1.
Endocrinological Toxicity Secondary to Treatment of Gastroenteropancreatic Neuroendocrine Neoplasms (GEP-NENs).
Alexandraki, KI, Daskalakis, K, Tsoli, M, Grossman, AB, Kaltsas, GA
Trends in endocrinology and metabolism: TEM. 2020;(3):239-255
Abstract
Gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) are increasingly recognized, characterized by prolonged survival even with metastatic disease. Their medical treatment is complex involving various specialties, necessitating awareness of treatment-related adverse effects (AEs). As GEP-NENs express somatostatin receptors (SSTRs), long-acting somatostatin analogs (SSAs) that are used for secretory syndrome and tumor control may lead to altered glucose metabolism. Everolimus and sunitinib are molecular targeted agents that affect glucose and lipid metabolism and may induce hypothyroidism or hypocalcemia, respectively. Chemotherapeutic drugs can affect the reproductive system and water homeostasis, whereas immunotherapeutic agents can cause hypophysitis and thyroiditis or other immune-mediated disorders. Treatment with radiopeptides may temporarily lead to radiation-induced hormone disturbances. As drugs targeting GEP-NENs are increasingly introduced, recognition and management of endocrine-related AEs may improve compliance and the quality of life of these patients.
2.
Supportive therapy in gastroenteropancreatic neuroendocrine tumors: Often forgotten but important.
Jin, XF, Spampatti, MP, Spitzweg, C, Auernhammer, CJ
Reviews in endocrine & metabolic disorders. 2018;(2):145-158
Abstract
Neuroendocrine tumors (NETs) are a group of rare and heterogeneous malignancies that can develop in various organs. A significant number of gastroenteropancreatic neuroendocrine tumours (GEP-NETs) is functionally active and presents with symptoms related to the secretion of biologically active substances, leading to the development of distinct clinical syndromes. There are various therapeutic approaches for GEP-NETs, including curative surgery, palliative surgery, local-ablative and loco-regional therapies as well as systemic therapeutic options including peptide receptor radionuclide therapy, cytotoxic therapy, and molecularly targeted therapies. Specific supportive therapy of patients with NETs includes management or prevention of hormone-related clinical syndromes and paraneoplastic states. Supportive therapy plays a key role in NET treatment. Supportive therapy includes debulking surgery and interventional radiologic techniques to reduce tumour bulk or load, as well as systemic medical treatment options to manage or prevent hypersecretion syndromes and treatment-related side effects. Supportive therapies are a type of of comprehensive treatment addressing the patient as a whole person throughout the process of NET treatment. Therefore, supportive therapy also encompasses psychosocial support, expert nursing, nutritional support and management of cancer related pain.
3.
Diabetes, pancreatic cancer and vitamin D. Is there a link?
Meerza, D, Naseem, I, Ahmad, J
Diabetes & metabolic syndrome. 2011;(4):218-21
Abstract
The role of vitamin D is not merely limited to maintaining skeletal health but also extends to maintaining glucose homeostasis by preserving insulin secretion and sensitivity and thus deficiency of vitamin D plays an important role in aetiopathogenesis of T2 diabetes. In addition to its many other roles, vitamin D has recently been found to have growth inhibiting affects on pancreatic cancer cells. Ecological studies have shown that there exists an inverse correlation between sun exposure and death rates for pancreatic cancer. Since vitamin D has promising role in both type 2 diabetes mellitus and pancreatic cancer, its deficiency may be associated to any or both of these chronic diseases. The present review thus aims to find correlation between diabetes and pancreatic cancer and if vitamin D is a common link between the two.
4.
Etiology and pathogenesis of necrolytic migratory erythema: review of the literature.
Tierney, EP, Badger, J
MedGenMed : Medscape general medicine. 2004;(3):4
Abstract
CONTEXT Necrolytic migratory erythema (NME) is a characteristic skin condition seen in the presence of a pancreatic glucagonoma. The presence of NME in the absence of a pancreatic tumor has been termed the pseudoglucagonoma syndrome. In such cases, NME is commonly associated with conditions, such as liver disease, inflammatory bowel disease, pancreatitis, malabsorption disorders (ie, celiac sprue), and other malignancies. There are many theories on the pathogenesis of NME, which include the direct action of glucagon in inducing skin necrolysis, hypoaminoacidemia-inducing epidermal protein deficiency and necrolysis, a nutritional or metabolic deficiency of zinc or essential fatty acids, liver disease, glucagon induction of inflammatory mediators, a substance secreted from pancreatic and other visceral tumors associated with NME, and generalized malabsorption. OBJECTIVE To present a review of the literature on the clinical presentation, etiology, pathogenesis, and treatment of NME. DESIGN Review of the literature on NME occurring in patients both with and without a pancreatic glucagonoma. METHODS We performed a PubMed review of the literature on the etiology and pathogenesis of NME to identify case reports and reviews published in both the internal medicine and dermatology literature. RESULTS Our literature review encompassed 17 primary case reports and literature reviews published in the dermatologic and internal medicine literature on NME in patients both with and without a pancreatic glucagonoma. Although we found no clear consensus among the investigators of a universally accepted pathogenesis for NME, we did identify 4 main categories of etiologic/pathogenetic mechanisms for NME (glucagon excess, nutritional deficiencies, inflammatory mediators, and liver disease) that were discussed by many of the investigators and validated by both clinical and scientific evidence. CONCLUSION The exact pathogenesis and treatment of NME remain ill-defined despite many case reports and studies on NME in the literature. The many systemic diseases and nutritional deficiencies that have been found to be associated with NME suggest a multifactorial model for the pathogenesis of the disease. The most comprehensive, postulated mechanism for NME involves a combination of zinc, amino acid, and fatty acid deficiencies (arising from a wide variety of causes, such as dietary insufficiency, malabsorption syndromes, liver disease, elevated glucagon levels, and disorders of metabolism) that contributes to increased inflammation in the epidermis in response to trauma and to the necrolysis observed in NME. The importance of gaining an understanding of the etiology and pathogenesis of NME lies in the fact that there is no universally accepted mechanism of pathogenesis for NME, and that the only treatment reported to resolve the rash in these patients is to adequately identify and treat the underlying associated systemic condition or nutritional deficiency.