Acquired cutis laxa in childhood Sweet's syndrome
ABSTRACT In Sweet's syndrome, the essential features are the characteristic morphology of the lesions, their histologic appearance, the dramatic response to corticosteroids and the absence of scarring. We report an 8-month-old infant in whom Sweet's syndrome was diagnosed and who developed acquired cutis laxa in the skin lesions.
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- "Because of underlying medical conditions, the follow-up is an important part of treatment and its results decide about further patient management with other specialists co-operation. For instance, recent observations in paediatric patients suggest an evaluation of dermatosis-related cardiac involvement in children suffering from post-SS cutis laxa . "
ABSTRACT: Diagnosis of paraneoplastic skin syndromes associating neoplastic processes is assumed as the crucial aspect of dermatological practice. Knowledge of clinical findings of dermatoses suggesting coincidence of malignant proliferative processes facilitates diagnostic and therapeutic procedures. We would like to present a case of Sweet's syndrome, qualified for comparative paraneoplastic skin syndromes. Sweet's syndrome, acute, febrile neutrophilic dermatosis, was first described by Robert Douglas Sweet in 1964 as a disorder characterized by fever, skin lesions of erythematous-infiltrative character, leukocytosis with neutrophilia and dense infiltrations of dermis by mature neutrophils. Sweet's syndrome aetiology is not fully understood, although cytokine abnormalities suggest that Th1 lymphocytes play an important role in pathogenesis of the dermatosis. Factors inducing Sweet's syndrome include: haematopoietic hyperplasia; neoplasms: genitourinary, breast, gastrointestinal; infections of the respiratory and alimentary system; inflammatory bowel diseases; drugs; pregnancy and vaccinations. Systemic corticosteroids are the "gold standard" of Sweet's syndrome treatment; potassium iodide or colchicine may also be used. Indomethacin, clofazimine, cyclosporine A and sulfones are the second-line drugs.Postepy Dermatologii I Alergologii 02/2014; 31(1):47-52. DOI:10.5114/pdia.2014.40661 · 0.66 Impact Factor
Article: Sweet Syndrome in Children[Show abstract] [Hide abstract]
ABSTRACT: The objective of this study was to describe the clinical features of Sweet syndrome in children. Our study population consisted of seven children diagnosed with Sweet syndrome over a 22-year period. Age, sex, appearance and location of lesions, associated signs and symptoms, past medical history, pathology, and subsequent disease course were documented for each patient. Fever and typical lesions were reported in most of patients in our study. The majority of patients presented with less-typical findings, such as pustules, vesicles, bullae, oral ulcerations, atrophic scars, and evidence of pathergy. Of the seven children in our study, four were found to have a preceding nonspecific upper respiratory or gastrointestinal infection, and two were diagnosed with an underlying hematologic malignancy. Our results suggest that atypical lesions are relatively common in children with Sweet syndrome and that underlying malignancy is associated with a minority of cases of pediatric Sweet syndrome.Pediatric Dermatology 01/1981; 29(1):38-44. DOI:10.1111/j.1525-1470.2011.01534.x · 1.52 Impact Factor
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ABSTRACT: Currently, most of esophageal diverticula arise as the result of a pulsion effect. Some esophageal motor disorders increase the intraluminal pressure and after some time, the diverticula grow through a weak point of esophageal wall. In these cases, the surgical treatment of choice is the myotomy associated with diverticulopexy or diverticulectomy. Adding a fundoplication is accepted to avoid the consequences of gastroesophageal reflux after myotomy in the epiphrenic diverticula surgery. There are other causes of esophageal diverticula that change the resistance of esophageal wall. Cutis laxa, a congenital or acquired connective disease, is a strange one. In our patient, a good result was reached modifying the standard technique accord to its ethiopathogenic mechanism.Diseases of the Esophagus 09/2010; 23(7):E39-41. DOI:10.1111/j.1442-2050.2010.01067.x · 2.06 Impact Factor