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Cancer-related anemia (CRA) is a common sign occurring in more than 30% of cancer patients at diagnosis before the initiation of antineoplastic therapy. CRA has a relevant influence on survival, disease progression, treatment efficacy, and the patients’ quality of life. It is more often detected in patients with advanced stage disease, where it represents a specific symptom of the neoplastic disease, as a consequence of chronic inflammation. In fact, CRA is characterized by biological and hematologic features that resemble those described in anemia associated to chronic inflammatory disease. Proinflammatory cytokine, mainly IL-6, which are released by both tumor and immune cells, play a pivotal action in CRA etiopathogenesis: they promote alterations in erythroid progenitor proliferation, erythropoietin (EPO) production, survival of circulating erythrocytes, iron balance, redox status, and energy metabolism, all of which can lead to anemia. The discovery of hepcidin allowed a greater knowledge of the relationships between immune cells, iron metabolism, and anemia in chronic inflammatory diseases. Additionally, chronic inflammation influences a compromised nutritional status, which in turn might induce or contribute to CRA. In the present review we examine the multifactorial pathogenesis of CRA discussing the main and novel mechanisms by which immune, nutritional, and metabolic components affect its onset and severity. Moreover, we analyze the status of the art and the perspective for the treatment of CRA. Notably, despite the high incidence and clinical relevance of CRA, controlled clinical studies testing the most appropriate treatment for CRA are scarce, and its management in clinical practice remains challenging. The present review may be useful to indicate the development of an effective approach based on a detailed assessment of all factors potentially involved in the pathogenesis of CRA. This mechanism-based approach is essential for clinicians to plan a safe, targeted, and successful therapy, thereby promoting a relevant amelioration of patients’ quality of life.

Advanced-stage cancer patients often suffer from anemia that closely resembles the anemia of chronic inflammatory diseases characterized by specific changes in iron homeostasis and absorption. i.v. iron improves the efficacy of recombinant human erythropoietin (rHuEPO) in anemic cancer patients undergoing chemotherapy. We report the results of an open-label, randomized, prospective trial aimed at testing the efficacy and safety of treatment with oral lactoferrin versus i.v. iron, both combined with rHuEPO, for the treatment of anemia in a population of 148 advanced cancer patients undergoing chemotherapy. All patients received s.c. rHuEPO-␤, 30,000 UI once weekly for 12 weeks, and were randomly assigned to ferric gluconate (125 mg i.v. weekly) or lactoferrin (200 mg/day). Both arms showed a significant hemoglobin increase. No difference in the mean hemoglobin increase or the hematopoietic response, time to hematopoietic response, or mean change in serum iron, C-reactive protein, or erythrocyte sedimentation rate were observed between arms. In contrast, ferritin decreased in the lactoferrin arm whereas it increased in the i.v. iron arm. In conclusion, these results show similar efficacy for oral lactoferrin and for i.v. iron, combined with rHuEPO, for the treatment of anemia in advanced cancer patients undergoing chemotherapy. The Oncologist 2010;15:894 -902

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Background There is little information on which to base the prognostic counselling as to whether an antenatally diagnosed fetal abdominal cyst will grow or shrink, or need surgery. This study aims to provide contemporary data on prenatally diagnosed fetal abdominal cysts in relation to their course and postnatal outcomes. Methods Fetal abdominal cysts diagnosed over 11 years in a single centre were identified. The gestational age at diagnosis and cyst characteristics at each examination were recorded (size, location, echogenity, septation and vascularity) and follow-up data from postnatal visits were collected. Results Eighty abdominal cysts were identified antenatally at 28+4 weeks (range 11+0–38+3). Most (87%) were isolated and the majority were pelvic (52%), simple (87.5%) and avascular (100%). Antenatally, 29% resolved spontaneously; 29% reduced in size; 9% were stable and 33% increased in size. Forty-one percent of cysts under 20 mm diameter increased in size, while only 20% of cysts with a diameter of over 40 mm increased in size. The majority of cysts were ovarian in origin (n=45, 56%), followed by intestinal (n=15, 18%), choledochal (n=3, 4%), liver (n=2, 3%) and renal/adrenal origins (n=2, 3%), respectively. In 16% (n=13), the antenatal diagnosis was not obvious. Seventy-five percent of the cysts that persisted postnatally required surgical intervention. Conclusion Most antenatally diagnosed fetal abdominal cysts were ovarian in origin. Though most disappeared antenatally, nearly three quarters required surgical intervention when present after birth. Cysts of intestinal origin are more difficult to diagnose antenatally and often require surgery.