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Sweet syndrome is a reactive, sterile, pustular dermatosis that occurs in association with infection, malignancy, or connective tissue disease or in response to the use of certain medications. Sweet syndrome secondary to azathioprine therapy is rarely reported. We describe 3 patients, 2 with inflammatory bowel disease and 1 with myasthenia gravis, who developed febrile pustulosis consistent with Sweet syndrome 1 to 2 weeks after treatment with azathioprine. Antibiotic therapy failed in all patients, but Sweet syndrome resolved with drug withdrawal and prednisone therapy. Because azathioprine is widely used, clinicians should be aware of this adverse reaction.

Pegylated interferon-alpha in combination with ribavirin currently represents the therapeutic standard for the hepatitis C virus infection. Interferon based therapy may be responsible for many cutaneous side effects. We report a case of drug-induced Sweet's syndrome secondary to hepatitis C antiviral therapy. To our knowledge, this is the first reported case of Sweet's syndrome in association with pegylated interferon-alpha therapy.

Background: Neutrophilic disease is characterized by aseptic visceral infiltration by normal polymorphonuclear leukocytes that can occur in any organ. Association with an underlying systemic disease, particularly haematological malignancy or inflammatory bowel disease, is frequent. This may produce a multisystem disorder, but diagnosis is usually based on skin lesions because of their clinical and histological accessibility. Pulmonary manifestations are the most common extracutaneous symptoms but may be misdiagnosed, as in our case report., Case Report: A 77-year-old woman with IgA myeloma presented with an inflammatory bullous plaque of the leg coupled with fever lasting one week. The clinical and histological examinations were evocative of a neutrophilic dermatosis such as Sweet's syndrome. Significant improvement was initially obtained with systemic corticosteroids and colchicine. The course became complicated by necrotic neutrophilic papulopustular lesions of the upper limbs and pulmonary manifestations, with fever and decline in overall condition occurring the day after administration of erythropoietin. A hypothesis of septic aetiology prompted antibiotic and antifungal therapy, which remained ineffective. The patient died the day after the second erythropoietin injection., Discussion: This case involved late identification of the aseptic neutrophilic aetiology of pulmonary manifestations. Several factors favouring their appearance and the fatal outcome may be suggested: the existence of a myeloma, association with myelodysplastic syndrome and the possible iatrogenic action of erythropoietin. To the best of our knowledge, this is the first reported case of extracutaneous neutrophilic infiltrate occurring in a patient treated with this haematopoietic hormone.

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.

Radiocontrast agents are known to be the cause of many cutaneous manifestations. The present report describes a unique case of a Sweet's syndrome-like neutrophilic dermatosis that recurred three times over 5 years following administration of a radiocontrast agent administered during the course of an intravenous pyelography.

Background: An association of Sweet syndrome with chronic myeloid leukemia (CML) has been recently observed in patients treated with tyrosine kinase inhibitors., Observations: We describe a 67-year-old patient with a 6-year history of Philadelphia chromosome translocation t(9;22)(q34;q11)-positive CML. The tyrosine kinase inhibitor AMN107 (nilotinib) kept the patient in chronic phase. After 10 months of taking nilotinib, he developed pneumonia with septic features. Seven days later, bullous skin infiltrations on the upper arms and a large, painful bullous swelling of the right neck occurred without any evidence of a viral, bacterial, or fungal blood infection. Findings from histologic examination showed massive infiltrations of the whole dermis with neutrophil granulocytes as well as with monocytoid histiocytic cells. Fluorescence in situ hybridization analysis of paraffin-embedded tissue revealed a BCR-ABL fusion, indicating the presence of t(9;22)(q34;q11). The addition of oral prednisolone to an adequate antibiotic treatment led to rapid resolution of the cutaneous infiltrations., Conclusions: Skin infiltrations consistent with Sweet syndrome can occur in patients with septic CML during the treatment with tyrosine kinase inhibitors, including nilotinib. Skin infiltrations can include specific CML cells.

Histiocytoid Sweet's syndrome is a recently described entity which has clinical features identical to typical Sweet's syndrome but is distinguished by a dermal cellular infiltrate composed not of mature neutrophils but of immature granulocytes. Herein, we report a case of bone marrow granulocytic maturation arrest and a histological histiocytoid Sweet's-like reaction pattern following trimethoprim-sulfamethoxazole therapy.

A 74-year-old psychotic female patient who was treated with clozapine developed Sweet's syndrome followed by agranulocytosis from which she later died. A link between these two conditions seems unlikely. Sweet's syndrome is characterised by an acute onset of fever, leukocytosis and erythematous plaques with dense neutrophilic infiltrates. Frequent counting of the numbers of neutrophiles is advisable when skin disorders appear during treatment with clozapine.

Drug-induced acute febrile neutrophilic dermatosis, or Sweet's syndrome, is rare and, to our knowledge, has not previously been associated with clindamycin therapy. We describe a 47-year-old woman with type 2 diabetes mellitus and end-stage renal disease requiring hemodialysis who developed Sweet's syndrome after receiving oral and intravenous clindamycin for a tooth infection. After the clindamycin was discontinued, the patient's clinical symptoms resolved over several days. Use of the Naranjo adverse drug reaction probability scale indicated a probable relationship between the patient's development of Sweet's syndrome and clindamycin therapy. Clinicians should be aware that Sweet's syndrome can occur with clindamycin treatment. Early recognition of this condition in conjunction with cessation of drug exposure, with or without antiinflammatory therapy, can produce complete recovery.

Sweet's syndrome (the eponym for acute febrile neutrophilic dermatosis) is characterized by a constellation of clinical symptoms, physical features, and pathologic findings which include fever, neutrophilia, tender erythematous skin lesions (papules, nodules, and plaques), and a diffuse infiltrate consisting predominantly of mature neutrophils that are typically located in the upper dermis. Several hundreds cases of Sweet's syndrome have been published. Sweet's syndrome presents in three clinical settings: classical (or idiopathic), malignancy-associated, and drug-induced. Classical Sweet's syndrome (CSS) usually presents in women between the age of 30 to 50 years, it is often preceded by an upper respiratory tract infection and may be associated with inflammatory bowel disease and pregnancy. Approximately one-third of patients with CSS experience recurrence of the dermatosis. The malignancy-associated Sweet's syndrome (MASS) can occur as a paraneoplastic syndrome in patients with an established cancer or individuals whose Sweet's syndrome-related hematologic dyscrasia or solid tumor was previously undiscovered; MASS is most commonly related to acute myelogenous leukemia. The dermatosis can precede, follow, or appear concurrent with the diagnosis of the patient's cancer. Hence, MASS can be the cutaneous harbinger of either an undiagnosed visceral malignancy in a previously cancer-free individual or an unsuspected cancer recurrence in an oncology patient. Drug-induced Sweet's syndrome (DISS) most commonly occurs in patients who have been treated with granulocyte-colony stimulating factor, however, other medications may also be associated with DISS. The pathogenesis of Sweet's syndrome may be multifactorial and still remains to be definitively established. Clinical and laboratory evidence suggests that cytokines have an etiologic role. Systemic corticosteroids are the therapeutic gold standard for Sweet's syndrome. After initiation of treatment with systemic corticosteroids, there is a prompt response consisting of dramatic improvement of both the dermatosis-related symptoms and skin lesions. Topical application of high potency corticosteroids or intralesional corticosteroids may be efficacious for treating localized lesions. Other first-line oral systemic agents are potassium iodide and colchicine. Second-line oral systemic agents include indomethacin, clofazimine, cyclosporine, and dapsone. The symptoms and lesions of Sweet's syndrome may resolved spontaneously, without any therapeutic intervention; however, recurrence may follow either spontaneous remission or therapy-induced clinical resolution.

Objective: To identify the side effect of all-trans retinoic acid (ATRA), and improve early therapeutic response in patients with acute promyelocytic leukemia (APL)., Method: The first case of Sweet's syndrome (SS) developed in a APL patient treated with ATRA was reported in mainland of China, and reviewed correlative literature., Results: Only 14 cases of SS associated with ATRA therapy in APL have been reported in the literature, including the present case. The median age was 49.5 years (9 -84) and 10 were women and 4 men. Of them, SS was restricted to the skin in 10 case, the other 4 muscle, fascia, kidney, and lung were involved. SS appeared after a median of 18 days of ATRA therapy (6 - 34 days). The median WBC count was 7.05 (0.80 - 23.00) x 10(9)/L. Four patients continued with the ATRA therapy without interruption, 13 patients treated with steroids and 12 responded. One patient improved without any treatment. Two cases of SS developed retinoic acid syndromes after ATRA therapy., Conclusion: Sweet's syndrome is a rare adverse effect of ATRA, and has similar features with inflammatory or infective dermatosis. The corticosteroids treatment could improve the systemic and cutaneous symptoms. When ATRA therapy was restarted after SS subsided, no recurrence of rashes was observed.

Objective: To systematically review the pertinent literature on drug-induced Sweet's syndrome (SS)., Data Sources: MEDLINE (1966-December 2006), International Pharmaceutical Abstracts (1970-December 2006), Science Citation Index (1945-December 2006), and EMBASE (1980-December 2006) were searched using the key terms Sweet's syndrome, drug-induced, and acute neutrophilic dermatitis., Study Selection and Data Extraction: All case reports of drug-induced SS located using the above databases were collected for causality assessment. In addition, relevant articles regarding the various causes and presentations of SS were selected to provide background information. Bibliographies of all relevant articles were reviewed for additional citations., Data Synthesis: All case reports of drug-induced SS were evaluated against an expanded Naranjo scale with specific criteria for SS. Tables were developed listing key criteria for evaluating the case reports for causality. Data were evaluated by quantity and quality of evidence, and an assessment was made as to whether there was a feasible pharmacologic mechanism to explain causality., Conclusions: Granulocyte colony-stimulating factor (G-CSF), all-trans retinoic acid (ATRA), and vaccines met 2 of 3 criteria for an association with SS. There are sufficient data and a plausible pharmacologic mechanism for G-CSF and ATRA. Vaccines meet the qualitative criteria and also have a plausible pharmacologic mechanism. The evidence regarding minocycline is of high quality; however, the quantity of evidence and a reasonable pharmacologic mechanism are lacking. A host of miscellaneous drugs have also been implicated in causing the disorder, all without sufficient evidence.

Sweet's syndrome-like (Sweet's-like) neutrophilic panniculitis is usually idiopathic, but is frequently associated with hematologic, inflammatory, and immunologic disease. Drug-related cases of Sweet's syndrome have been reported. Of relevance, chemotherapy with the retinoid all-trans-retinoic acid (ATRA) infrequently induces Sweet's-like neutrophilic panniculitis that occurs concomitantly with neutrophilic differentiation. The pathologic features are limited to the adipose tissue or include both the dermis and the subcutaneous fat; the neutrophilic infiltrate can be observed in the lobules, the septae, or both. We present this case because of the unusual subcutaneous neutrophilic infiltrate consistent with Sweet's-like neutrophilic lobular panniculitis in a patient with acute promyelocytic leukemia receiving ATRA chemotherapy. This case highlights the important connection between ATRA and Sweet's syndrome.

Background: We report a case of juvenile acne aggravated in the form of Sweet's syndrome by isotretinoin treatment. The late onset of ulcerative-hemorrhagic rectocolitis in this patient raised doubts about a possible relationship between Sweet's syndrome, acne and inflammatory colitis., Patients and Methods: A 19 year-old male patient with no disease history of note was treated for juvenile polymorphous acne resistant to standard topical acne treatment using isotretinoin (Roaccutane) at a dose of 0.5 mg/kg/d. After one week of treatment, the patient presented a fever of 38.5 degrees C, joint pain and congestive, erythematous-edematous, maculopapular plaques in ring-like layout subsequently becoming pustular and necrotic. These lesions occurred on the face, neck and pinna of the ear. Some nodules were also noted on the lower limbs. Biological tests and histology examination of a skin biopsy were evocative of Sweet's syndrome. The outcome was rapidly favorable following discontinuation of isotretinoin and institution of systemic corticosteroids (0.5 mg/kg/d). Two years later, ulcerative-hemorrhagic rectocolitis was diagnosed with episodes of bloody diarrhea., Discussion: Treatment of acne with isotretinoin can occasionally induce inflammatory episodes of acne. To date there have been no reported cases of isotretinoin-induced Sweet's syndrome. The subsequent onset of ulcerative-hemorrhagic rectocolitis provides an indication of the complexity of the pathogenic mechanisms involved.

Granulocyte colony stimulation factor (G-CSF) is commonly used in the treatment of chemotherapy-induced myelosuppression. We report the case of a 62-year-old man with chronic lymphocytic leukemia who presented with neutropenic fever and sepsis. After treatment with G-CSF he developed Sweet's syndrome. Sweet's syndrome is a rare disorder but has been associated with cancer recurrence as well as administration of G-CSF. We present clinical and pathologic images that highlight the salient features of this entity., ((c) 2006 Wiley-Liss, Inc.)

Sweet's syndrome is an acute febrile neutrophilic dermatosis. This syndrome can be idiopathic, para-inflammatory, paraneoplastic, drug-induced, or pregnancy-related. In this paper, a case of Sweet's syndrome associated with ofloxacin therapy in a patient with Crohn's disease is reported.

A 33-year-old man with advanced testicular cancer underwent high-dose chemotherapy combined with peripheral blood stem cell transplantation. After administration of granulocyte colony-stimulating factor (G-CSF), multiple infiltrative erythema was identified on the face, thigh, and lower leg. A dermatologist diagnosed this as Sweet's syndrome caused by G-CSF; consequently G-CSF administration was stopped. When the skin lesions had improved, phlebitis was found at the injection site of the peripheral vein catheter. The patient then suffered from sudden left chest pain and dyspnea. Chest computed tomography showed the characteristic findings of septic pulmonary emboli (SPE). He was treated by the administration of vancomycin, fluconazole, and pazufloxacin mesilate. Although Sweet's syndrome and SPE are rare diseases, the presence of these diseases must be considered when performing chemotherapy for urological malignancy.

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.

Sweet's syndrome is an uncommon acute skin disease, associated with a variety of medical problems. The drug-induced variant is even rarer. We describe two cases of this syndrome associated with the administration of the proteasome inhibitor bortezomib. The diagnostic criteria for drug-induced Sweet's syndrome as proposed by Walker and Cohen were fulfilled. Vasculitis and neutrophilic eccrine hidradenitis were excluded.

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 is an acute febrile neutrophilic dermatosis marked by attacks of painful, plaque-forming inflammatory papules accompanied by fever, arthralgias, peripheral leukocytosis, a diffuse dermal neutrophilic infiltrate, and prompt resolution of symptoms and lesions with glucocorticoid therapy. There are many reports of drug-induced Sweet's syndrome to various medications including all- trans -retinoic acid, carbamazepine, hydralazine, levonorgestrel/ethinyl estradiol, minocycline, trimethoprim/sulfamethoxazole, and granulocyte colony-stimulating factor. We describe the first known case of Sweet's syndrome induced by pegfilgrastim, a pegylated form of granulocyte colony-stimulating factor with unique pharmacologic properties that may induce Sweet's syndrome in patients with no history of neutrophilic dermatoses associated with granulocyte colony-stimulating factor therapy.

Background: Imatinib mesylate has become one of the main chemotherapeutic agents currently used to treat patients with chronic myeloid leukemia (CML). Although cutaneous reactions to this drug have been documented before, this is the first time that Sweet syndrome has been reported with its use., Observations: We report a case of Sweet syndrome secondary to the administration of imatinib to treat CML. On 2 separate occasions, a 53-year-old African American woman with CML developed neutrophilic dermatosis consistent with Sweet syndrome after chemotherapy with imatinib., Conclusion: Greater awareness of the adverse effects of imatinib and the characterization of its cutaneous adverse effects will lead to improved surveillance for and treatment of those adverse effects.

Sweet's syndrome is an acute febrile neutrophilic dermatosis that is a known complication of the administration of filgrastim, a drug that causes increased neutrophil proliferation and differentiation. This complication has not previously been reported during treatment with sargramostim, a hematopoietic cytokine with activity that overlaps filgrastim. We report a case of Sweet's syndrome in association with sargramostim treatment following chemotherapy for acute myelogenous leukemia. A suspected second episode occurred after subsequent chemotherapy and sargramostim treatment. Physicians should be aware of this possible association because the signs and symptoms of Sweet's syndrome are easily mistaken as being due to infection., (Copyright 2004 Wiley-Liss, Inc.)

Ulcerative colitis is an inflammatory bowel disease often associated with extra-intestinal manifestations, such as dermatological disorders. Of these, the most frequent are erythema nodosum and pyoderma gangrenosum, the two neutrophilic forms of dermatosis. Another is Sweet' s syndrome, which results in a sudden eruption of tender, raised erythematous or violaceous plaques/papules or nodules, less frequent vesicles, pustules or bullae, involving face, neck, arms and trunk. This skin disorder is frequently observed in patients with leukaemia or connective tissue diseases, while it is very rare in patients with inflammatory bowel disease. The present report deals with the case of a febrile diffuse skin eruption in a 53-year-old patient with moderately active ulcerative colitis after few days' treatment with steroids and azathioprine. At first, the dermatosis was addressed to an idiosyncrasy to azathioprine, which was, therefore, promptly discontinued. Histological examination of skin biopsies revealed the presence of features typical of a Sweet's syndrome. The eruption gradually improved as well as the patient's general condition, until complete regression was achieved following steroid treatment.

Background: Sweet's syndrome may occur during medullar aplasia, especially after treatment with exogenous growth factors such as G-CSF. In this context, Sweet's syndrome presents particular histological features that we detail in this observation., Case Report: A 50 year-old man was treated for multiple myeloma with a mobilizating chemotherapy prior to autologous stem cell transplantation. Four days after the onset of G-CSF, he presented with a febrile generalized eruption of erythematous infiltrated lesions. Histological examination of a skin biopsy showed a neutrophilic infiltrate associated with atypical xanthomized histiocytes and vascular hyperplasia with marked endothelial turgescence. Treatment with a short cause of oral corticosteroids was efficient., Discussion: The classical histological features of Sweet's syndrome consist in a dermal neutrophilic infiltrate with edema. In our patient, we noticed the presence of atypical histiocytes among the dermal neutrophilic infiltrate. These histiocytes are described in maculo-papular eruptions induced by G-CSF, and should not be confused with a malignant infiltrate associated with a hemopathy. Vascular hyperplasia may be related to the angiogenic properties of G-CSF. Knowledge of these histological features would enable clinicians and histologists to recognize the appropriate diagnosis.

A woman fitted with a Mirena intrauterine system (IUS) for menorrhagia presented with a short history of fever and progressive skin lesions. Histological examination of a skin biopsy was compatible with the clinical diagnosis of Sweet's syndrome. Treatment was with topical and oral steroids, however the condition relapsed on reduction of the steroid dose. Symptoms finally resolved on removal of the IUS and the patient remained symptom free at 9-month follow-up. There have been previous reports of Sweet's syndrome in association with hormonal contraceptives, however this is believed to be the first reported case in association with a Mirena IUS.

Acute febrile neutrophilic dermatosis (Sweet syndrome) has been reported in a few adults receiving all-trans retinoic acid for acute promyelocytic leukemia. The authors report a case of Sweet syndrome associated with the administration of all-trans retinoic acid for acute promyelocytic leukemia in a pediatric patient.

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.

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.

We report a case of Sweet's syndrome associated with retinoic acid syndrome in a patient with acute promyelocytic leukemia treated with all- trans retinoic acid (ATRA). Sweet's syndrome appeared on day 6 of ATRA therapy for promyelocytic leukemia. It was associated with a mild retinoic acid syndrome, an inflammatory syndrome occurring in 25% of patients treated with ATRA and characterized by features of capillary leakage with systemic inflammatory signs. The ATRA therapy was discontinued for 11 days and treatment with corticosteroids improved the systemic and cutaneous signs. Only 11 cases of Sweet's syndrome associated with ATRA have been previously reported in the literature, involving only the skin in eight cases, the skin and muscles in two cases, and the lung, kidney, fascia, and muscles in one case. Sweet's syndrome was followed by retinoic acid syndrome in one of these cases. The previously reported cases are reviewed, and the mechanisms of Sweet's and retinoic acid syndromes and the link between them are discussed.