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Welcome to TODAYS CME

This case report provides an update on a patient with neuroendocrine tumor (carcinoid) of the stomach, including their symptoms, diagnosis, and management. It also discusses the prevalence, risk factors, and pathology of gastrointestinal neuroendocrine tumors.

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Welcome to TODAYS CME

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  1. Welcome to TODAYS CME

  2. Neuroendocrine Tumor(carcinoid) of stomach : A case report and update Dr. Md. Rashedul Islam MD(Thesis Part Student) Department of Medical Oncology National Institute of Cancer Research & Hospital

  3. Chief complains: 1.Upper abdominal pain for 0ne and half year. 2.Anorexia and nausea for one year 3.Weight loss for 6 months On examination Mildly anemic (Hb%-9 gm/dl) Epigastric tenderness without clinically palpable mass USG of whole abdomen-normal(10/7/2017) Endoscopy report-Peptic ulcer disease (17/7 /2017).

  4. She was treated conservatively by local physician. symptomatic improvement lasted for 6 months, then she again visited with same complains and evaluated properly. • Upper GI endoscopy- Gastropathy(07/9/2018) • 2nd endoscopy revealed -Polypoid,ulcerated& mobile growth seen at the lower end of oesophagus involving the cardiac part of stomach (24/10/2018) and biopsy was taken

  5. Digital barium swallow of esophagus: no organic lesion. (out side the NICRH) Spiral CT scan of whole abdomen-Thickening of the wall of lower end of esophagus .post contrast scan revealed enhancement of the thickened wall. (16/10/2018) HPR: -suggestive of poorly differentiated adenocarcinoma(27/10/2018)

  6. After proper investigations and evaluation she was diagnosed as a case of Ca- esophagus involving the cardiac part of stomach and admitted at NIDCH for surgical management. Oesophagogastostomywith feeding jejunostomy was done 13/12/2018. HPR :- CARCINOID TUMOR with lymphnode metastasis (pT3N3Mx) (15/12/2018)

  7. Patient was advised for IHC but due to financial issues, patient denied, so we advised for slide review. Slide Review:- Small cell neuroendocrine carcinoma(17/02/19)

  8. Patient admitted at medical Oncology department of NICRH for further management. We evaluated the patient properly and advised for palliative systemic chemotherapy with Cisplatin and Etoposide.

  9. Neuroendocrine Tumor Neuroendocrine tumors (NET) of the gastrointestinal tract (carcinoid tumors) are uncommon The incidence of gastrointestinal (GI) NETs is 6.2 per 100,000 Small bowel NETs (midgut carcinoids) are more common than both foregut and hindgut & also can remain small (<1 cm) and still metastasize to regional lymph nodes and liver Risk factors for the development of midgut carcinoid tumors include age , male sex, increased body mass index, and menopausal hormone therapy

  10. These tumors are indolent and patients survive a long time • The prevalence is quite high, making them the second most prevalent GI tract tumor, second only to colon cancer • Some are clinically silent and have been detected only at autopsy (incidence 8%) • In 1907, Oberndorfer first used the term carcinoid, meaning “cancer-like,” to describe a rare ileal tumor with less malignant behavior than the large bowel carcinomas

  11. They are derived from the diffuse neuroendocrine system that is composed of peptide- and amine-producing cells that may secrete different hormones depending on the site of origin • There is currently no single system for staging for NETs at all anatomic site • Critical factors in NET pathology include key features are • Embryologic site of origin (foregut, midgut, hindgut), • Functional status (defined as hormone secretion associated with symptoms of hormone excess), and • Grade

  12. The recent 2010 World Health Organization pathology classification relies mainly on proliferation rates as measured by Ki67 antibody staining or mitotic index. • Low-grade tumors (grade 1) are the most common and have a mitoticindex of fewer than two mitoses/10 high power field (hpf) and a Ki67 <3% • Intermediate-grade tumors (grade 2) have a mitotic index of 2 to 20 mitoses/10 hpf and a Ki67 3% to 20% • High-grade tumors (grade 3) have a mitotic index >20 mitoses/10 hpfand a Ki67 >20%.

  13. General Diagnostic Principle • Diagnosis of GI and pulmonary NET is often incidental • Patient with functional tumor can present with symptoms of hormone excess • Elevated serum hormone markers can be a surrogate marker of symptoms of hormone excess or tumor growth • ChromograninA levels are elevated in approximately 80% of patients with GI NETs • Urine 5-hydroxyindoleacetic acid (5-HIAA), the primary metabolite of serotonin, is elevated in carcinoid syndrome.

  14. Abnormal levels (>5 mg/24 hours) of 5-HIAA are diagnostic of carcinoid syndrome • Less common NETs may also be identified by the specific hormone and syndrome that is produced • Imaging play an important role in diagnostic evaluation of GI and pulmonary NET like CT scan, MRI, SRS • Ga-68 DOTATATE is a newer somatostatin-based scintrigraphy that is thought to be more sensitive than octreoscan

  15. PET-CT with FDG has poor sensitivity for well differentiated NETs • ¹³¹I-meta-iodobenzylguanidine scan in patients with small intestine is useful in patients whose tumors secrete catecholamines • CT-enteroclysis is a newer imaging modality designed to image tumors of the small bowel

  16. Staging and Grading

  17. Management

  18. Oncological principles of management in patients with NETs depend on many factors and require a multidisciplinary approach • Treatment often requires individualization • Surgery is the only definitive cure but is rarely possible in patients with metastatic disease, and other approaches are therefore necessary • Anti-proliferative treatment decisions depend on: • Origin of the primary tumour • Histological differentiation • Tumour grade (or proliferative capacity)

  19. Evaluation and treatment of Local gastric NETs

  20. Endoscopic resection of prominent tumor Hypergastrinemic/type 1 (atropic gastritis, or High gastric Pᴴ Vit B12 level EUS as clinically indicated Metastatic disease Abdominal multiphasic CT/MRI Somatostatin receptor based imaging(68 Ga-dotatate or SRS EUS as clinically indicated Other biochemical evaluation as clinically indicaed Consider testing for inherited genetic syndromes Resect primary Gastrinoma EGD Gastric biopsy Serum Gastrin level Consider gastric Pᴴ Hypergastrinemic/type2 Zollinger-Ellison syndrome,noatropicgastritis,low gastric Pᴴ Primary gastrinoma not resected Metastatic disease Radical resection with lymphadenectomy Or Endoscopic surgical wedge resection EUS Abdominal multiphasic CT/MRI Somatostatin receptor based Imaging Normal gastrin/ type 3

  21. Consider endoscopic Surveillence and endoscopic resection of prominent tumor and/or Consider Octreotide or Lanreotide And Manage gastric hypersecretion with high dose PPI Primary gastrinoma not resected

  22. Management of Locoregional advance disease And/or distant metastasis of GI tract NETs

  23. Multiphasic CT/MRI of abdomen and pelvis • Chest CT as clinically indicated • Somatostatin based Imaging or Somatostatin receptor scintigraphy • Biochemical evaluation as clinically indicated If complete resection possible Resect primary+ metastasis Refer for surveillance Observe with imaging or Octreotide/Lanreotide Asymptomatic low tumor burden Multiphasic CT/MRI of abdomen and pelvis Every 3-12 mo Chest CT as clinically indicated Consider resection of primary tumor Locally symptomatic primary tumor Octreotide/Lanreotide Or Alternative frontline therapy Clinically significant tumor burden

  24. If disease progression • Everolimus(10mg/d) • or • PRRT with 177 lu-dotatate(if somatostatin receptor positive and progression on octreotide) • Or • Hepatic directed therapy for hepatic predominant disease • Arterial embolization or • Hepatic chemoembolization or • Radioembolization or • Cytoreductive therapy • Or • Interferon alpha-2B • Or • Cytotoxic chemotherapy If no other option is feasible Multiphasic CT/MRI of abdomen and pelvis Every 3-12 mo Chest CT as clinically indicated If disease progression on Octreotide or Lanreotide Clinically significant tumor burden

  25. Systemic therapy for well differentiated NETs Streptozocin based Combination chemotherapy with either 5 FU or Doxorubicin Molecular targeted therapy Either with Everolimus Or Sunitinib Temozolamide based Combination chemotherapy with capcetabine Oxaliplatin based Combination chemotherapy with FOLFOX/ CapOx

  26. Systemic therapy for poorly differentiated NETs Cisplatin based Combination chemotherapy with Etoposide Irinotecan based Combination with leucovorin and 5 FU(FOLFIRI) Temozolamide based Combination chemotherapy with capcetabine Oxaliplatin based Combination chemotherapy with FOLFOX/ CapOx

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