ObjectiveTo explore the clinical manifestations, pathogenesis, prognosis and the therapeutic modalities of the patients with solid tumors combined with remarkable hematologic abnormalities. MethodsGastric cancer in a paitnet was diagnosed by endoscopy as well as pathological biopsy and myeloproliferative neoplasms (MPNs) were excluded through bone marrow examinations. Therefore, the primary and metastatic malignancies were excised. ResultsAlthough surgical operation improved the hematologic changes, the high tumor load caused the poor prognosis. ConclusionThe solid tumors may present with hematologic manifestations which is similar to the symptoms of MPNs; it belongs to the para-neoplastic phenomenon and may be an independent poor prognostic factors.
目的 探討內鏡下治療膽管乳頭狀瘤的價值。方法 6例經病理學檢查證實的膽管乳頭狀瘤患者在行“膽道探查+ T管引流術”后6～8周行膽道鏡下高頻電刀燒灼術，對術后治療效果進行評估。結果 6例患者術后膽汁引流量逐漸增多至100～400 ml/d(平均250 ml/d)，膽汁黏稠度明顯減輕，黃疸減退。術后隨訪1～3年，平均2年，3例患者術后黃疸、腹痛明顯減輕，至今無復發； 2例在繼續治療中； 1例患者隨訪半年，T管引流通暢，但因嚴重肺部感染并發多器官功能衰竭死亡。結論 內鏡下高頻電刀燒灼治療膽管乳頭狀瘤能有效緩解患者的臨床癥狀，明顯提高患者的生存質量。
目的 增加對治療相關性繼發白血病的認識。 方法 報道非霍奇金淋巴瘤治療后2年繼發急性髓細胞白血病M6型1例，結合文獻討論治療相關性白血病的發病機制、治療、預后。 結果 1例73歲非霍奇金淋巴瘤患者接受R（Rituxmab，利妥昔單抗）－CHOP環磷酰胺+多柔比星+長春新堿+潑尼松方案規律化學治療。治療結束24+個月后，經骨髓涂片及細胞免疫分型診斷為急性髓細胞白血病M6型，染色體檢查為：44～48，XY，del（5）（q12q33），-8，-10，der（12）t（4；12）（q11-q12；p13），其一般情況急劇惡化并死亡。 結論 治療相關性白血病的發生可能與烷化劑等化療藥物使用和免疫受損等有關，利妥昔單抗導致第二腫瘤的發生暫時不能除外。治療相關性白血病常伴有復雜染色體核型，其病情發展迅速，治療效果差，生存期明顯縮短。Objective To improve the understanding of secondary therapy-related leukemia. Methods The clinical data of one patient with non-Hodgkin lymphoma which transformed into acute myeloid leukemia M6 2 years after chemotherapy were studied. We discussed the pathogenesis, treatment and prognosis of therapy-related leukemia with literature review. Results A 73-year-old patient diagnosed to have non-Hodgkin’s lymphoma accepted R-CHOP chemotherapy.Two years after the treatment, the disease finally developed into acute myeloid leukemia M6 confirmed by cytogenetics, bone marrow morphology and flowcytometry analysis. The chromosome analysis demonstrated complex karyotypes as 44-48, XY, del (5) (q12q33), -8, -10, der (12) t (4; 12) (q11-q12; p13). His general status deteriorated rapidly and soon after the patient died. Conclusions Occurrence of therapy-related leukemia may be due to the administration of alkylating agents, topoisomerase inhibitors and damage of immune function. Therapy-related leukemia often occurs with complex karyotypes and progresses rapidly with poor treatment response.