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Spider angioma is a cutaneous nevus caused by a vascular abnormality, characterized by a central red area with radiating reddish, web-like extensions. It is typically associated with liver cirrhosis, hyperestrogenism, and alcohol consumption. In this case report, we present a unique instance of a patient who developed spider angioma at the injection site of the meningitis vaccine as a long-term adverse effect. The lesion was treated with electrocautery and diminished within one week of treatment. This case highlights the potential for spider angioma to develop as a long-term adverse effect of the meningitis vaccine, a possibility that has not been previously reported. Further research is required to understand the underlying mechanisms and identify potential risk factors for this rare adverse effect.
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BACKGROUND: Fragile histidine triad (FHIT) is a tumor suppressor gene that is commonly inactivated in human tumors. Interestingly, the normal pattern of FHIT expression is largely unknown. AIM: This study is aimed to characterize the expression of FHIT protein in normal human tissues. MATERIALS AND METHODS: A total of 119 normal human tissue specimens were analyzed for the FHIT expression using immunohistochemistry technique. The inclusion criteria included: normal/inflammatory tissue with no evidence of cellular atypia. RESULTS: All studied specimens were stained positively with FHIT and showed either nuclear or cytoplasmic expression. Interestingly, the pattern of FHIT staining was similar among different specimens from each organ. FHIT is located predominantly in the nucleus, although cytoplasmic staining is also present in some cell types. Oral squamous epithelium, breast ductal epithelium, squamous and tubal metaplastic epithelium of the uterine cervix, esophageal squamous epithelium, salivary glands, and bronchial epithelia all strongly expressed the nuclear protein. In connective tissue, FHIT has shown strong cytoplasmic expression in histocytes including macrophages and dendritic cells, fibroblasts, and myofibroblasts. CONCLUSION: Documentation of the pattern of FHIT expression in normal tissues will contribute to our understanding of the normal function of this protein and to interpretation of potentially altered FHIT expression in human tumors.
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INTRODUCTION: Giant cell lesions are characterised histologically by multinucleated giant cells in a background of ovoid to spindle-shaped mesenchymal cells. There is a major debate whether these lesions are separate entities or variants of the same disease. Our aim was to study the nature of multinucleated and mononuclear cells from peripheral giant cell granuloma (PGCG), and central giant cell granuloma (CGCG) and giant cell tumor (GCT) of long bones using immunohistochemistry evaluation and to determine whether there is a correlation between recurrence and the markers used. MATERIALS AND METHODS: Ki-67, p53, Vimentin, smooth muscle specific actin, CD68 and alpha-1-antichymotrypsin were used to study 60 giant cell lesions. These included 26 CGCG, 28 PGCG, and 6 GCT cases using an avidin-biotin-complex immunohistochemistry standard method. RESULTS: All studied cases showed the same results except the percentage of Ki-67 positive mononuclear cells in PGCG was significantly higher than that of both CGCG and GCT (p<0.05). Interestingly, no statistical correlation between recurrence and the markers used was found. CONCLUSION: Our results may suggest that these lesions have the same histogenesis. The mononuclear stromal cells, both histiocytic and myofibroblastic, are thought to be responsible for the behavior of these lesions whereas the multinucleated cells are considered as reactive. This might support the argument that PGCG, CGCG and GCT are different variants for the same disease. Further studies using molecular techniques are required to elucidate why some of these lesions behave aggressively than others.