Neuroendocrine Tumors of the Rectum a 10-year Review of Management
Globe J Clin Cases. 2022 Jul 26; 7(14): 1865–1875.
Colorectal neuroendocrine carcinoma: A example report and review of the literature
Tomoaki Yoshida
Partition of Gastroenterology and Hepatology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata 951-8510, Japan
Division of Gastroenterology and Hepatology, Nagaoka Chuo Full general Infirmary, Niigata 940-0861, Japan
Kazunori Hosaka
Division of Gastroenterology and Hepatology, Graduate School of Medical and Dental Sciences, Niigata Academy, Niigata 951-8510, Japan
Division of Gastroenterology and Hepatology, Nagaoka Chuo Full general Infirmary, Niigata 940-0861, Japan
Koji Doumori
Partition of Gastroenterology and Hepatology, Nagaoka Chuo General Hospital, Niigata 940-0861, Nippon
Hiromitsu Oka
Sectionalisation of Gastroenterology and Hepatology, Nagaoka Chuo General Hospital, Niigata 940-0861, Japan
Akito Sato
Division of Gastroenterology and Hepatology, Nagaoka Chuo General Hospital, Niigata 940-0861, Japan
Yasuo Fukuhara
Division of Gastroenterology and Hepatology, Nagaoka Chuo General Infirmary, Niigata 940-0861, Japan
Shoji Watanabe
Partitioning of Gastroenterology and Hepatology, Nagaoka Chuo General Hospital, Niigata 940-0861, Japan
Tomomi Sato
Partitioning of Gastroenterology and Hepatology, Nagaoka Chuo Full general Hospital, Niigata 940-0861, Japan
Akira Yoshikawa
Division of Gastroenterology and Hepatology, Nagaoka Chuo General Hospital, Niigata 940-0861, Japan
Takashi Tomidokoro
Segmentation of Gastroenterology and Hepatology, Nagaoka Chuo General Hospital, Niigata 940-0861, Japan
Shuji Terai
Division of Gastroenterology and Hepatology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata 951-8510, Nihon
Received 2022 Mar 6; Revised 2022 May 13; Accepted 2022 Jun 26.
Abstract
BACKGROUND
Colorectal neuroendocrine carcinoma (NEC) is a rare tumor that demonstrates aggressive growth pattern with ingrowth into the tract, metastasis to the other organs, and invasion to the surrounding organs; these clinical characteristics effect in poor prognosis. Surgical resection appears as an effective approach; notwithstanding, because it is difficult to accurately diagnose NEC during the early stage and owing to its ambitious growth pattern, development of a reliable standard chemotherapy regimen and direction strategies are essential.
Instance SUMMARY
Hither, we report the case of patient with NEC showing an aggressive growth pattern that resulted in the rupture of the tumor to the outside the colon after stenting of the internal colonic stenosis. In addition, the tumor invaded into the duodenum, thereby causing duodenal stenosis that required an additional stent in the duodenum. This aggressive growth pattern is one of the main features of the NEC that is different from adenocarcinoma. To clarify the clinical characteristics, we reviewed 60 recently reported cases, including data on tumor location, size, treatment, and prognosis.
Determination
We consider that the information presented here is of great significance for the diagnosis, handling, and management of symptoms of the patients with NEC.
Keywords: Neuroendocrine carcinoma, Colon, Colorectal mixed adenoneuroendocrine carcinoma, Growth, Example report
Cadre tip: The aggressive growth design of the rare tumor colorectal neuroendocrine carcinoma (NEC) results in the rapid growth into the tract, metastasis to the other organs, and invasion to the surrounding organs. The overall prognosis has been poor compared with invasive colon adenocarcinoma. The aggressive growth pattern of this tumor could issue in the colonic stenosis, tumor rupture exterior the colon, and invasion to the surrounding organs. Because of its rarity and poor prognosis, clinical information has not been all the same summarized; we have summarized the information obtained from 60 cases reported to appointment. The information summarized in the nowadays study would exist of great importance to assist physicians for the diagnosis, treatment, and management of the symptoms of patients with NEC.
INTRODUCTION
Neuroendocrine carcinoma (NEC) of colon and rectum is a rare neuroendocrine tumor (Internet) type that accounts for < 1% of all colorectal malignancies[one]. The clinical progression of NECs includes highly ambitious growth and rapid dissemination along with a high tendency for metastasis[two]. Moreover, these tumors could be detected at avant-garde stage[3]. The three-twelvemonth overall survival (OS) was estimated to be 5%–27%[one,4,five], and response to chemotherapy was reported as the but predictive factor in patients with metastasis[1]. Because of its ambitious nature and high recurrence rate of the NEC, adjuvant chemotherapy constitutes a critical part of the treatment and significantly improves survival[4]. Although platinum-based regimens are widely used equally commencement-line chemotherapy for the handling of patients with advanced NEC, no standard regimen has yet been established. A previous study has reported that some cases who received chemotherapy showed the complete response (CR) or partial response (PR) to the avant-garde NEC; still, more than half of patients showed progressive response[half dozen].
Additionally, some NEC cases showed aggressive progression and outward growth with the invasion of surrounding tissues. These aggressive tumors pb to serious health issues such every bit colonic obstacle and internal organ exclusion. The manage-ment of such wellness issues is sometimes challenging; moreover, an appropriate therapeutic strategy has not still been proposed because of rareness of the aggressive NEC.
Here, we attempted to present a patient with NEC that showed aggressive tumor progression. Although the patient received various therapeutic options, such as chemotherapy or intestinal self-expandable metallic stent, all those treatments have been unsuccessful yet.
CASE PRESENTATION
Chief complaints
A 55-year-old human being was admitted to our hospital with a huge abdominal mass. He complained of palpable intestinal mass, while painless mass two months prior to the presentation.
History of past affliction
He had no pregnant history of past disease.
Physical test
Concrete exam showed a palpable tumor and a relatively soft mass associating with poor movability in the right upper quadrant.
Laboratory examinations
Laboratory findings showed an elevated white blood jail cell count (9740 /µL), platelet count (37.3 × 104 /µL), C-reactive protein (4.99 mg/dL), lactate dehydrogenase (328 IU/L), and hemoglobin level (9.iv g/dL). Carcinoembryonic antigen showed mild elevation of 9.five ng/mL, while other tumor markers were in normal range (Table 1).
Tabular array 1
Results of laboratory investigation on the day of admission
| WBC | 9740 /μL |
| RBC | 344 × 10four /μL |
| Hb | 9.four one thousand/dL |
| Ht | 29.one% |
| Plt | 37.3 ×x4 /μL |
| TP | six.7 one thousand/dL |
| Alb | 3.8 g/dL |
| BUN | 12.iii mg/dL |
| Cre | 0.85 mg/dL |
| AST | 12 IU/L |
| ALT | ix.0 IU/50 |
| LDH | 328 IU/L |
| ALP | 166 IU/Fifty |
| γ-GTP | 43 IU/L |
| T-bil | 0.4 mg/dL |
| CRP | 5.0 mg/dL |
| CEA | 7.4 ng/mL |
| CA19-9 | ane.0 U/mL |
Further progress, diagnosis, treatment and effect
Intestinal dissimilarity-enhanced computed tomography (CT) showed an irregularly shaped, x cm, likewise as an enhanced mass in the transverse colon at the hepatic flexure (Figure 1A) and suspicious of metastatic tumors in the liver (Effigy 1B). Colonoscopy showed the mass in the correct transverse colon with pregnant stenosis (Figure 1C) due to submucosal superlative of the tumor (Figure 1D), while the lumen had a necrotic tissue (Figure 1E) evidenced by colonic enema with water-soluble contrast medium showing an irregular shape in the lumen of colon (Effigy 1B). Post-obit the mucosal biopsy for the histological analysis, a self-expandable metal stent was successfully placed. Even so, the patient re-admitted to our hospital because of the sudden onset and astringent abdominal hurting at v days later on the placement. The contrast-enhanced CT of the abdomen showed intraperitoneal free-air associated with the colon tumor (Figure 1F). The hematoxylin and eosin (HE) staining showed that the tumor cells were poorly differentiated (Figure 2A) with hemorrhage in the tumor (Figure 2B) and significantly stained positively for Synaptophysin (Figure 2C). In addition, Ki67 staining showed a highly proliferative design with the Ki67 index of ninety% (Figure 2nd).
Imaging findings. A: Contrast-enhanced computed tomography (CT) of the belly shows an irregularly shaped and enhanced mass (10 cm) at the correct colonic flexure. White arrow indicates the tumor; B: CT showed multiple low-density tumors in the liver with no enhancement consequence. Black arrows bespeak the tumors; C: Colonic enema with water-soluble dissimilarity medium (Gatrografin®) shows an irregular shape in the lumen of colon. Black arrow indicates the stenotic and irregular lesion; D: Colonoscopy showed the mass in the right transverse colon with significant stenosis due to submucosal elevation of the tumor. Black pointer indicates the submucosal pinnacle; E: Colonoscopy showed the necrotic tissue in the lumen of the tumor. White arrow indicates the necrotic lesion; F: Perforation of the colon by stenting. Black arrow indicates the free-air and intratumoral air outside the stent.
Histological findings of the tumor. A: Hematoxylin-eosin staining showed that the tumor cells were poorly differentiated; B: Complicated with the intratumoral bleeding; C: Tumor cells underwent immunohistochemical staining for Synaptophysin. Black arrows bespeak the positively stained cells; D: A high proliferative fraction of immunohistochemical staining for Ki67 staining. Blackness arrows indicate the positively stained cells.
FINAL DIAGNOSIS
Based on these findings, the tumor was diagnosed with NEC, and the tumor showed perforation to the exterior the colon probably due to the expandable growth of the tumor.
TREATMENT
The tumor showed severe invasion to the surrounding tissues; therefore, it was considered to be curatively unresectable, and anastomosis betwixt the ileum and left colon was surgically developed that followed by chemotherapy.
Upshot AND FOLLOW-UP
Although the patient was treated with multiple chemotherapies, such as irinotecan + cisplatin (as the kickoff-line therapy) and etoposide + carboplatin (every bit the 2nd-line therapy); nonetheless, the tumor showed no significant response, and disease was speedily progressed due to this invasive growth, in which the tumor induced the bile duct and duodenal obstruction past tumor progression. An additional stent for the duodenal stenosis was besides placed; withal, the appetite and general condition did not recover and he died 4 mo after the diagnosis.
Give-and-take
The Earth Wellness Organization classification, published in 2010, divides NETs of the digestive tracts into Cyberspace course (G) 1, Cyberspace G2, and NECs, based on mitotic counts and the Ki-67 proliferation index, regardless of tumor size, extent, or location, and besides the colorectal NEC is a rare tumor with the incidence charge per unit of 0.1%[i]. In addition, NEC and colorectal mixed adenoneuroendocrine carcinoma (MANEC) revealed loftier-grade cancer cells evidenced by high level of Ki-67 alphabetize (> 20%). The advanced NEC typically associates with the expansive growth pattern similar to that associates with the phase II colon cancer, i.eastward., yellowish ulcer and raised margin of non-neoplastic mucosa like submucosal tumor[v]. Colorectal NEC involves high malignant potential with poor differentiation and loftier invasiveness, while its prognosis is worse than colorectal adenocarcinoma. The median survival rate and relative survival (%) at 5 years of NEC and adenocarcinoma were 7.i–14.7 and 36.0 mo, and 8.0%–16.3% and 50.two%, respectively. In add-on, MANEC showed significantly poor Bone compared with adenocarcinoma[3]. Because of the aggressive progression, NEC was mainly detected at advanced stage in comparison with adenocarcinoma resulted in the fact that 57.9%–67.five% of NEC patients were initially diagnosed with the stage Four compared with the finding that 25.2% of cases with adenocarcinoma were diagnosed with stage 4[1,3,6]. These findings advise that neuroendocrine differentiation is the cause of higher malignant potential and worse prognosis. Tabular array ii presents the characteristics of 59 cases with advances NEC and MANEC, while the terms "colon" and "neuroendocrine carcinoma" were searched in PubMed, and the available clinical information was summarized.
Table 2
Summary of the cases reported to appointment
| No. | Ref. | Year | Age | Gen-der | Diagn-osis | Loca-tion | Size (mm x mm) | Posit-ive for Ki-67 (%) | Steno-sis (%) | Symp-tom of Obstruc-tion | Inva-sion to Surroun-ding Tissu-eastward | Metas-tasis | Sur-gery | CT | RT | Chemo-thera-py | Re-sponse to Chemo-thera-py | Over-all Sur-vival (mo) |
| 1 | 12 | 1996 | 65 | F | ECC | A | 150 | Northward/A | 100 | + | - | + | - | + | - | P | PD | 3 |
| 2 | 13 | 1998 | lxx | M | ECC | R | 80x55 | N/A | 60 | - | - | + | + | + | - | P | PD | 15 |
| 3 | 14 | 1999 | 54 | F | MAENC | South | 60 | N/A | N/A | - | + | + | + | + | - | F | N/A | Northward/A |
| 4 | 14 | 1999 | 46 | M | NEC | R | 160x130x40 | N/A | 100 | - | - | + | + | + | - | P | PD | 8 |
| 5 | 15 | 2002 | 50 | F | small cell carcinoma | R | 45x55 | North/A | fifty | - | - | + | + | + | - | P | CR | 54, alive |
| 6 | 16 | 2002 | 76 | M | MANEC | C | 45x45x15 | Northward/A | Northward/A | - | Northward/A | + | + | + | - | N/A | N/A | N/A |
| 7 | 17 | 2002 | 67 | F | small cell carcinoma | A | Northward/A | North/A | N/A | - | North/A | N/A | N/A | N/A | Northward/A | Due north/A | N/A | Northward/A |
| 8 | eighteen | 2003 | 61 | F | ECC | R | Due north/A | N/A | 60 | - | + | + | + | + | - | P | PD | 5 |
| nine | 19 | 2004 | 78 | M | ECC | R | 47x43 | N/A | sixty | - | - | + | + | + | - | P | PD | 6 |
| 10 | 20 | 2004 | 38 | M | NEC | T | 100 | Northward/A | 100 | + | + | - | + | + | - | P | PR | fourteen |
| 11 | 21 | 2004 | 79 | M | MANEC | R | 30x20 | N/A | thirty | - | - | + | + | + | + | F | PR | 21, alive |
| 12 | 22 | 2006 | 34 | M | ECC | T | 170x110 | Northward/A | 100 | - | + | + | + | + | - | P | PD | 8 |
| thirteen | 23 | 2006 | 48 | M | ECC | R | 120x100 | Due north/A | 50 | - | + | + | + | + | + | P | SD | 24, alive |
| 14 | 24 | 2006 | 62 | M | NEC | A | 45x25 | N/A | 60 | - | + | + | + | + | - | F | PD | 11 |
| 15 | 25 | 2006 | 71 | M | NEC | D | 40x50 | N/A | 50 | - | - | + | + | + | - | F | PD | vi |
| 16 | 26 | 2007 | 53 | K | NEC | R | 32x27 | 40 | 30 | - | + | + | + | + | - | P | PR | 51 |
| 17 | 27 | 2007 | 45 | M | ECC | C | 42 | North/A | fifty | - | - | + | + | + | + | P | PR | 67 |
| eighteen | 28 | 2007 | 44 | F | MANEC | T | 80x75x50 | Northward/A | 100 | N/A | N/A | + | + | + | - | N/A | Due north/A | N/A |
| xix | 29 | 2007 | 38 | F | ECC | T | 29x27 | N/A | 50 | - | + | + | + | + | - | F | PD | 9 |
| 20 | 30 | 2008 | 63 | M | ECC | A | 50x70 | N/A | 100 | - | - | + | + | + | - | F | PD | 41 |
| 21 | 31 | 2008 | 56 | K | ECC | C | 40x50 | N/A | N/A | - | - | + | + | + | - | P | PD | half-dozen |
| 22 | 7 | 2008 | 61 | M | ECC | R | 50 | N/A | 100 | + | + | + | + | + | + | F | PR | 50, alive |
| 23 | 32 | 2009 | 79 | F | ECC | S | 115x35 | N/A | 100 | +/- | + | + | + | + | - | P | SD | xiv, alive |
| 24 | 33 | 2010 | 78 | Chiliad | NEC | Southward | 82x74 | N/A | Northward/A | - | + | + | + | + | - | F | SD | 10 |
| 25 | 34 | 2010 | 59 | Thou | ECC | N/A | N/A | 80 | North/A | N/A | North/A | + | Due north/A | N/A | Northward/A | Northward/A | N/A | Northward/A |
| 26 | 35 | 2011 | 63 | Yard | NEC | A | N/A | N/A | Northward/A | N/A | - | + | + | + | - | F | PR | eleven |
| 27 | 36 | 2011 | 70 | M | NEC | A | 74x51 | N/A | threescore | - | - | + | + | - | - | - | N/A | North/A |
| 28 | 37 | 2011 | 74 | F | NEC | A | Due north/A | 90 | 100 | + | - | + | + | - | - | - | North/A | i |
| 29 | 38 | 2011 | 76 | F | NEC | A | N/A | 66.3 | l | - | - | + | + | + | - | P | PR | 27, alive |
| thirty | 39 | 2012 | 54 | Yard | MANEC | R | xxx | North/A | 50 | - | N/A | North/A | + | + | - | F | Northward/A | N/A |
| 31 | 40 | 2012 | 76 | F | NEC | T | 183x115 | N/A | 100 | - | + | - | + | + | - | F | PD | 42, alive |
| 32 | 41 | 2012 | 74 | F | NEC | A | N/A | 75 | 30 | - | - | + | - | + | - | P | PR | 8 |
| 33 | 42 | 2012 | 57 | F | NEC | Northward/A | North/A | 80 | 30 | - | N/A | + | N/A | N/A | North/A | N/A | N/A | N/A |
| 34 | 43 | 2012 | 81 | F | NEC | C,A | N/A | N/A | 100 | N/A | N/A | + | + | - | - | - | N/A | vi |
| 35 | 44 | 2012 | 68 | F | NEC | S | 30 | North/A | 50 | - | Northward/A | + | - | - | - | - | N/A | 0.5 |
| 36 | 45 | 2013 | 51 | M | NEC | R | Due north/A | N/A | 50 | - | - | + | + | + | - | F | PR | 12, alive |
| 37 | 46 | 2013 | 68 | K | NEC | R | North/A | N/A | 50 | - | - | + | + | + | + | P | PR | 7 |
| 38 | 47 | 2014 | 77 | M | NEC | A | 40x35 | 20-30 | thirty | - | - | + | + | + | - | F | PD | 8, live |
| 39 | 48 | 2014 | 71 | 1000 | MANEC | T | 70x45 | 25 | 80 | + | - | + | + | + | - | F | PD | xiii |
| 40 | 49 | 2014 | 48 | M | MANEC | South | N/A | Northward/A | 100 | + | + | + | + | + | + | F | PD | 3 |
| 41 | 50 | 2014 | 63 | F | NEC | A | N/A | sixty-70 | 100 | + | - | + | + | + | - | P | PD | 10 |
| 42 | 51 | 2014 | 39 | M | MANEC | T | N/A | 80 | 50 | - | - | + | + | + | - | F | PD | 7 |
| 43 | 52 | 2014 | 55 | F | MANEC | A | N/A | N/A | 30 | - | Northward/A | North/A | North/A | Northward/A | Due north/A | Due north/A | N/A | N/A |
| 44 | 53 | 2014 | 34 | F | MANEC | D | N/A | N/A | 100 | + | + | N/A | + | Due north/A | N/A | N/A | N/A | Northward/A |
| 45 | 54 | 2015 | 74 | F | MANEC | C | 70x18 | <20 | 100 | + | + | - | + | + | - | F | SD | 10, alive |
| 46 | 55 | 2015 | 44 | M | NEC | A | 170x110x80 | N/A | 100 | + | + | - | + | + | - | P | SD | 84, alive |
| 47 | 56 | 2016 | 70 | M | MANEC | D | 100 | 82.9 | 100 | - | + | + | + | + | - | F | CR | 30, alive |
| 48 | 57 | 2016 | 48 | F | NEC | S | 93x40 | >xc | 100 | +/- | - | + | - | + | - | P | PR | ii |
| 49 | 58 | 2016 | 70 | M | NEC | S | 15 | N/A | 25 | - | - | + | - | + | - | P | N/A | N/A |
| 50 | 59 | 2016 | 67 | M | NEC+SCC | C | 60x50 | >40 | 100 | + | + | + | + | + | - | P | PD | iii |
| 51 | threescore | 2017 | 49 | F | ECC | T | 100x100 | N/A | 100 | - | + | - | + | - | - | - | N/A | 10, alive |
| 52 | 61 | 2017 | 60 | M | NEC | Anus | 20 | 90 | Northward/A | - | - | + | - | + | - | Northward/A | PR | N/A |
| 53 | 62 | 2017 | 68 | M | MANEC | A | 30 | 75 | 30 | - | - | - | + | + | - | P | SD | N/A |
| 54 | 63 | 2017 | 32 | M | MANEC | C | 80x55 | N/A | seventy | +/- | - | + | + | + | - | F | SD | 6, alive |
| 55 | 64 | 2017 | 61 | F | NEC | T | 50 | ninety | 100 | + | Due north/A | - | + | - | - | - | Northward/A | Northward/A |
| 56 | 65 | 2018 | 74 | M | NEC | S | 60x50 | 90 | 100 | - | + | + | + | + | - | F | SD | 36, live |
| 57 | 66 | 2018 | 68 | Yard | NEC+SCC | D | 35x35 | lxxx | 100 | +/- | - | + | + | + | - | P | PD | N/A |
| 58 | 67 | 2018 | 40 | F | NEC | R | 45x36x44 | N/A | fifty | - | N/A | + | - | + | + | P | CR | N/A |
| 59 | 68 | 2018 | 77 | G | ECC | T | North/A | Due north/A | 100 | + | - | + | + | - | - | - | N/A | 2 |
| threescore | North/A | Our Instance | 55 | K | NEC | T | 100x100 | 90 | 100 | + | + | + | - | + | - | P | PD | four |
Although a reliable handling guideline has not presented yet, chemo-therapy plays a key part in treat-ment of patients with advanced NEC. Platinum-based chemotherapy, as a therapeutic strategy, is oft used and the response rate is 42% to NEC that is relatively lower than that of 67% for small cell lung cancer[half dozen]. A previous study proposed the effectiveness of 5-fluorouracil (5-FU)-based chemotherapy[7]; however, equally mentioned earlier, a standard regimen for NEC has not been developed yet. It has also been reported that a regimen for the MANEC, comprising neoplasms with both neuroendocrine carcinomatous and adenocarcinomatous components, depends on which component dominantly contributes. In the present research, the number of patients with NEC and MANEC was 44 and 13, and the mean historic period was 61.five and 56.2 years sometime, respectively (other two patients were diagnosed as the combination of NEC with squamous cell carcinoma). Too, 29 patients were died due to these tumors, while fifteen patients were saved by treatment with tumor resection and chemotherapy. The Os of 48 patients who received the tumor resection was xix.2 mo, which was significantly higher than 3.four mo belonged to 7 patients who did non undergo surgical resection. These results highly reveal that surgical resection is essential to prolong prognosis. Even so, a poor prognosis was observed in the bulk of those patients considering of the delayed diagnosis like to our case, and nosotros therefore were unable to perform the surgical treatment. To follow the chemotherapy, an constructive stenting for the obstructive tumor is vital for treatment and also for quality of life (QOL) of the patients every bit meaning rapid tumor progression in both within and outside the colon are clinical features of NEC and may cause intestinal tract obstruction and besides stenosis of the surrounding organs, including minor intestine. The rapid growth resulted in the huge tumor upon the diagnoses, as our findings showed that the average bore of NEC was 76.viii mm, and growth toward outside of the colon, outward invasion, which was observed in 42% of the patients, and similar results reported past a previous written report[v]. Importantly, MANEC, associating with a rapid growth pattern in NEC, showed sixty% of outward growth, indicating that the college growth rate of the tumor cells represents this aggressive and infiltrative growth blueprint. In our case, colonic and duodenum self-expandable metal stent (SEMS) were inserted for direct colonial obstacle and infiltrative growth toward the duodenum. Generally, stenting in the gastrointestinal tract for cancerous obstruction due to the adenocarcinoma has been reported as an effective and condom strategy with the clinical success rate of 90.5%–95.5%, too as an adverse issue rate of 3.5%–7.6%[eight-ten]. In addition, it is extremely rare to detect out the tumor perforation, post-obit the stent placement with the rate of two% that might occur at the necrotic tissue of the tumor[11]. The master reason of the tumor perforation following SEMS insertion in our case is likely due to the rapid growth of the NEC tumor cells at both inside and outside the colon, evidenced by the tumor necrosis appeared in the endoscopic findings and 90% of positive cells by Ki67 staining that led to the vulnerability of the mass structure. As successful induction of the chemotherapy could lead to the better survival period (Table 2), stenting is of great importance to manage the symptoms and QOL. The summary of the chemotherapy induced in the recent cases are summarized in Table ii[7,12-68]. Equally shown in Table 2, 24 NEC patients received platinum-based chemotherapy and 11 NEC patients received 5-FU-based chemotherapy as the beginning-line regimen. In particular, 9 MANEC patients received 5-FU-based chemotherapy, and but 1 patient received platinum-based chemotherapy, probably targeting the component of adenocarcinoma. The responses to the platinum-based and v-FU-based chemotherapy were (CR, 2; PR, vii; stable illness (SD), iii; and progressive disease (PD), 11; and (CR, 0; PR, 3; SD, 2; and PD, vi), respectively. Therefore, evolution of an constructive chemotherapy-based regimen is essential besides.
Consequently, exertion is essential to detect NEC in early stage, thereby the correct diagnosis is of great importance, while NEC and MANEC are frequently misdiagnosed equally adenocarcinoma or another malignant tumor at the kickoff imaging or histological report[5]. Thus, to diagnose accurately, detailed endoscopic observation and histological research are required. A study suggested that fluorodeoxyglucose positron emission tomography (FDG-PET) assembly with high-sensitivity to tumor, as well as high-proliferation (e.g., NEC)[12], therefore FDG-PET is precious to diagnose tumor with clinical feature of NEC.
At present, early diagnosis followed by the surgical resection is the most favorable clinical course for meliorate prognosis, and if impossible, conscientious making determination for chemotherapy and stenting for obstruction is significant. Furthermore, NEC with higher cell proliferation not only may cause the intestinal obstruction, but likewise the invasive growth to the surrounding organs, leading to the tumor rupture after stenting within the tract, thus careful consideration is essential for making a right clinical decision. In item, the placement of stent needs to be highly taken into business relationship as information technology is significantly different from the colorectal adenocarcinoma in terms of the cell growth pattern, and clinical characteristics.
CONCLUSION
Equally a result, as the rapid growth pattern of NEC is difficult to be managed, early diagnosis and careful management with the understanding of the disease are essential. Still, accumulated information related to this rare illness may assist physicians to finer care for patients with the help of evolution of chemotherapy, stenting method, too every bit upgrading medical devices. We hope that the results of the present study can enhance the information related to NEC and besides assistance the scholars to better empathise the disease.
Footnotes
Informed consent argument: Written informed consent was obtained from the patient.
Conflict-of-interest argument: The authors have no conflicts of interest to declare.
Care Checklist (2016) argument: The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the Care Checklist (2016).
Manuscript source: Invited Manuscript
Peer-review started: March 11, 2019
First decision: May 13, 2019
Article in press: June 27, 2019
Specialty blazon: Medicine, enquiry and experimental
Country of origin: Japan
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Contributor Information
Tomoaki Yoshida, Division of Gastroenterology and Hepatology, Graduate Schoolhouse of Medical and Dental Sciences, Niigata Academy, Niigata 951-8510, Japan. Sectionalisation of Gastroenterology and Hepatology, Nagaoka Chuo Full general Hospital, Niigata 940-0861, Japan.
Republic of kenya Kamimura, Division of Gastroenterology and Hepatology, Graduate School of Medical and Dental Sciences, Niigata Academy, Niigata 951-8510, Nippon. pj.ca.u;31020x#&atagiin.dem@k;31020x#&aynek.
Kazunori Hosaka, Segmentation of Gastroenterology and Hepatology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata 951-8510, Nippon. Division of Gastroenterology and Hepatology, Nagaoka Chuo General Hospital, Niigata 940-0861, Nihon.
Koji Doumori, Partition of Gastroenterology and Hepatology, Nagaoka Chuo General Hospital, Niigata 940-0861, Japan.
Hiromitsu Oka, Partition of Gastroenterology and Hepatology, Nagaoka Chuo General Hospital, Niigata 940-0861, Japan.
Akito Sato, Sectionalisation of Gastroenterology and Hepatology, Nagaoka Chuo General Hospital, Niigata 940-0861, Japan.
Yasuo Fukuhara, Division of Gastroenterology and Hepatology, Nagaoka Chuo General Hospital, Niigata 940-0861, Nippon.
Shoji Watanabe, Partition of Gastroenterology and Hepatology, Nagaoka Chuo Full general Hospital, Niigata 940-0861, Japan.
Tomomi Sato, Division of Gastroenterology and Hepatology, Nagaoka Chuo Full general Hospital, Niigata 940-0861, Nihon.
Akira Yoshikawa, Division of Gastroenterology and Hepatology, Nagaoka Chuo General Hospital, Niigata 940-0861, Nihon.
Takashi Tomidokoro, Partitioning of Gastroenterology and Hepatology, Nagaoka Chuo Full general Hospital, Niigata 940-0861, Nippon.
Shuji Terai, Division of Gastroenterology and Hepatology, Graduate Schoolhouse of Medical and Dental Sciences, Niigata University, Niigata 951-8510, Japan.
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