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Medical Studies/Studia Medyczne
Bieżący numer Archiwum Artykuły zaakceptowane O czasopiśmie Suplementy Rada naukowa Bazy indeksacyjne Prenumerata Kontakt Zasady publikacji prac
vol. 35
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Zaktualizowany przegląd zmian torbielowatych w trzustce

Pradhyumna Muralidharan
Jeffrey Pradeep Raj
Pavani Nathala

Medical Intensive Care Unit, St. Johns Medical College, Bengaluru, India
Department of Clinical Pharmacology, Seth G.S Medical College & King Edward Memorial Hospital, Mumbai, India
Division of Infectious Diseases, University of Louisville, KY, USA
Medical Studies/Studia Medyczne 2019; 35 (2): 153–163
Data publikacji online: 2019/06/28
Plik artykułu:
- An updated review.pdf  [0.13 MB]
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A pancreatic cystic lesion (PCL) is a collection of fluid in the pancreas, which often presents a therapeutic and diagnostic challenge. Pancreatic cystic lesions are broadly classified as non-neoplastic and neoplastic cystic lesions. Neoplastic lesions are further broadly subcategorised into mucin-producing and non-mucin-producing [1]. The majority of cystic pancreatic lesions are incidental findings in patients undergoing abdominal imaging performed for unrelated reasons. The prevalence of such incidental lesions is approximately 2.5%, and their frequency increases with age to as much as 10% in those aged 70 years [2]. A non-malignant pseudocyst is the most common cystic lesion and is noted in individuals with a history of pancreatitis. In high-risk populations with a family history of pancreatic cancer or a hereditary predisposition to malignancy, non-pseudocyst cystic lesions may be identified in as many as one-third of patients [3]. Cystic pancreatic lesions have diverse histological and imaging appearances, and they also differ in clinical presentation, growth pattern, and risk of malignancy [3]. Patients with pancreatic cysts have an increased risk of pancreatic malignancy compared with the general population (relative risk: 22.5, 95% CI: 11.0–45.3) and the risk increases with the size of the cyst [3, 4]. The classic example of a non-mucin-producing cystic neoplasm is a serous cystadenoma. Papillary cystic neoplasms (e.g. solid pseudopapillary tumours) and cystic pancreatic neuroendocrine tumours are additional examples. Thus, the management decision for a pancreatic cyst, whether to perform conservative or surgical resection, takes into consideration the risk of malignancy, the cost of cyst analysis, cyst surveillance, the anatomical location of the cyst, the patient’s age, and overall health status [1]. A recent review suggests that the mortality rate from pancreatic resection for pancreatic cyst is 2.1% with a morbidity rate of 30%, which highlights the importance of appropriate management decisions and tailored therapy, despite the guidelines [5]. In this current review, we aim to provide an insight into the pathogenesis, clinical features, and management of various cystic pancreatic neoplasms (Table 1). The first step in evaluating a cyst is to perform magnetic resonance imaging (MRI) with magnetic resonance cholangiopancreatography (MRCP) to further evaluate the cyst if not already done. A dedicated pancreatic protocol computed tomography (CT) scan is an alternative for patients who are unable to undergo MRI/MRCP. The use of MRI and CT helps to identify the pancreatic cyst with an accuracy of 40–90% for MRI and 40–81% for CT [6]. Endoscopic ultrasound (EUS) has also been recommended as a part of the imaging modality because it helps to identify pancreatic cystic neoplasms (PCN) with features that should be considered for surgical resection, but it cannot explain the exact type of PCN. Contrast-enhanced EUS (CH-EUS) helps in evaluating the mural nodule, vascularity, or septations, which helps to see any malignant transformation. EUS-fine needle aspiration (FNA) improves the diagnostic accuracy and helps to differentiate mucinous from non-mucinous PCN, as well as malignant from benign PCN.


The incidence of pancreatic cysts in the US is estimated to be between 3% and 15% [7]. Another large study from the US that reviewed around 25,000 records of radiological, surgical, and pathological reports revealed the incidence rate of pancreatic cystic lesions to be 1.2%. Of the 49 cysts resected in this study, half were asymptomatic lesions. Twenty-nine percent of the resected cysts were classified as benign, 51% as premalignant, and 20% as malignant [8, 9]. Pancreatic cysts are detected in approximately 2.4% of patients who undergo abdominal imaging with multidetector-row CT or MRI for unrelated reasons [10]. Pancreatic cystic neoplasms account for more than 50% of pancreatic cysts, even in patients with a history of pancreatitis [8, 11]. In another case series involving 212 patients, 37% had asymptomatic lesions. Of these incidental pancreatic cystic lesions, 42% were premalignant, and 17% harboured in-situ or invasive cancer [12]. These data demonstrate that a significant percentage of neoplastic cysts are discovered incidentally [13].

Intraductal papillary mucinous neoplasm (IPMN)

Intraductal papillary mucinous neoplasms are cystic lesions (typically ≥ 1.0 cm) lined by intraductal dysplastic epithelium, which secrete excessive mucin, causing cystic dilation of the pancreatic ducts (PDs) [14]. IPMN on the basis of involvement of the PDs are classified as main duct IPMN (MD-IPMN), branch duct IPMN (BD-IPMN), or mixed variant IPMN involving both the main PD and its side branches [14]. IPMN also have various histological subtypes, such as: gastric, intestinal, pancreatobiliary, and oncocytic. BD-IPMN are usually of the gastric type, which is MUC5AC positive, is low grade, and only a small proportion turn into carcinoma. Main duct IPMNs usually have intestinal-type epithelium and a large and complex invasive property [15]. Progression to cancer can occur in all morphologic variants of IPMN. The survival rates are worse if progression occurs from invasive adenocarcinoma originating in gastric-type IPMNs, when compared to other types of IPMNs. Intestinal-type histology is found more frequently in MD-IPMN and is associated with intermediate to high risk of dysplasia and is therefore thought to cause more aggressive disease than gastric-type histology [16, 17]. The oncocytic type has papillae with oncocytic cells and is MUC6 positive [18, 19]. The oncocytic type is large and has a less invasive property, and it gets a clinical diagnosis of cystadenocarcinoma but has a good prognosis. The pancreatobiliary type is the least common, and it is also referred to by some as a high-grade version of the gastric type. The risk of progression of IPMN does not decrease even after resection, so investigations such as CT, MRCP/EUS, physical examination, and blood tests for tumour markers and glycohaemoglobin twice a year in patients with IPMN, even if they have undergone resection, are recommended [20]. All types of IPMN have a risk of developing PDAC more with BD-IPMN than with MD-IPMN [21].
IPMNs usually occur in the seventh decade of life and occur more frequently in males, with the highest male-to-female ratio of 3 : 1 seen in the Asian population [13, 22]. Although the true incidence of IPMNs is unknown, they are reported to be the most common PCN. IPMNs account for approximately 1% to 3% of pancreatic exocrine neoplasms and 20% to 50% of all PCNs [23, 24]. The site of occurrence of main duct IPMN is often the pancreatic head (> 50% of the time), whereas BD-IPMN is often multifocal, with 21–41% of those with BD-IPMNs having a multifocal disease, with > 2 cysts of various sizes throughout the pancreas [23]. BD-IPMNs are usually asymptomatic when small with no calcification and no common capsule. A cross-sectional study by Capurso et al., involving 390 patients, demonstrated that history of diabetes (especially with prior insulin use), chronic pancreatitis, and family history of pancreatic adenocarcinoma might increase the risk of IPMN development [25]. BD-IPMNs are more inactive, with a mean frequency of malignancy and invasive carcinoma around 25% and 18%, respectively, compared with 61% and 43% in MD-IPMN [23].
Symptomatic patients present with nonspecific symptoms such as abdominal pain, malaise, nausea/vomiting, and weight loss, whereas those with invasive carcinoma present with weight loss, diabetes mellitus, and/or painless jaundice [26, 27]. Laboratory investigation involves analysis of cyst fluid and estimation of carcinoembryonic antigen (CEA)/CA – 19 [28, 29]. IPMNs have clear, viscous fluid on physical examination (indicated by positive “string sign”) and an elevated CEA > 192 ng/ml (CEA has a sensitivity of 73%, specificity of 84%, and accuracy of 79% in differentiating mucinous from non-mucinous pancreatic cystic lesions). Serum CA 19-9 and CEA do not help in differentiating between benign and malignant mucinous cysts of the pancreas [30]. A study by Wu et al. involving DNA analysis of IPMNs revealed that 66% contained a GNAS mutation, 81% KRAS, and 51% both GNAS and KRAS [30]. Imaging techniques such as EUS are increasingly used to differentiate the types of IPMNs and in treatments such as intracystic injection of ethanol or ethanol/paclitaxel for cyst ablation [31]. EUS is used for the detection of mural nodules and invasive nature, as well as for detecting malignant characteristics. EUS-guided needle aspiration can be useful for obtaining the fluid CEA, amylase levels, and cytology of the cyst [32]. In centres with high expertise a combination of EUS-FNA and cytological interpretation helps to identify small BD-IPMNs [32, 33]. In a recent investigation it was shown that preoperative FNA-EUS is not associated with gastric or peritoneal cancer seeding. According to one meta-analysis, EUS-FNA accurately diagnosed IPMNs 72% of the time [34, 35].
The Sendai Guidelines from 2006, expanded in 2012 (now called the Fukuoka Guidelines), for the management of IPMN stated that surgical resection is the recommended modality for MD-IPMN when the pancreatic duct (PD) diameter is > 10 mm [36]. These guidelines also recommend resection of suspected BD-IPMN with cyst size > 3 cm or cyst size < 3 cm and the presence of mural nodules, dilation of the main PD > 6 mm, thick irregular wall, thick septa, and solid nodules identified on imaging [37]. A recent meta-analysis by Yamao et al. showed that the Sendai Consensus Guidelines had a low PPV (11–52%) but a high NPV (90–100%) for predicting malignancy in BD-IPMN [38]. Because the management of BD- IPMN is challenging, due to its less aggressive progression, imaging follow-up through CT/MRI is necessitated based on the size of the lesion. BD-IPMN smaller than 1 cm are evaluated annually, those measuring 1–2 cm are evaluated every 6–12 months, and those measuring 2–3 cm are imaged at intervals of 3–6 months [37]. The absolute criteria for surgical resection of BD-IPMN include jaundice, cytology positive for high-grade dysplasia or cancer, and the presence of contrast-enhanced mural nodule > 5 mm or solid mass. The relative indications for surgical resection include growth rate of 0.5 mm/year, increased serum CEA 19-9 level, main pancreatic ductdiameter between 5 mm and 9.9 mm, cyst diameter > 40 mm, symptoms such as new onset diabetes, mural nodule < 5 mm. Patients with IPMN and with no indication for surgery should undergo a 6-month follow-up in the first year, and then yearly follow-up is required. Patients undergoing partial pancreatectomy for IPMN require lifelong follow-up. Several studies have shown increased risk of malignancy ranging from 12–47% if the cyst size in IPMN is over 30 mm [39]. With regards to the prognosis, for patients with resected non-invasive IPMN, the 5-year survival rate is 90% to 95%. Whereas, for patients with IPMNs with an associated invasive carcinoma, the 5-year survival rates are reported to be between 36% and 60% [27]. Postoperatively patients need yearly follow-up evaluations of benign IPMNs and imaging follow-up in addition to measurement of serum markers (CEA and CA19-9) after resection of invasive IPMN, according to the International Association of Pancreatology [37, 40, 41]. 5 Extrapancreatic neoplasm is common in 20–30% of patients with IPMN; these include neoplasm of GIT, skin, breast, renal cell, thyroid, and prostate malignancies [42]. HGD, positive margins of the resected tissue, and family history are predictors for its recurrence. With respect to family history, He et al. found that patients with a family history of pancreatic cancer develop recurrence after resection of non-invasive IPMN (23% vs. 7%, p < 0.05), and family history was the pre-operative predictor of recurrence [43].

Serous cystic tumours (SCN)

Serous cystic neoplasm is benign, and no deaths are recorded due to dissemination/malignant behaviour of SCN; specific mortality due to SCN is nearly zero [44, 45]. They are cystic tumours that are histologically composed of cuboidal, glycogen-rich epithelial cells. They are filled with serous fluid and are classified according to the degree of dysplasia, as either serous cystadenoma (SCA) or serous cystadenocarcinoma (SCAC) [46–48]. SCN is more common in women, and patients are usually diagnosed during the fifth or sixth decade of life [49]. They account for approximately 16% of resected pancreatic cystic tumours and are most common in the body or tail of the pancreas but can involve the entire organ [50, 51]. Up to 90% of patients with von Hippel-Lindau syndrome have been reported to develop SCN [50]. Serous cystadenomas can be divided into microcystic, honeycomb, and oligocystic/macrocystic forms [52].
On CT a central fibrous scar with calcification can be seen in up to 30% of these lesions and is pathognomonic for SCNs [53, 54]. Microcyst is seen in 70% cases; they appear solid or show macrocavities, and can be confused as mucinous cystic neoplasm (MCN) on CT. They appear as multiple cysts (> 6) and each measuring < 2 cm in diameter [50]. The honeycomb pattern is seen in 20% of patients and shows multiple small cysts that appear as solid masses on CT and maintain high signal intensity on T2-weighted MRI [50]. The oligocystic (macrocystic) pattern is the least common (< 10%) and can be difficult to distinguish from MCN based on MRI or CT [55]. The absence of communication on imaging with the pancreatic duct helps in the differentiation of MCN and SCN from IPMN [56]. Needle-based confocal laser endomicroscopy (nCLE) is an emerging imaging technique performed during EUS-FNA and provides real-time images of the internal structure of the pancreatic cyst [57–59]. In the CONTACT study by Napoléon et al., a superficial vascular network pattern was used to identify SCA with a sensitivity of 69%, a specificity of 100%, positive predictive value of 100%, negative predictive value of 82%, and accuracy of 87%. CEA levels are low in patients with SCA [60, 61]. In a study of 450 patients, van der Waaij et al. revealed that CEA levels below 5 ng/ml suggested an SCA or pseudocyst (PC) with 50% sensitivity and 95% specificity [62]. The size of 60% of SCNs is stable, and the remaining 40% increase in size, but the growth is slow and new onset of symptoms are rare [63].
Management in the form of surgical resection is indicated only if the lesion is > 4 cm in size, the patient is symptomatic, and if there is uncertainty with regard to the nature of the cyst [60, 64, 65]. Follow-up imaging in a non-resected patient is controversial with regards to the length of time; some studies support follow-up for up to 2 years [66]. In patients who have had a surgical resection, postoperative surveillance is unnecessary, unless histology showed SCAC [66].

Mucinous cystic neoplasm (MCN)

Mucinous cystic neoplasms are premalignant or malignant cysts forming epithelial tumours of the pancreas, which are histologically composed of columnar, mucin-producing epithelium with an underlying ovarian-type stroma, which is a unique finding, and some authors consider it as a prerequisite for diagnosis [67]. MCN are more common in women (> 95%) and are usually located in the distal pancreas (> 95%), with a peak incidence in the fifth decade [68–71]. They can arise from the neck, body, or tail of the pancreas [23]. The World Health Organisation has classified MCN into three stages: benign (adenomatous), low-grade malignant (borderline), and malignant (carcinoma in situ and invasive) [72].
Imaging techniques such as CT reveal the presence of septae, which are better visualised on T1-weighted images with intravenous gadolinium administration. The cysts have high signal intensity on T2-weighted images, and in 15% of cases, peripheral eggshell calcifications may be found on CT, which indicates an increased likelihood of invasive cystadenocarcinoma [73–75]. Cyst fluid analysis with CEA level ≥ 480 ng/ml combined with viscosity > 1.6 has also been shown to predict mucinous cysts accurately. Higher levels of CEA (i.e. > 800 ng/ml) have revealed 98% specificity, 48% sensitivity, and 79% accuracy in differentiating mucinous cystadenoma (MCA) or mucinous cystadenocarcinoma (MCAC) from SCA or PC (pseudocyst) [61]. In addition, estimation of amylase levels is also diagnostic; cyst fluid amylase levels < 250 U/l have been shown to have a sensitivity of 44% and specificity of 98% in the diagnosis of SCA, MCA, or MCAC and can be used to exclude PC [61].
Management in an elderly patient is through observation, in case the lesion is < 3 cm and mural nodules are absent. If the size is over 40 mm, then surgical resection is mandatory. Surgical resection is also required if MCN is symptomatic or if there is a mural nodule, irrespective of the size [76]. However, the size of MCN needs to be monitored; some evidence suggests that there is rapid growth of the MCN during pregnancy and that the chances of rupture also increase [77]. Hence, during pregnancy monitoring must be done. If the size is between 30 mm and 40 mm, other comorbidities such as age, patient preference, and surgical risk should be taken into consideration. When the size is less than 40 mm, then MRI and EUS should be done either individually or using a combination of both [78]. In invasive carcinoma distal pancreatectomy with lymph node dissection and splenectomy is recommended if imaging shows high-grade dysplasia. In low risk cases, malignancy can be treated with distal pancreatectomy with splenic preservation with or without preservation of splenic vessels or PSP. A PSP can be considered if there are chances of long-term development of diabetes. However, early morbidity and longer hospitalisation are major drawbacks [79]. Distal pancreatectomy is indicated in young individuals, considering the risk of progression to malignancy [37]. Studies have reported a 5-year survival of 94.7–100% in patients with non-invasive MCN and 57–62.5% in those with invasive MCN [80]. In patients with invasive carcinoma, disease recurrence ranges from 37% to 83% at 5 years. In the presence of an invasive lesion, repeat CT or MRI every 6 months to check for local recurrence and distant metastases is mandated [81].

Solid pseudopapillary neoplasm (SPN)

Solid pseudopapillary neoplasms are low potential malignant tumours, which are uncommon and account for less than 4% of the resected pancreatic cystic lesions [82]. SPNs without histological criteria of malignant behaviours, such as angioinvasion, perineural invasion, or infiltration of the surrounding parenchyma, may metastasise. Therefore, all SPNs are classified as low-grade malignant neoplasms [82]. SPNs metastasise to the liver or peritoneum in 10–15% of cases [83]. SPNs are rare; hence, most studies are retrospective, making comparison difficult [84]. SPNs are genetically characterised by the activation of beta-catenin and its target genes in the WNT signalling pathway [85]. They occur more commonly in women and generally present during the third and fourth decades of life [86, 87]. SPNs can occur throughout the pancreas but usually occur in the pancreatic body or tail [88, 89]. Macroscopically, SPNs appear as large, well-demarcated, solitary, mixed solid, and cystic heterogeneous masses. It is thought that these tumours begin as solid masses with poorly supported small vessels; therefore, cells distant to these vessels undergo swelling and degenerative change resulting in a pseudopapillary pattern and cystic spaces [90]. The cytological analysis includes branching papillae with myxoid stroma surrounded by monomorphic neoplastic cells [91]. The neoplastic cells are similar to neuroendocrine tumour cells. Thus, it is important to perform appropriate immunostains (vimentin, CD10, and -catenin) to differentiate this neoplasm [90, 92]. Clinical presentation is generally nonspecific with symptoms like abdominal discomfort, increased abdominal girth, poor appetite, and nausea, which commonly occur from tumour compression of adjacent organs [48].
On CT, SPNs appear as well-circumscribed, encapsulated masses with varying areas of soft tissue and necrotic foci. The capsule is usually thick and enhancing. Peripheral calcification has been reported in 30% of patients, but no septations are visualised [93]. On MRI, the neoplasm is seen as a well-defined lesion with a mix of high and low signal intensity on T1- and T2-weighted images, which reflects the complex nature of the mass. Areas filled with blood products demonstrate high signal intensity on T1-weighted images [94]. On EUS, SPNs are usually well-defined, hypoechoic masses. They may be solid, mixed solid and cystic, or cystic [95]. Internal calcifications can be seen in some patients. The reported diagnostic accuracy of EUS-FNA for SPN based on cytology and immunohistochemistry is 65% [90]. The cyst fluid CEA is low, reflecting the presence of non-mucinous epithelium [29].
Management of SPNs is mainly surgical, taking into consideration the malignant potential (in 10–15% of individuals) of the lesion [96]. Surgeries such as distal pancreatectomy, central pancreatectomy, local resection, enucleation, and pancreaticoduodenectomy are performed depending on the site of the tumour [97]. Common metastatic sites include the liver, IVC wall, and spleen [98]. Despite its malignant potential, SPN does have a favourable prognosis, with a 5-year survival rate of around 95% after surgical resection [97]. Postoperative surveillance should be continued for at least 5 years, considering that the mean recurrence period is 4 years. Elderly patients, male patients, and those with aneuploidy DNA content have a poor prognosis and increased mortality [97, 99].


The detection of PCL is on the rise due to increased use of imaging techniques. The preliminary approach to a PCL begins with performing good-quality MRI imaging of the pancreas to identify malignant and mucinous cysts [100]. EUS-FNA has emerged as the modality of choice to evaluate further and sample PCL [101]. Although the AGA guidelines recommend utilisation of EUS in the presence of three high-risk factors, it would be reasonable to perform EUS even in the presence of one risk factor, considering the malignant potential [102]. EUS can further aid in diagnosis with direct visualisation using Spyglass technology and needle confocal laser endomicroscopy [103]. It would be ideal if the cyst biology could be accurately predicted via molecular analysis of aspirated cyst fluid [104]. Cytology is useful if malignancy is detected, with its high positive predictive value and 90% specificity. In addition, increased expression of IL-1, IL-5, and IL-8 has also been linked to high-grade dysplasia or malignancy [104]. Elevated cyst fluid vascular endothelial growth factor-A (VEGF-A) > 8500 pg/ml has 100% sensitivity and 97% specificity for SCA [105]. A recent study stated that a composite of clinical and molecular markers improved sensitivity and specificity for MCN and IPMN to 90–94% and 84–97%, respectively [106]. Consensus guidelines for surgical management do exist, but considering the morbidity involved in the surgery, risk stratification methods are essential. Considering the guidelines as mentioned above and various diagnostic techniques, each case needs to be tailored considering the malignant risk, surgical risk, and life expectancy. This would thereby help in optimising therapy and avoid unnecessary burden both in terms of monetary and non-monetary forms to the patient. Broadening the dimensions of research is essential in controversial areas of management of cystic neoplasms of the pancreas.

Conflict of interest

The authors declare no conflict of interest.


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Address for correspondence:

Jeffrey Pradeep Raj MD
Department of Clinical Pharmacology
Seth GS Medical College & King Edward Memorial Hospital Mumbai, India
E-mail: jpraj.m07@gmail.com
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