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Table of Contents
LETTER TO EDITOR
Year : 2018  |  Volume : 1  |  Issue : 2  |  Page : 173-176

Synchronous primary of periampullary and lung cancer: A case report and review of literature


Department of Medical Oncology, Tata Memorial Hospital, Mumbai, Maharashtra, India

Date of Web Publication17-May-2019

Correspondence Address:
Vikas Talreja
SFS Flat, No. 886, Pocket GH 13, Paschim Vihar, New Delhi - 110 087
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/CRST.CRST_4_19

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How to cite this article:
Talreja V, Noronha V, Joshi A, Patil V, Prabhash K. Synchronous primary of periampullary and lung cancer: A case report and review of literature. Cancer Res Stat Treat 2018;1:173-6

How to cite this URL:
Talreja V, Noronha V, Joshi A, Patil V, Prabhash K. Synchronous primary of periampullary and lung cancer: A case report and review of literature. Cancer Res Stat Treat [serial online] 2018 [cited 2019 Aug 24];1:173-6. Available from: http://www.crstonline.com/text.asp?2018/1/2/173/258542



Multiple primary lung cancer may present in synchronous or metachronous form. Synchronous multiple primary lung cancer is defined as multiple lung lesions that develop at the same time, whereas metachronous multiple primary lung cancer describes multiple lung lesions that develop at different times, typically following treatment of the primary lung cancer. Patients with previously treated lung cancer are at risk for developing metachronous lung cancer; but, with the success of computed tomography (CT) and positron emission tomography (PET), the ability to detect both synchronous and metachronous lung cancer has increased. Multiple primary malignancies are divided according to Moertel's [1] definition into synchronous and metachronous: (1) synchronous refers to tumors diagnosed within 6 months and (2) metachronous refers to tumor which are diagnosed after 6 months of diagnosis of the first tumor. Metachronous malignancies are said to have a better prognosis than synchronous malignancies,[2],[3] while that of synchronous malignancies is said to be worse. Which malignancy must be dealt with first or are both to be dealt with at the same time are questions yet to be answered. Treatment strategies in cases of double malignancy depend on treating the malignancy that is more advanced first, or sometimes both malignancies could be treated simultaneously. If both are amenable to surgical resection as in two of our cases, both the malignancies may be dealt with at the same time. The prognosis of the patients with dual malignancies depends on the aggressiveness and the stage of presentation of the more advanced tumor.[4] We describe a case report of periampullary and lung cancer synchronous primary treated sequentially at our center.

A 49-year-old man, occasional alcoholic with comorbidities of diabetes on insulin and hypertension on olmesartan for the last 5 years, presented with chief complaints of dyspepsia and pain in the abdomen for 15 days. Investigation suggested the following: hemoglobin: 13.0 g/dl, total leukocyte count: 9.93 × 10^9/L with total bilirubin: 0.32 mg/dl, albumin: 4.0 g/dl, globulin: 2.9 g/dl: CEA: 3.69 ng/ml, and CA 19-9: 389.55 U/l.

Endoscopic ultrasound done on May 28, 2018, was suggestive of ill-defined hypoechoic lesion noted at the head of pancreas with involvement of the portal vein with dilated main pancreatic duct.

Magnetic resonance cholangiopancreatography was done on May 28, 2018, suggestive of the focal lesion at the distal common bile duct (CBD) at ampulla with cutoff of distal CBD and main pancreatic duct. Ampullary growth biopsy using side viewing endoscopy done on May 30, 2018 revealed moderately differentiated adenocarcinoma. He underwent endoscopic retrograde cholangiopancreatography (ERCP) guided self-expanding metallic stent 10 mm × 60 mm.

Contrast-enhanced CT (July 19, 2018) showed the right lung lower lobe lesion – 2.2 cm × 2.1 cm with the right paratracheal and subcarinal lymph node. Fluorodeoxyglucose (FDG) positron emission CT scan done on August 9, 2018, was suggestive of hypermetabolic abnormal increased FDG uptake noted in periampullary soft tissue, partially extending into biliary drainage stent (SUVmax – 12.15). Dilatation of proximal biliary tree was noted, with pneumobilia FDG avid cavitary lesion (maximum wall thickness >1.5 cm) noted in the right lung lower lobe measuring 2.2 cm × 2 cm × 2.6 cm (SUVmax – 6.15) and FDG avid mediastinal nodes: right paratracheal and subcarinal, larger measuring 1.7 cm (SUVmax – 8.91) [Figure 1] and [Figure 2]. Bronchoscopy was within normal limits. Left lung biopsy: on immunohistochemistry, tumor cells were positive for CK7, CK19, and TTF1 and negative for CDX2 and CK20 suggestive of adenocarcinoma of primary pulmonary origin. Endobronchial ultrasound was suggestive of level 4R, and level 7 lymph node involved by malignancy.
Figure 1: Abnormal increased fluorodeoxyglucose uptake noted in periampullary soft tissue, partially extending into biliary drainage stent (SUVmax12.15). Dilatation of proximal biliary tree noted, with pneumobilia

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Figure 2: Fluorodeoxyglucose avid cavitary lesion (maximum wall thickness >1.5 cm) noted in the right lung lower lobe measuring 2.2 cm × 2 cm × 2.6 cm (SUVmax6.15). Fluorodeoxyglucose avid mediastinal nodes: Right paratracheal and subcarinal, larger measuring 1.7 cm (SUVmax8.91)

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The final diagnosis was T2N0M0 periampullary cancer with synchronous right lung adenocarcinoma cT1cN2 Stage IIIA.

He was planned for neoadjuvant chemotherapy in view of multistation N2 disease.

The patient received 3 cycles of 3-weekly pemetrexed (500 mg/m2) and cisplatin (75 mg/m2), completed on 8th Oct 2018, with no major toxicities. The response FDG-PET CT was suggestive of FDG uptake noted in ill-defined soft tissue lesion noted in the lower lobe of the right lung: 21 mm × 16 mm, SUVmax – 4.66. Mediastinal nodes had responded to neoadjuvant chemotherapy (NACT). No uptake/lesion was seen in periampullary region.

He underwent robotic right lower lobectomy with mediastinal lymph node dissection on November 8, 2018.

The histopathological report of lobectomy was that no lesion/tumor was identified in the lung parenchyma on gross examination. Microscopically residual viable adenocarcinoma in an acinar and lepidic growth pattern with no lymphovascular invasion or visceral pleura involvement. All margins were negative. The adjacent lung is unremarkable. Right interlobar, hilar, peribronchial, and right paratracheal lymph nodes were free of tumor. His postoperative contrast CT of thorax and abdomen (October 12, 2018) was unremarkable with stent seen in situ.

He underwent Whipple surgery (December 11, 2018) (Pancreas Pylorus Preserving Pancreaticoduodenectomy whereby no residual tumor was identified, and lymphovascular invasion was not seen. Perineural invasion was absent. Transection margins were negative. All nodes were negative (along cystic duct, anterior pancreaticoduodenal nodes, posterior pancreaticoduodenal nodes, superior pancreatic nodes, inferior pancreatic nodes, and periportal node).

He was planned for one cycle adjuvant pemetrexed (500 mg/m2) and cisplatin 75 (mg/m2) 3-weekly in view of endobronchial ultrasound suggestive of positive lymph node before neoadjuvant therapy and is now doing well.

Surgical resection of adenocarcinoma of the pancreas or periampullary area provides the only possibility of long-term survival. Although resection traditionally had been associated with relatively high morbidity and mortality, over the past several decades, advances in anesthesia, operative techniques, and postoperative care have led to marked improvements in perioperative outcomes.[5],[6] Despite these improvements, the 5-year survival rate after surgical resection remains poor, ranging from 26% for patients with pancreatic adenocarcinoma [7],[8],[9] to 70% for patients with ampullary carcinoma. Patients who have advanced locoregional or metastatic disease identified at the time of exploration have an even worse prognosis.[10],[11],[12] Thus, there has been considerable debate regarding the best way to manage this cohort of patients. For those individuals with advanced locoregional disease, Lillemoe et al. reported that palliative pancreaticoduodenectomy resulted in improved long-term survival compared with traditional surgical palliation – even in patients with residual local disease. The role of surgical resection in the setting of evident low-volume metastatic disease, however, is much more controversial. Specifically, in the setting of hepatic metastasis, resection of the primary pancreatic or periampullary adenocarcinoma has been discouraged.[13],[14]

Mehdi et al.[15] have shown that second primary tumors are usually more aggressive, treatment resistant and metastasize early, require a more aggressive treatment strategy, and usually have a poor outcome. On the other hand, Agrawal [16] has noted that synchronous malignancies can be treated successfully. The outcome of the patient that we managed successfully is similar to the observation of Agrawal. The diagnosis of multiple primary tumors is now increasing due to an increased awareness of possibility of a second malignancy; the higher use and sensitivity of diagnostic methods as well as the recent improvements in cancer treatment and survival will further lead to higher prevalence of multiple cancers. As patients with a history of cancer tend to undergo regular follow-up, this could lead to earlier diagnosis of new malignancies at curable stages.[17] To define a second primary malignancy, International Agency for Research on Cancer has laid down a few rules and guidelines [18],[19] which include the following:

  1. The existence of two or more primary cancers does not depend on time
  2. Both tumors are confined to primary sites, and no direct connections between the tumors exist
  3. One tumor should only be recognized in an organ or a pair of organs or tissue (as defined by the code of the International Classification of Diseases)
  4. Rule 3 does not apply if tumors in an organ are of a different histology
  5. Be different in histological type when diagnosis of pathology is available.


Warren and Gates [20] have defined multiple primary malignancies as follows:

  1. The tumor has to have definite features of malignancy
  2. The tumor has to be separate and distinct from the index tumor
  3. The possibility of the tumor being a metastasis of the index tumor has to be ruled out.


Although the mechanism involved in the development of multiple primary cancer has not been clarified, some factors such as heredity, constitution, environmental and immunological factors, carcinogenic viruses, radiological and chemical treatments have been implicated as some of the possible mechanisms.[21],[22],[23]

With the advent of the armamentarium of therapeutic options that we have nowadays, successful management of these tumors is possible given the stage of presentation of the individual tumors. We conclude that all hope is not lost when a patient presents with dual malignancy. Patient selection and treatment in specialized centers are the most important criteria in these scenarios. Risk–benefit ratio and long-term survival have to be assessed before offering major therapeutic interventions. The prognosis of these patients does not depend on the occurrence of two primary tumors but on the aggressive biology of the tumor and the stage of presentation of each individual tumor.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Moertel CG. Multiple primary malignant neoplasms: Historical perspectives. Cancer 1977;40:1786-92.  Back to cited text no. 1
    
2.
Marrano D, Viti G, Grigioni W, Marra A. Synchronous and metachronous cancer of the stomach. Eur J Surg Oncol 1987;13:493-8.  Back to cited text no. 2
    
3.
Kim JH, Rha SY, Kim C, Kim GM, Yoon SH, Kim KH, et al. Clinicopathologic features of metachronous or synchronous gastric cancer patients with three or more primary sites. Cancer Res Treat 2010;42:217-24.  Back to cited text no. 3
    
4.
Chowdary T, Sivaraj SM, Rao GV, Thirunavukkarasu S. Dual malignancies: Do they have a worse prognosis than their individual counterparts. Arch Int Surg 2015;5:29-32. Available from: http://www.archintsurg.org/article.asp?issn=2278-9596;year=2015;volume=5;issue=1;spage=29;epage=32;aulast=Chowdary. [Last accessed on 2019 Jan 08].  Back to cited text no. 4
    
5.
Crist DW, Sitzmann JV, Cameron JL. Improved hospital morbidity, mortality, and survival after the Whipple procedure. Ann Surg 1987;206:358-65.  Back to cited text no. 5
    
6.
Winter JM, Cameron JL, Campbell KA, Arnold MA, Chang DC, Coleman J, et al. 1423 pancreaticoduodenectomies for pancreatic cancer: A single-institution experience. J Gastrointest Surg 2006;10:1199-210.  Back to cited text no. 6
    
7.
Pawlik TM, Abdalla EK, Barnett CC, Ahmad SA, Cleary KR, Vauthey JN, et al. Feasibility of a randomized trial of extended lymphadenectomy for pancreatic cancer. Arch Surg 2005;140:584-9.  Back to cited text no. 7
    
8.
Sohn TA, Yeo CJ, Cameron JL, Koniaris L, Kaushal S, Abrams RA, et al. Resected adenocarcinoma of the pancreas-616 patients: Results, outcomes, and prognostic indicators. J Gastrointest Surg 2000;4:567-79.  Back to cited text no. 8
    
9.
Pawlik TM, Gleisner AL, Cameron JL, Winter JM, Assumpcao L, Lillemoe KD, et al. Prognostic relevance of lymph node ratio following pancreaticoduodenectomy for pancreatic cancer. Surgery 2007;141:610-8.  Back to cited text no. 9
    
10.
Di Giorgio A, Alfieri S, Rotondi F, Prete F, Di Miceli D, Ridolfini MP, et al. Pancreatoduodenectomy for tumors of Vater's ampulla: Report on 94 consecutive patients. World J Surg 2005;29:513-8.  Back to cited text no. 10
    
11.
Beger HG, Treitschke F, Gansauge F, Harada N, Hiki N, Mattfeldt T, et al. Tumor of the ampulla of Vater: Experience with local or radical resection in 171 consecutively treated patients. Arch Surg 1999;134:526-32.  Back to cited text no. 11
    
12.
Qiao QL, Zhao YG, Ye ML, Yang YM, Zhao JX, Huang YT, et al. Carcinoma of the ampulla of vater: Factors influencing long-term survival of 127 patients with resection. World J Surg 2007;31:137-43.  Back to cited text no. 12
    
13.
Klapdor R, Seutter E, Lang-Pölckow EM, Reichle H, Hinrichs A. Locoregional/systemic chemotherapy of locally advanced/metastasized pancreatic cancer with a combination of mitomycin-C and gemcitabine and simultaneous follow-up by imaging methods and tumor markers. Anticancer Res 1999;19:2459-69.  Back to cited text no. 13
    
14.
Lillemoe KD, Cameron JL, Yeo CJ, Sohn TA, Nakeeb A, Sauter PK, et al. Pancreaticoduodenectomy. Does it have a role in the palliation of pancreatic cancer? Ann Surg 1996;223:718-25.  Back to cited text no. 14
    
15.
Mehdi I, Shah AH, Moona MS, Verma K, Abussa A, Elramih R, et al. Synchronous and metachronous malignant tumours expect the unexpected. J Pak Med Assoc 2010;60:905-9.  Back to cited text no. 15
    
16.
Agrawal R. Synchronous dual malignancy: Successfully treated cases. J Cancer Res Ther 2007;3:153-6.  Back to cited text no. 16
    
17.
Luciani A, Balducci L. Multiple primary malignancies. Semin Oncol 2004;31:264-73.  Back to cited text no. 17
    
18.
Jensen OM, Storm HH. Cancer registration: Principles and methods. Reporting of results. IARC Sci Publ 1991;95:108-25.  Back to cited text no. 18
    
19.
Ećimović P, Pompe-Kirn V. Second primary cancers in laryngeal cancer patients in Slovenia, 1961-1996. Eur J Cancer 2002;38:1254-60.  Back to cited text no. 19
    
20.
Warren S, Gates O. Multiple primary, malignant tumors: A survey of the literature and statistical study. Am J Cancer 1932;16:1358-414.  Back to cited text no. 20
    
21.
Koubková L, Hrstka R, Dobes P, Vojtesek B, Vyzula R. Second primary cancers –R. Seco, incidence and the future. Klin Onkol 2014;27:11-7.  Back to cited text no. 21
    
22.
Pedersen-Bjergaard J, Larsen SO. Incidence of acute nonlymphocytic leukemia, preleukemia, and acute myeloproliferative syndrome up to 10 years after treatment of Hodgkin's disease. N Engl J Med 1982;307:965-71.  Back to cited text no. 22
    
23.
Hemminki K, Boffetta P. Multiple primary cancers as clues to environmental and heritable causes of cancer and mechanisms of carcinogenesis. In: Buffler P, Rice J, Baan R, et al. (eds): Mechanisms of Carcinogenesis: Contributions of Molecular Epidemiology. IARC Sci Publ No 157. Lyon: International Agency for Research on Cancer, IARC Sci Publ 2004. p. 289-97.  Back to cited text no. 23
    


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