Erythema marginatum secondary to streptococcal infection is classically associated with acute rheumatic fever and fulfills one of the Jones criteria for this diagnosis. We describe a case of streptococcal associated erythema marginatum without rheumatic heart disease in a 12 year old male with post streptococcal arthralgia and myalgia. The rash was originally suggestive of urticaria. He was initially seen with a five week history of fever. Examination and laboratory evaluation did not yield an acute infectious etiology for his fever. However anti-streptolysin O and anti-deoxyribonuclease B were very elevated. Historically, he had a sore throat 3 weeks prior to his presentation and had been treated by his PCP with amoxicillin; no cultures were done. Based on this history and his elevated anti-streptococcal antibody titers, he was started on cefadroxil and non-steroidal antiinflammatory drugs. Several days after antibiotics were started and several weeks after his fever and arthralgia symptoms had begun, he developed a trunk and upper arm rash with raised, erythematous borders. Dermatology diagnosed it as urticaria and cetirizine was recommended. The antibiotic was switched to azithromycin but the rash persisted. He was referred to rheumatology who diagnosed a post-streptococcal syndrome. He was started on penicillin under close observation and no changes in the rash were noted. His aches improved in a matter of days. Dermatology biopsied his rash and the histopathology was consistent with both urticaria and published reports of erythema marginatum. Electrocardiogram and serial echocardiographs were normal. His anti-streptococcal titers returned to near normal in 12 months. His elevated inflammatory markers normalized. This case demonstrates a post-streptococcal syndrome with a rash suggestive of urticaria, but was later confirmed to be erythema marginatum in the absence of carditis. Confirming the diagnosis of erythema marginatum was critical, since it enabled a diagnosis of rheumatic fever which had direct implications for prophylactic treatment.
This article has been removed: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal) This meeting abstract has been removed by the Publisher. Due to an administrative error, abstracts that were not presented at the ISDN 2014 meeting were inadvertently published in the meeting's abstract supplement. The Publisher apologizes to the authors and readers for this error.
Oral squamous cell carcinoma (OSCC) is the most frequent cancer and constitutes a major health problem in India, representing the leading cause of death. The aim of the present investigation was to study the major chromosomal aberrations (CA) like deletion, translocation, inversion and mosaic in OSCC patients of South India. Genetic factors play an important role in the etiology of OSCC. Totally 300 oral sumucosa fibrosis symptoms patients were chosen from various hospitals from southern india by advent screening like Toluidine blue staining and brush biopsy. Finally 103 severely affected OSCC patients were selected. 5ml of peripheral blood samples were taken from affected patients. Equal numbers of normal healthy control subjects were chosen after signing a consent form. Cytogenetic studies were performed by using Giemsa-banding technique and finally the results were ensured by spectral karyotyping (SKY) technique. In the present investigation, major CA like deletion, translocation, inversion and mosaic were identified in experimental subjects. Results showed frequent CA in chromosomes 3p, 3q, 8p, 7p, 9p, 11q, 17p, 19q and X. In comparison with experimental subjects, the control subjects exhibited very low levels of major CA (P<0.05). In the present study, the high frequency of centromeric rearrangements indicates a potential role for mitotic irregularities associated with the centromere in OSCC tumorigenesis, interesting chromosomal regions which may harbor susceptibility genes. Identification of chromosome alterations may be helpful in understanding the molecular basis of the disease in a better manner.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B45.
This article has been removed: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal) This meeting abstract has been removed by the Publisher. Due to an administrative error, abstracts that were not presented at the ISDN 2014 meeting were inadvertently published in the meeting's abstract supplement. The Publisher apologizes to the authors and readers for this error.
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