and keratinocyte dyskeratosis/apoptosis. The term "neutrophilic fixed drug eruption" has been used to describe cases in which the inflammatory infiltrate is predominantly neutrophilic. The infiltrate can extend deeper in the dermis, potentially mimicking a neutrophilic dermatosis such as Sweet syndrome. We present two cases and review the literature to discuss the possibility that a neutrophilic inflammatory infiltrate may be an expected finding in FDE, rather than a histopathologic variant., (© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Iododerma is an uncommon dermatosis caused by excessive iodine exposure and is associated with significant morbidity and mortality. Because of its heterogenous clinical presentation and variable histopathological findings, which depend on the time the skin biopsy is performed, the diagnosis of iododerma is often delayed. We report a rare case of acute iododerma in a woman with end-stage diabetic nephropathy with antecedent radioiodine contrast exposure, presenting histopathologically as cryptococcoid neutrophilic dermatosis (CND). We underscore important clinicopathological pitfalls to avoid misdiagnosis with similar overlapping entities such as Sweet syndrome, review all published cases of CND and draw novel insights into its associated entities., (© 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

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.)

We report the case of a 64-year-old woman treated with ibrutinib for a chronic lymphocytic leukemia with 17p deletion, who developed several erythematous, painful, and papulo-nodular skin lesions in the limbs, neck, and face. The skin biopsy was consistent with the diagnosis of neutrophilic dermatosis. Rechallenge with ibrutinib at full dose was followed by the recurrence of the same skin lesions, strongly suggesting a direct relationship.

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.

Neutrophilic dermatosis (ND) confined to postmastectomy lymphedema, localized Sweet syndrome, is a newly recognized disease. In this study, the authors describe a 44-year-old obese woman with chronic myelogenous leukemia in molecular remission on dasatinib therapy, who presented with a painful urticarial eruption limited to lipo-lymphedematous skin and accompanied by malaise, episodic fever, diarrhea, neutrophilia, and leukocytosis. Initially transient and migratory, the rash became fixed, papular, and vesicular and showed minimal response to corticosteroids. Biopsy demonstrated sparse perivascular and interstitial dermal neutrophilic infiltrates, without vasculitis or significant dermal edema. Aggregates of neutrophils were found within and surrounding lymphangiectases. Biopsy of a new onset papule 3 weeks later demonstrated papillary dermal edema, denser neutrophilic infiltrate, and vasculitis-like changes. These 2 histopathologic patterns of ND, early and late, resemble neutrophilic urticarial dermatitis (also known as neutrophilic dermatitis with systemic inflammation) and Sweet syndrome, respectively. Extensive workup did not reveal evidence of relapsed chronic myelogenous leukemia, infection, or a coexisting systemic inflammatory disease. Dasatinib was discontinued and the eruption gradually resolved over 2.5 months. Still in molecular remission (no detectable BCR-ABL gene fusion), dasatinib therapy was recommenced at 3-month follow-up. After 10 months, she complains of malaise and arthralgia, but no cutaneous symptoms. The evolution and slow resolution of this ND in lipo-lymphedematous skin implicate poor lymphatic clearance of factors, antigenic and/or toxic, involved in the pathogenesis of ND.

Sweet syndrome (SS) is an acute febrile neutrophilic dermatosis that can be associated with malignancy and medications. A 60-year-old man presented with erythematous, edematous, and ulcerated plaques in the extensor surface of the upper extremities, after a ketoconazole course due to pityrosporum folliculitis. Skin biopsy showed a dense dermal neutrophilic infiltrate, associated with marked papillary dermal edema. Blood count showed leukocytosis and neutrophilia. Skin lesions resolved spontaneously with discoloration after 2 weeks of discontinuation of ketoconazole. Although most cases of drug-induced SS are associated with granulocyte colony-stimulating factor, other medications need to be considered. This is the first reported case of ketoconazole-induced SS despite its widespread use.

Sweet's syndrome (SS) is a dermatosis with systemic symptoms characterized by tender, red nodules or papules, occasionally covered with vesicles, pustules or bullae, usually affecting the upper limbs, face and neck. SS is frequently observed in patients with leukemia or connective tissue diseases, while it is rather seldom in patients with inflammatory bowel disease. The exact pathogenesis of SS is only partially understood. We report the case of a 50-year-old patient with indeterminate colitis, presenting with a febrile diffuse papulopustular and necrotizing skin eruption that healed with significant scarring and appeared 14 days after onset of treatment with azathioprine. Histological examination revealed the presence of features typical of SS, gene expression analysis very high levels of interleukin-1β (IL-1β) mRNA in lesional skin, and immunohistochemistry high levels of IL-1β at the protein level. SS associated with azathioprine is being increasingly reported and is reviewed herein.

Drugs may elicit a considerable variety of clinical signs, often affecting the skin and the mucous membranes. The most common are maculopapular exanthemas and urticaria, more rarely pustules, bullae vasculitic lesions, and lichenoid lesions may also be observed. Apart from the morphology, the chronology of the occurrence and the evolution of single skin lesions and exanthema are also paramount in the clinical diagnosis of cutaneous drug hypersensitivity. Often, the skin represents the only organ manifestation; however, it may be the herald for a systemic involvement of internal organs, such as in severe drug-induced hypersensitivity syndromes or anaphylaxis., (Copyright (c) 2010 Elsevier Inc. All rights reserved.)

Bortezomib, a proteasome inhibitor approved for the treatment of multiple myeloma, has been reported to be associated with Sweet syndrome. However, careful review of the histopathology of the first reported case and our case revealed similar histologic and immunohistochemical findings (a mononuclear dermal infiltrate) and not the usual neutrophilic infiltrate of Sweet syndrome. We suggest that the dermatitis induced by bortezomib is best classified as "histiocytoid Sweet syndrome."

Background: Phenylbutazone frequently induces a range of potentially dangerous adverse reactions. We report a case of Sweet's syndrome with sialadenitis induced by phenylbutazone., Case-Report: A 54-year-old woman presented lumbar pains treated with phenylbutazone for three days. Six days later, she exhibited inflammation of the submaxillary and parotid salivary glands, followed by an erythematous, oedematous, pustular and febrile eruption, with failure of antibiotic therapy. Laboratory data showed leukocytosis and neutrophilia, anaemia, an elevated platelet count and liver dysfunction. The infectious and autoimmune tests were negative. The skin biopsy confirmed Sweet's syndrome. Clinical and biological abnormalities resolved on administration of systemic steroids., Discussion: Phenylbutazone-induced sialadenitis is rare and presents unrecognized adverse effects that may be associated with a systemic reaction. In the present case report, Sweet's syndrome met the criteria for drug-induced Sweet's syndrome. There appears to have been a systemic reaction caused by a hypersensitivity mechanism, in the same way as sialadenitis.

Granulocyte colony-stimulating factor (GCSF) is a recombinant human growth factor widely used in haematology. It is known to cause cutaneous vasculitis and neutrophilic dermatoses. We present three cases of Sweet's syndrome (SS) associated with GCSF use. Raised GCSF levels have been demonstrated in patients with SS. GCSF is the best understood mechanism by which neutrophil accumulation occurs and shows a dose-dependent effect in provoking SS.

This case report describes a case of Sweet syndrome (SS) related to use of furosemide in a 46-year-old female who was admitted for treatment of congestive heart failure. Three days after administration of furosemide, the patient had a fever and a skin eruption appeared on her wrists, forearms, and legs. Biopsy of the skin lesion was consistent with SS. Infection was thought to be unlikely because of negative blood cultures, echocardiography, and other imaging studies. Careful review of her medications revealed that the patient received furosemide before the appearance of the skin eruption and fever. After discontinuation of furosemide, the patient's skin lesion and fever resolved. A MEDLINE search from June 1966 to May 2004 revealed only one reference documenting the association of SS with furosemide administration. Patients who have development of SS without an obvious cause should have their medication list closely reviewed.

Sweet's syndrome was first described in 1964. It is characterized by an acute onset of non-pruritic, painful reddish nodules on the head and neck, chest and/or the upper limbs, mostly accompanied by fever, general malaise and leucocytosis. Histopathological examination shows a diffuse dermal neutrophilic infiltrate. The pathogenesis is still not fully understood, and different diseases have been shown to be associated with this syndrome. However, although still very rare, there is an increase of reports on Sweet's syndrome induced by drugs. We describe a 30-year-old man who experienced acute neutrophilic dermatosis after systemic treatment with minocycline. Additionally, there is a strong possibility that the same patient developed a drug-induced Sweet's syndrome after oral administration of tetracycline and doxycycline.

Sweet's syndrome and related neutrophilic dermatoses have been associated with a variety of medications. Celecoxib is a new cyclo-oxygenase-2 inhibitor recently approved for arthritis. We describe a 57-year-old man who experienced tender pustulopapular lesions on the dorsal aspects of the hands, neck, and legs 1 week after starting celecoxib. Histopathologic examination of the lesion showed a diffuse dermal neutrophilic infiltrate, edema of the papillary dermis, spongiform pustules, and no leukocytoclastic vasculitis. These findings were consistent with Sweet's syndrome. Without realizing a possible association, the patient rechallenged himself with a second course of the medication, which resulted in a rapid exacerbation of his lesions. After discontinuing the medication for the second time, the patient has had complete clearing of his lesions. To our knowledge, this is the first report of Sweet's syndrome associated with this new class of nonsteroidal anti-inflammatory drugs.

This is the second reported case of minocycline-induced Sweet's syndrome (and the first such case to appear in the American literature). The syndrome developed in a 32-year-old man 10 days after minocycline therapy for acne was begun and resolved rapidly after discontinuation of the medication and start of oral prednisone therapy.

A case is presented of a Sweet's syndrome-like eruption in association with the oral contraceptive. A 46 year old caucasian woman developed recurrent episodes of erythematous tender plaques on her trunk six weeks after commencement of the oral contraceptive (OC). Her condition clinically and histologically resembled Sweet's dermatosis. On cessation of the OC there was complete resolution of her lesions and she remains well 12 months later. This is the first report, to our knowledge, of a neutrophilic reaction to the oral contraceptive, and we believe that drugs may be implicated in the aetiology of atypical neutrophilic reactions simulating Sweet's syndrome in patients who are otherwise well.