Меланома кожи у детей встречается очень редко и по ряду характеристик отличается от меланомы кожи у взрослых. Ранняя диагностика этой высокозлокачественной опухоли является главным условием успешного лечения. При определении заболевания у детей обычно используют те же методы, что и у взрослых. Адекватность такого подхода требует проверки. Цель исследования-описание процедур постановки диагноза для крупного врожденного пигментного новообразования кожи у ребенка. Описание клинического случая врожденной опухоли в области лучезапястного сустава у девочки 5 мес. По месту жительства было высказано предположение о гемангиоме. При диагностике в НИИ детской онкологии и гематологии НМИЦ онкологии им. Н. Н. Блохина проведены ультразвуковое исследование, магнитно-резонансная томография, трепанобиопсия, открытая биопсия. Материалы последней исследованы гистологически на препаратах, окрашенных гематоксилином и эозином, и иммуногистохимически путем детекции индикаторов пролиферации клеток, антигенов меланоцитарного ряда дифференцировки, белков, используемых как маркеры собственно меланомы, антигенов тканевой совместимости. Сделано заключение: узловая пигментная меланома кожи. Проведено иссечение опухоли. Безрецидивный период на момент подготовки сообщения-12 мес. Заключение. Описаны процедуры диагностики и лечения 5-месячной девочки с врожденным пигментным новообразованием кожи в области лучезапястного сустава. В процессе диагностики использованы подходы, применяемые при выявлении более частой и лучше изученной меланомы кожи у взрослых. Для подтверждения адекватности использованных в работе методов в диагностике пигментных новообразований кожи у детей целесообразно продолжение исследований.
Results of ELISA investigation of the pretreatment sPD-1 and sPD-L1 content in blood serum of 133 bone neoplasms patients aged 6-70 years and 57 practically healthy control persons aged 12-70 years are described. In 14 patients the neoplasms were of a benign character, in 16 - borderline giant-cell bone tumor was diagnosed, and in 103 - malignant bone lesions including 39 osteosarcomas and 42 chondrosarcomas were revealed. The sPD-1 receptor concentrations in blood serum did not differ between control healthy persons and primary bone tumor patients, while serum sPD-L1 level in bone tumor patients was statistically significantly increased (p<0.0000001). By means of ROC curve construction a cut-off sPD-L1 level of 16.5 pg/ml was found that imposed 75,9% sensitivity and 75,4% specificity in relation to healthy control. However, the frequency of sPD-L1 levels exceeding 16.5 pg/ml was approximately similar in benign, borderline and malignant bone tumor patients. Analysis of the pattern of sPD-1 and sPD-L1 circulation in the peripheral blood of patients with the most prevalent malignant bone tumors - osteosarcoma and chondrosarcoma - demonstrated that in both sarcoma types sPD-L1 level was significantly higher than in control, but in patients with chondrogenic tumors the soluble ligand sPD-L1 dominates in the circulation, while in those with osteogenic tumors - sPD-1 receptor prevails. In particular, sPD-1 level is statistically significantly higher in patients with typical osteosarcoma than in those with typical chondrosarcoma (p=0.002437), and sPD-L1/sPD-1 concentration ratio in chondrosarcoma is highly significantly more than 2-fold higher than in osteosarcoma (0.81 and 0.35 respectively; p=0.000284). The sensitivity of sPD-L1 ≥16.5 pg/ml test in typical osteosarcoma patients’ group comprised only 70.2%, and in those with typical chondrosarcoma - 84.6%. Serum sPD-1 and sPD-L1 concentrations in osteosarcoma and chondrosarcoma patients were not associated with the indices of tumor advancement, its histological grade, localization in the osseous system, and type of affected bone. Thus, it can be concluded that the ratio between circulating soluble forms of the receptor and the ligand of PD-1/PD-L signaling pathway differs between patients with chondrogenic and those with osteogenic tumors, sPD-L1 being diagnostically valuable mostly for chondrogenic bone neoplasms.
Hyperparathyroid crisis (HPC) in children suffering from urine stone disease is developed because of fast and acute raise of calcium content in blood. Diagnostics and treatment process of children with urine stone disease and further developed HPC was examined. The crisis developed due to a sharp increase in concentration of parathyroid hormone in blood serum. Due to successful diagnostics and treatment, two patents were cured, and, because of late entering and HPC complications with comatose state, the taken treatment was not successful.
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