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.

/pdf/sweet-s-syndrome-a-comprehensive-review-of-an-acute-febrile-1noo2fa818.pdf

Sweet's syndrome – a comprehensive review of an acute febrile neutrophilic dermatosis

Sweet's syndrome, also referred to as acute febrile neutrophilic dermatosis, is characterized by a constellation of symptoms and findings: fever, neutrophilia, erythematous and tender skin lesions that typically show an upper dermal infiltrate of mature neutrophils, and prompt improvement of both symptoms and lesions after the initiation of treatment with systemic corticosteroids. Hundreds of patients with this dermatosis have been reported. The manifestations of Sweet's syndrome in these individuals have not only confirmed those originally described by Dr Robert Douglas Sweet in 1964, but have also introduced new features that have expanded the clinical and pathologic concepts of this condition. The history, clinical characteristics, laboratory findings, associated diseases, pathology, and treatment options of Sweet's syndrome are reviewed. The evolving and new concepts of this dermatosis that are discussed include: (i) Sweet's syndrome occurring in the clinical setting of a disease-related malignancy, or medication, or both; (ii) detection of additional sites of extracutaneous Sweet's syndrome manifestations; (iii) discovery of additional Sweet's syndrome-associated diseases; (iv) variability of the composition and/or location of the cutaneous inflammatory infiltrate in Sweet's syndrome lesions; and (v) additional efficacious treatments for Sweet's syndrome.

Sweet's syndrome revisited: a review of disease concepts

OBJECTIVE: To assess the nature and rates of complications and recurrences after completion lymph node dissection (CLND) following positive sentinel lymph node biopsy (SLNB) in melanoma patients. SUMMARY BACKGROUND DATA: In contrast to SLNB, CLND is associated with considerable morbidity. CLND delays nodal recurrence, thereby prolonging disease-free survival (DFS), but not overall melanoma-specific survival. Elaborate studies on morbidity and recurrence rates after CLND are scarce. Therefore, many controversies concerning extent and nature of CLND exist. METHODS: We conducted a retrospective study on 100 melanoma patients, on whom we performed CLND between October 1999 and December 2005. The median observation period was 38.8 months. RESULTS: We performed a total of 102 CLNDs, [46.1% axillary (47/102), 42.2% groin (43/102), 11.8% neck (12/102)]. Groin dissection (GD) and axillary dissection (AD) led to comparable morbidity (47.6% and 46.8%), but complications were more severe in GD, mandating additional surgery in 25.6% (11/43), versus 8.5% (4/47) in AD. Of the GD patients, 18.5% (8/43) were readmitted for complications compared with 10.4% (5/47) of AD patients. Only 8.3% (1/12) of ND patients suffered complications, mandating neither readmittance nor further surgery. During the median observation period, 65 (65%) of these patients showed DFS, and 35 (35%) exhibited recurrences after a median DFS of 12.5 months. Of the recurrences, 31.4% were nodal, 42.9% distant, and 25.7% local/in-transit. Of our AD patients, 28.3% suffered recurrences (13/46), as did 33.3% of the GD (14/42) and 66.7% of the ND patients (8/12). CONCLUSIONS: CLND is fraught with considerable morbidity. Local control of the dissected nodal basins was achieved with a modified radical approach in ADs (levels I + II only) and, to a lesser extent, GDs, but not in NDs. Clinical trials are necessary to establish guidelines on the extent of lymphatic dissection.

Morbidity and recurrence after completion lymph node dissection following sentinel lymph node biopsy in cutaneous malignant melanoma.

Melanoma is rarely described in the pediatric population. However, recent studies show that the incidence may be increasing. The diagnosis of melanoma presents unique challenges in this age group. There may be predisposing factors that affect children more than adults. A high index of suspicion is necessary in order to make a timely diagnosis. Prompt surgical treatment by individuals with expertise in care of patients with melanoma with potentially curative excision and appropriate lymph node evaluation is important to optimize survival. Careful review of all specimens by an experienced dermatopathologist is important. Through cooperation with adult trials and potential inclusion of pediatric patients in evaluations of new therapies, further progress against this disease can hopefully be addressed in all age groups.

Melanoma in children and adolescents

Background: Sweet disease, also known as acute febrile neutrophilic dermatosis, is a multisystem inflammatory disorder characterized by painful erythematous plaques and aseptic neutrophilic infiltration of various organs. Skin biopsies typically demonstrate dermal infiltration with neutrophils in the absence of vasculitis. Sweet disease responds to systemic corticosteroids. The CNS can also be involved. Methods: The authors performed a survey on neuro-Sweet disease (NSD) in Japan and obtained detailed information about 16 cases. They analyzed 42 cases, including 26 cases documented in the literature, and assessed clinical and laboratory criteria for the diagnosis. Results: Thirteen cases also fulfilled the criteria for the diagnosis of Behçet disease. The clinical features of 27 cases, which the authors classified as probable NSD, are as follows: 1) both sexes are almost evenly affected; 2) people of ages 30 to 70 years are affected; 3) encephalitis and meningitis are common neurologic manifestations; 4) any region of the CNS can be involved, resulting in a variety of neurologic symptoms; 5) there is a strong human leukocyte antigen-Cw1 association; 6) systemic corticosteroids are highly effective for most of the neurologic manifestations, although recurrences are not infrequent. Conclusions: Neuro-Sweet disease is a distinct entity that may account for some cases of idiopathic encephalomeningitis.

[Neuro-Sweet disease].

background The superiorly based nasalis myocutaneous island pedicle flap with bilevel undermining is a recently described bipedicled flap used for repair of nasal tip and supratip defects This flap was used for the repair of small to medium-size defects of the nasal tip and supratip regions



objective To describe a single-pedicled modification of this flap for the reconstruction of lateral nasal defects at or above the alar groove



methods With the use of diagrams and fresh cadaver dissection, we demonstrate the method of preparing, raising, and placement of this new flap We further elucidate in an illustrative way the efficacy of bilevel undermining as it is used for achieving greater flap mobility Finally, we show representative cases with pre- and postoperative results



results We describe the senior author's 4-year experience in the development of this flap



conclusion The nasalis myocutaneous island pedicle flap with bilevel undermining, a new method for repair of lateral nasal defects at or above the alar groove, yields excellent functional and cosmetic results Bilevel undermining is a new and valuable method of achieving greater tissue mobility in muscle-based flaps

Nasalis myocutaneous island pedicle flap with bilevel undermining for repair of lateral nasal defects.

Acute febrile neutrophilic dermatosis, or Sweet's syndrome, was first described in 1964 and consists of a triad of erythematous cutaneous plaques infiltrated by neutrophils in association with fever and leukocytosis. Sweet's syndrome has been reported to be associated with conditions ranging from upper respiratory tract infections to inflammatory bowel disease to rheumatoid arthritis. We report a patient with a 2-year history of Sweet's syndrome in whom idiopathic progressive bilateral sensory neural hearing loss (IPBSNHL) developed. IPBSNHL is a suspected immunologically mediated hearing loss first described by McCabe in 1979. On the basis of this association, hearing evaluation should be considered in the initial and subsequent examinations of the patient with Sweet's syndrome. (J Am Acad Dermatol 2000;42:932-5.)

https://www.jaad.org/article/S0190-9622(00)90276-7/pdf

Sweet’s syndrome in a patient with idiopathic progressive bilateral sensorineural hearing loss☆☆☆

Background.Reconstruction of full-thickness defects of the nasal tip is one of the most challenging aspects of cutaneous oncologic surgery. It is imperative that the cutaneous surgeon be intimately familiar with all the available surgical options to provide for the best postoperative outcome.Objecti

Superiorly based nasolabial interpolation flap for repair of complex nasal tip defects.

Early clinical observation in cancer patients suggested that tumors spread in a methodical, stepwise fashion from the primary site, to the regional lymphatics, and only then to distant locations. Based on these observations, the regional lymphatics were believed to be mechanical barriers, at least temporarily preventing the widespread dissemination of tumor. Despite evidence now available disputing its validity, this barrier theory has guided the surgical management of the regional lymphatics in cancer patients for more than a century, influencing the use of such surgical modalities as therapeutic lymph node dissection, elective lymph node dissection, and most recently lymphatic mapping and sentinel lymph node biopsy. No published randomized controlled trial exists that demonstrates improved overall patient survival for cancer of any type, including melanoma, after surgical excision of regional lymphatics. This article will review the biology of lymphatics as it relates to regional tumor metastasis, and based on available information, offer practical recommendations for the clinical dermatologist and their patients who have cutaneous melanoma.

Cutaneous melanoma: therapeutic lymph node and elective lymph node dissections, lymphatic mapping, and sentinel lymph node biopsy.

WE ARE WRITING to warn and remind clinicians that ultraviolet (UV) light (sunburn) and trauma to an otherwise benign melanocytic nevus may result in transient histologic changes simulating melanoma in situ. These changes, including epidermal melanocyte atypia and Pagetoid spread, may simulate invasive melanoma when associated with a junctional nevus. The importance to the clinician is to recognize these effects and consider alternative timing for biopsy of normal appearing nevi that have been recently traumatized or exposed to UV light. A common scenario conveyed by patients referred to our practice for excision of pigmented lesions is that a family member or friend noticed a mole during a vacation to a sunny climate while the patient was wearing a bathing suit. Frequently the patient received a significant amount of UV light or sunburn at the time the mole was noted. The anxiety associated with the recognition of this nevus, even if clinically benign, prompts many patients to seek medical care immediately after returning from their vacation, while evidence of recent heavy sun exposure is still present. The physician, when confronted with this history, often biopsies the lesion in question. While the lesion may in fact be a benign nevus, a subsequent diagnosis of atypical nevus or melanoma is made, leading to a chain of events with life-long ramifications. The patient is referred for excision and diagnostic examination that may include sentinel node biopsy, possible adjuvant therapy and life-long follow-up. Thus the importance of the correct initial diagnosis cannot be overemphasized. Although much is known about the impact of UV irradiation on melanocytes, only a handful of articles have addressed the histologic consequences of acute erythemogenic doses of UV light on melanocytic nevi. 1–5

Sunburn, trauma, and the timing of biopsies of melanocytic nevi.

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