Primary liver tumors in children are rare with malignant hepatoblastoma being the most common neoplasm. In this report, we describe the diagnosis and clinical management of a large liver tumor in a 3-year-old child that displayed the features of both, conventional hepatoblastoma and malignant teratoma. Pathological assessment on a pre-operative bioptical specimen showed an immature teratoid tumor with no area of hepatoblastic differentiation present. Histological and immunhistological examination of the resected tumor specimen additionally showed tumor areas of very different differentiation pattern intermixed with each other, namely areas of hepatoblastoma-typical and neuroblastoma-like morphology as well as areas of rhadomyosarcomatous differentiation.After chemotherapy the tumor size increased and an extended right hemihepatectomy was performed. Post-operatively, the general condition of the child improved and adjuvant chemotherapy was started two weeks later. 36 months after initial diagnosis the patient is healthy, in good general condition, and without any sign of residual tumor disease.Overall, we describe the diagnosis and clinical management of a large liver tumor in a 3-year-old child that displayed the features of both, conventional hepatoblastoma and malignant teratoma and was designated as mixed hepatoblastoma and teratoma. Though mesenchymal tumor portions can occur within hepatoblastomas, most commonly osteoid or chondroid, our case is different as it presents a large spectrum of mesenchymal and epithelial differentiation pattern in most of the lesion.
Functional dysphagia therapy (FDT) is a noninvasive procedure that can accompany percutaneous endoscopic gastrostomy (PEG) treatment and supports transitioning from tube to oral feeding. In this retrospective study, we investigated the outcome of FDT with or without PEG feeding. Patients with dysphagia were divided into two groups: those with PEG feeding (N = 117) and those with exclusively oral feeding (N = 105). Both groups received functional training (oral motor skills/sensation, compensatory swallowing techniques) from speech-language therapists. Functional oral intake, weight, Barthel index, and speech and language abilities were evaluated pre- and post-training. The non-PEG group showed a significant post-treatment improvement in functional oral intake, with diet improvement from pasty consistency to firm meals in most cases. However, even severely disordered patients (with PEG feeding) showed a significant increase in functional oral intake, still requiring PEG feeding post-treatment but able to take some food orally. The sooner a PEG was placed, the more functional oral intake improved. Significantly more complications and higher mortality occurred in the PEG group compared to the group with exclusively oral feeding. Dysphagia treatment in the elderly requires a multiprofessional setting, differentiated assessment, and functional training of oral motor skills and sensation and swallowing techniques.
Epstein-Barr virus (EBV)-associated B-cell post-transplantation lymphoproliferative disorder (PTLD) is a severe complication following stem cell transplantation. This is believed to occur as a result of iatrogenic immunosuppression leading to a relaxation of T-cell control of EBV infection and thus allowing viral reactivation and proliferation of EBV-infected B-lymphocytes. In support of this notion, reduction of immunosuppressive therapy may lead to regression of PTLD.We present a case of an 18-year-old male developing a monomorphic B-cell PTLD 2 months after receiving an allogenic stem cell transplant for acute lymphoblastic leukemia. Reduction of immunosuppressive therapy led to regression of lymphadenopathy. Nevertheless, the patient died 3 months afterwards due to extensive graft-vs.-host-disease and sepsis. As a diagnostic lymph node biopsy was performed only after reduction of immunosuppressive therapy, we are able to study the histopathological changes characterizing PTLD regression. We observed extensive apoptosis of blast cells, accompanied by an abundant infiltrate comprising predominantly CD8-positive, Granzyme B-positive T-cells. This observation supports the idea that regression of PTLD is mediated by cytotoxic T-cells and is in keeping with the observation that T-cell depletion, represents a major risk factor for the development of PTLD.
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