The present study was designed to identify the role of folate, B12, homocysteine, and polymorphisms of methylene tetrahydrofolatereductase (MTHFR) gene in cervical carcinogenesis among 322 women from Kerala, South India. Serum folate, vitamin B12 (chemiluminescence assay), and homocysteine (EIA) along with genetic polymorphisms of MTHFR gene (polymerase chain reaction/restriction fragment length polymorphism) were analyzed for 136 control subjects, 92 low-grade squamous intraepithelial lesions (LSIL) subjects, and 94 invasive cervical cancer cases (ICC). Statistically significant associations between MTHFR polymorphisms, serum homocysteine, and folate levels with cervical carcinogenesis were not evident, but we found that these parameters acted as effect modifiers of serum vitamin B12. The risk estimates observed for B12 became prominent only when there was a deficiency in serum folate levels [LSIL-odds ratio (OR): 14.9 (95% CI: 2.65 to 84.4); ICC-OR = 8.72 (95% CI = 1.55 to 48.8)] or when MTHFR A1298C polymorphic variant was present [LSIL-OR = 9.8 (95% CI = 2.61 to 36.7); ICC-OR = 10.0 (95%CI = 2.5 to 39.3)]. The statistical significance of this effect modification was further studied using an interaction model, where only folate was observed to have an influence on B12 levels as suggested by the odds ratio of 7.11 (95% CI = 0.45 to 111.9) obtained for ICC group, implicating a synergistic role of these 2 vitamins in invasive cervical cancer.
JXG is a disorder classified under histiocytosis. It usually affects children and commonly presents with skin lesions. Intracranial lesions are uncommon and usually solitary. We present the case of a child who had extensive intracranial involvement with multiple enhancing solid lesions in the cerebellum, brain stem, thalami, and bilateral cerebral hemispheres on MR imaging.
Neurocysticercosis (NCC) is a common cause of morbidity in many developing countries and a common cause of seizure disorder in children and adults. The 4 stages of NCC are vesicular, vesicular colloidal, granular nodular, and nodular calcified.1 The appearance on MR imaging would depend on the stage of the disease. Most commonly, NCC presents as isohypointense lesions on T1-weighted MR imaging. To our knowledge, extensive hyperintense signals on T1-weighted images have not been described for NCC. A young man 22 years of age presented with headache on and off for 5-6 months. There was no history of seizures, which was also very unusual in his case. Plain and contrast MR imaging of the brain was performed. T1-weighted images revealed multiple hyperintense foci of varying sizes, in bilateral cerebral, cerebellar hemispheres and the brain stem (Fig 1). The T1 hyperintense signals were thicker in the right cerebellar hemisphere (Fig 2). Multiple other lesions were revealed on gradient images, which were not demonstrated on routine MR images. These multiple extensive T1 hyperintense signals were confirmed to be calcifications on CT, which was performed subsequent to the MR imaging. Few of the T1 hyperintense lesions showed mild enhancement on contrast administration.The MR imaging appearance and contrast characteristics would depend on the stage of the parasitic cyst. The unusual appearance of such extensive T1 hyperintense signals, as seen in our patient, has not been described earlier and is probably due to calcifications, which are known to appear hyperintense on T1-weighted MR imaging.
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