口服枸橼酸铁水合物治疗尼拉帕尼所致贫血的疗效观察：1例
抽象的
使用聚腺苷二磷酸核糖聚合酶抑制剂进行维持治疗可能会产生不良反应，包括血液毒性，并可能限制癌症患者的治疗潜力。尼拉帕尼引起的贫血会对生活质量产生负面影响。亚铁（例如柠檬酸亚铁钠）、叶酸或维生素 B12 无法改善贫血。口服柠檬酸铁水合物可增加循环铁水平和肝铁蓄积，改善接受血液透析的肾衰竭患者的肾性贫血。三价铁的吸收率被认为远高于亚铁。
入院患者为一名 57 岁的日本女性，患有 IIIB 期卵巢癌，接受了初次减瘤手术和标准卡铂 - 紫杉醇化疗联合贝伐单抗，随后接受尼拉帕尼 (200 mg/天) 维持治疗。患者开始口服 SFC (100 mg/天) 以治疗尼拉帕尼相关贫血。然而，在开始尼拉帕尼治疗后 3 个月内，她需要三次两单位的浓缩红细胞输血。患者被诊断为尼拉帕尼相关贫血。开始尼拉帕尼治疗 1 个月后的血液检查结果如下：红细胞，211×104/μL；血红蛋白，7.0 g/dL；红细胞比容，20.8%；网织红细胞，0.2%；血小板计数，18.0×104/μL。患者改用口服柠檬酸铁水合物（剂量为 500 mg/天），并恢复尼拉帕尼治疗。患者未出现 3 级尼拉帕尼相关血液学毒性，并实现了输血独立性。
柠檬酸铁水合物可能是一种安全、有效且耐受性良好的口服药物，用于治疗尼拉帕尼相关贫血患者。
背景
卵巢癌是妇科恶性肿瘤死亡的主要原因 [1]。上皮性卵巢癌 (EOC) 的一线治疗包括减瘤手术和以铂类/紫杉烷为基础的联合化疗 [2]。聚（ADP-核糖）聚合酶 (PARP) 抑制剂改变了 EOC 的治疗策略 [3,4]。根据合成致死概念，患有 BRCA 突变和/或同源重组缺陷 (HRD) 的 EOC 患者可从 PARP 抑制剂中获益 [4,5,6,7]。因此，对于患有 BRCA 突变或 HRD 的晚期 EOC 患者，PARP 抑制剂（如尼拉帕尼）可作为有效的维持治疗。与尼拉帕尼相关的不良事件包括血液学异常（贫血、血小板减少和白细胞减少）和胃肠道症状（恶心和疲劳）[8]。 25.3–28.7% 的患者会出现 3 级或 4 级贫血，可通过减少剂量、中断、停药或输注红细胞 (RBC) 进行治疗 [9]。贫血通常发生在尼拉帕尼维持治疗后 3 个月内 [10]。值得注意的是，补充铁、叶酸或维生素 B12 是否能改善 PARP 抑制剂引起的贫血仍不清楚。
本文报道了一位 57 岁日本女性因服用尼拉帕尼导致贫血而接受口服柠檬酸铁水合物 (FCH) 治疗的病例。口服 FCH 可能是治疗尼拉帕尼导致贫血的一种选择。
病例介绍
A 57-year-old nulliparous Japanese woman visited our clinic for the first time, presenting with dull left lower abdominal pain lasting for a few weeks. Transvaginal ultrasound (TVS) showed a left unilocular ovarian cystic mass, measuring 60 mm, containing a solid component on the cul-de-sac of Douglas (Fig.1). The patient was referred to the Department of Gynecology, Nara Medical University Hospital in September 2020 for the diagnosis of ovarian tumor. The patient was a housewife with normal social, emotional, and cognitive development and had normal environmental and employment history. There was no past medical, surgical, and medication history. She had never smoked or consumed alcohol. Neurological examinations were unremarkable. Evaluation of the patient’s family history revealed that her father died of lung cancer, all three of her paternal uncles succumbed to colon cancer, two paternal aunts died of gastric cancer and colon cancer, respectively, and one maternal uncle was treated for leukemia. In addition, her paternal grandfather died of gastric cancer. All three of her brothers are fine. Vital signs on admission showed a body temperature of 36.3 °C, blood pressure of 132/74 mm Hg, and respiratory rate of 20/minute. She was obese (weight 79 kg, height 158 cm, body mass index 31.6 kg/m2). A pelvic mass was palpated on the left side of the uterus during physical examination. Pelvic magnetic resonance imaging (MRI) showed a 57 × 41 × 39 mm cystic mass with solid component originating in the left adnexa. The cystic part is of liquid signal, the solid component had high signal intensity on T2-weighted imaging (T2WI), and had low signal intensity on T1-weighted imaging (T1WI), with hyperintensity on diffusion-weighted images (DWI) (Fig.2). In addition,18F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) scan revealed increased FDG uptake in solid components of the tumor [maximum standardized uptake value (SUVmax): 19.9] (Fig.3). No distant metastases were detected with staging CT and FDG-PET/CT. The patient had elevated serum levels of cancer antigen (CA) 125 (89 U/mL), but CA19-9 and carcinoembryonic antigen (CEA) were within the normal range. Imaging studies suspected ovarian malignancy, and she received primary debulking surgery. Following surgery, the pathological evaluation revealed the International Federation of Gynecology and Obstetrics (FIGO) stage IIIB high-grade serous ovarian cancer (pT3bN1M0). The patient underwent complete cytoreductive surgery. On postoperative day 27, the patient received the first cycle of combination chemotherapy comprising paclitaxel (175 mg/m2; 3-hour infusion) and carboplatin (at a dose corresponding to an area under the curve of 5 mg/mL/minute). The patient subsequently received five cycles of standard carboplatin–paclitaxel chemotherapy combined with bevacizumab (15 mg/kg every 3 weeks). Genetic analysis of peripheral blood DNA revealed that BRCA1 and BRCA2 gene mutations were absent, but tissue samples from a pretreatment tumor biopsy were positive for the homologous recombination deficiency (HRD) test (Myriad Genetics, Inc.). The patient received oral niraparib maintenance therapy at a bolus of 200 mg daily after first-line chemotherapy. Figure4and Table1show the laboratory data. Her RBC count, hemoglobin, white blood cell count, and platelet count were 297 × 104/μL, 10.5 g/dL, 35 × 102/μL, and 21.1 × 104/μL, respectively, when she started niraparib therapy. Immediately after the start of niraparib treatment (that is, 6 months after surgery), sodium ferrous citrate (SFC) was orally administered to treat anemia. Forty days after the start of niraparib therapy, peripheral blood cell counts, hematocrit levels, platelet counts, white blood cell count, and neutrophil count decreased to 231 × 104/μL, 7.8 g/dL, 9.6 × 104/μL, 18 × 102/μL, and 323/μL, respectively (Table1). Niraparib therapy was discontinued, but hemoglobin levels were further reduced to 7.0 g/dL. The patient had transient neutropenia and thrombocytopenia. Blood examination showed macrocytic anemia [mean corpuscular volume, 99.1 fL (82–98 fL); mean corpuscular hemoglobin, 33.8 pg (26–32 pg/mL); and mean corpuscular hemoglobin concentration, 35.1 g/dL (31–34 g/dL)]. Furthermore, blood tests showed high serum ferritin levels 350 ng/mL (10–148 ng/mL) and reticulocyte 3.5% (0.5–2.0%), low serum total iron-binding capacity 260 μg/dL (263–457 μg/dL), and serum levels of iron 141 μg/dL (32–170 μg/dL), bilirubin 0.6 mg/dL (0.4–1.5 mg/dL), lactate dehydrogenase 190 U/L (120–225 U/L), folic acid 8.0 ng/mL (2.1–10.1 ng/mL), vitamin B12 401 pg/mL (180–914 pg/mL), and transferrin 211 mg/dL (190–320 mg/dL) were in the normal range. Chest radiography, electrocardiogram, abdominal ultrasound, and thorax, abdominal, and pelvic computerized tomography were normal. Therefore, the patient was diagnosed with niraparib-related anemia. Nirapari

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