Sweet's syndrome: systemic signs and symptoms and associated disorders.

OBJECTIVE: To characterize the findings associated with acute febrile neutrophilic dermatosis (Sweet's syndrome [SS]) and the response of SS to treatment. DESIGN: We retrospectively reviewed 48 cases of SS encountered at the Mayo Clinic between 1980 and 1992. MATERIAL AND METHODS: Histopathologic specimens and medical records were studied to determine initial manifestations, patterns of involvement, systemic signs and symptoms (including mucosal, musculoskeletal, hematologic, pulmonary, hepatic, and renal findings), and conditions associated with SS. RESULTS: In patients with SS, the typical manifestations are the acute onset of tender, erythematous or violaceous nodules or plaques in association with fever, leukocytosis, and dermal neutrophilia. In our study group, the cutaneous lesions most frequently involved the arms and legs. Of our 48 patients, 26 (54%) had a hematopoietic, plasma cell, or malignant disorder, and many of these patients had associated anemia, especially the male patients. No single laboratory finding specifically indicated an association with serious systemic disease. Most patients were treated with a tapering dose of prednisone, which yielded a good response. CONCLUSION: Clinical acumen and appropriate laboratory tests are the main requirements for detection of hematologic disorders, internal malignant diseases, or other systemic conditions associated with SS.

An unusual case of severe griseofulvin-alcohol interaction.

Drug-alcohol interactions in patients who present to emergency departments with a severe "disulfiram-like" illness (including vomiting, diarrhea, flushing, tachycardia, and hypotension) must be recognized and treated appropriately. We report a case of such an interaction caused by oral griseofulvin and alcohol. Emergency physicians should be aware of this potential interaction.

Low-dose atrial natriuretic factor and furosemide in experimental acute congestive heart failure.

This study was designed to address three objectives in an experimental model of acute congestive heart failure (CHF) in the dog produced by rapid ventricular pacing. The first objective was to characterize cardiorenal and humoral responses before and during 2 h of acute CHF. The second objective was to determine the modulating action of iv furosemide upon these biologic responses to acute CHF, testing the hypothesis that furosemide-mediated natriuresis is associated with activation of the renin-angiotensin-aldosterone system (RAAS) compared with the control group. The third objective was to determine the modulating action of continuous low-dose atrial natriuretic factor (ANF) administration during acute CHF upon these biologic responses, testing the hypothesis that exogenous low-dose ANF would prevent activation of the RAAS and enhance the natriuretic action of furosemide. In the control group (Group 1; N = 6), plasma ANF increased after the onset of CHF; GFR and sodium excretion were maintained without activation of this RAAS despite arterial hypotension. In Group 2 (N = 6), furosemide in acute CHF increased sodium excretion but in association with a decrease in GFR and activation of the RAAS. Low-dose exogenous ANF and furosemide (Group 3; N = 6) in acute CHF were associated with a maintenance of GFR, no activation of the RAAS, and potentiation of furosemide-induced natriuresis. In summary, these studies demonstrate that furosemide potently increases sodium excretion in acute CHF, but with a decrease in GFR and activation of the RAAS. Low-dose ANF in acute CHF with furosemide maintains GFR, attenuates activation of the RAAS, and potentiates natriuresis.

Sweet syndrome: acute febrile neutrophilic dermatosis.

Sweet, in 1964, described a skin condition characterized by fever, leukocytosis, tender erythematous plaques, and, histopathologically, a predominantly neutrophilic dermal inflammation. However, other dermatologic conditions can present with similar clinical and histological features. Therefore, diagnostic criteria are important for the correct diagnosis. Use of systemic steroids is the treatment of choice for Sweet syndrome. A number of other medications can be useful at times, such as potassium iodide, dapsone, indomethacin, and colchicine.