Nutritional and vitamin status in patients with neuroendocrine neoplasms

Abstract

Symptoms of gastroenteropancreatic located neuroendocrine neoplasms (GEP-NENs) are often related to food intake and manifest as abdominal pain or diarrhoea which can influence patients nutritional status. Malnutrition is common in cancer patients and influences quality of life, treatment options and survival but is also present in up to 40% of patients with GEP-NENs. As part of malnutrition there are often deficiencies in fat-soluble vitamins, mainly vitamin D. Little knowledge exists on trace elements. Several factors influence the development of malnutrition such as size and localisation of the primary tumour as well as metastases, side effects from treatment but also hormone production of the tumour itself. One of the main influencing factors leading to malnutrition is diarrhoea which leads to dehydration and electrolyte disturbances. Treatment of diarrhoea should be guided by its cause. Screening for malnutrition should be part of routine care in every GEP-NEN patient. Multidisciplinary treatment including dietician support is necessary for all malnourished patients with GEP-NENs.

Bone Metabolism and Vitamin D Implication in Gastroenteropancreatic Neuroendocrine Tumors

“…Nutritional status in GEP-NET patients is deeply affected by the excessive production of gastrointestinal hormones, surgical resection changing the anatomy of the gastrointestinal tract, and treatment with SSA and chemotherapy. All these factors cause malabsorption with a consequent deficit of vitamin D and other electrolytes involved in bone metabolism [19,22,70]. Vitamin D deficiency is highly prevalent in GEP-NET patients [21,22,29,30].…”

“…Nevertheless, surgical treatment can influence nutritional status, causing diarrhea for several reasons. As previously discussed, the extent of the intestinal resection and the anatomical position of the resected region are the main factors with an impact on bowel transit time, vitamin B12 action, bile acid secretion, fat-soluble vitamins absorption and digestion [19,67,70].…”

NAD- and NADPH-Contributing Enzymes as Therapeutic Targets in Cancer: An Overview

“…Early on, elevated NAD levels exert a protective effect against oncogenesis [31][32][33][34], later on, elevated NAD levels enhance cancer cell survival and progression [35][36][37]. Demonstrating the effect of restricting the NAD pool in halting cancer progression requires the inhibition of vital pathways, and the reduction of redundancy [38].…”

“…Both reactions are catalyzed by nicotinamide riboside kinase 1/2 (NRK1/2) [27][28][29] (Figure 1). NMN supplementation is also available, however in order to be internalized in the cell, it has been postulated that NMN must be converted to NR by cell membrane protein CD73 (also known as ecto-5-nucleotidase) [28,30].Early on, elevated NAD levels exert a protective effect against oncogenesis [31][32][33][34], later on, elevated NAD levels enhance cancer cell survival and progression [35][36][37]. Demonstrating the effect of restricting the NAD pool in halting cancer progression requires the inhibition of vital pathways, and the reduction of redundancy [38].…”

Differential Diagnosis and Management of Diarrhea in Patients with Neuroendocrine Tumors

“…CS is predominantly associated with NETs of the midgut with extensive liver metastases, since a large amount of tumor-secreted substances are not completely metabolized by hepatic cells and enter the systemic circulation, causing CS. The diagnosis of CS is clinical, based on the presence of symptoms of diarrhea (80% of the patients), hot flushes (50-85% of the patients) and wheezing (10-20% of the patients) (Table 1), and biochemical [21]. In detail, serotonin is metabolized into 5-hydroxyindoleacetic acid (5-HIAA), a biomarker measurable in the urine, which can be used to monitor treatment response in patients with CS [22].…”