scholarly journals Clostridium difficile Infection Leading to Intestinal Pneumatosis in a Patient with a Recent Diagnosis of Pancreatic Cancer Local Recurrence: A Case Report and Literature Review

2021 ◽  
pp. 1111-1117
Author(s):  
Angel Ayumi Tome Uchiyama ◽  
Moisés de Souza Martins Lopes ◽  
Maira Nacimbem Marzinotto Vana ◽  
Renata D’Alpino Peixoto
Keyword(s):  
Pancreatic Cancer ◽  
Clostridium Difficile ◽  
Rare Event ◽  
Cancer Recurrence ◽  
Pneumatosis Intestinalis ◽  
Ductal Adenocarcinoma ◽  
Intestinal Pneumatosis ◽  
Gastrointestinal Dysmotility ◽  
Increased Risk ◽  
Adenocarcinoma Of The Pancreas

<i>Clostridium difficile</i> infection (CDI) causing pneumatosis intestinalis (PI) is a rare event, described mostly in immunocompromised patients. We present the case of a 65-year-old female diagnosed with adenocarcinoma of the pancreas who underwent a duodenopancreatectomy with lymphadenectomy and adjuvant gemcitabine and capecitabine. Four months after the end of chemotherapy, she experienced abdominal pain and intermittent diarrhea which became aggravated within 6 months. CT scans revealed diffuse intestinal pneumatosis and recurrence of ductal adenocarcinoma. We hypothesize that local pancreatic cancer recurrence may lead to gastrointestinal dysmotility with consequent increased risk for CDI. The patient had almost complete resolution of PI during the CDI treatment, thus we believe that the CDI was directly responsible for PI in this case.

scholarly journals Diabetes-Related Complications and Pancreatic Cancer Incidence in the Multiethnic Cohort

2020 ◽  
Vol 4 (5) ◽  
Author(s):  
Albert J Farias ◽  
Anna H Wu ◽  
Jacqueline Porcel ◽  
Loïc Le Marchand ◽  
Lynne R Wilkens ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Pancreatic Cancer ◽  
Cancer Incidence ◽  
Conditional Logistic Regression ◽  
Ductal Adenocarcinoma ◽  
Control Analysis ◽  
Metabolic Complications ◽  
Multiethnic Cohort ◽  
Increased Risk ◽  
Incident Cases

Abstract Background People with diabetes are at an increased risk of developing pancreatic cancer. However, it is unclear whether diabetes-related complications are associated with risk of pancreatic cancer. Methods A nested matched case-control analysis was conducted among the fee-for-service Medicare participants of the prospective Multiethnic Cohort (n = ∼123 000). Between 2001 and 2014, 433 incident cases of pancreatic ductal adenocarcinoma were matched to 1728 controls by birth year, sex, race and ethnicity, and age at cohort entry. Participants were linked to data from the California and Hawaii cancer registries and Medicare claims. We used the diabetes complications severity index (DCSI) for the presence of 7 complications within 2 years prior to the diagnosis date of the index case. Multivariable conditional logistic regression was used to examine the association of DCSI with pancreatic cancer incidence. Results Diabetes was present among 45.4% of cases and 34.1% of controls. Cases had higher DCSI score compared with controls (score ≥4: 32.8% in cases; 21.2% in controls). The most prevalent diabetes-related complications for cases were cardiovascular disease (61.2%), nephropathy (31.2%), and cerebrovascular disease (21.7%). Individuals with diabetes (odds ratio [OR] = 1.48, 95% confidence interval [CI] = 1.14 to 1.91), nephropathy (OR = 1.75, 95% CI = 1.32 to 2.33), cardiovascular disease (OR = 1.88, 95% CI = 1.45 to 2.44), and metabolic complications (OR = 6.61, 95% CI = 2.49 to 17.50) were at increased risk of pancreatic cancer. For every 1-unit increase in DCSI score, participants had 18% greater risk of pancreatic cancer (OR = 1.18, 95% CI = 1.11 to 1.25). Conclusions Participants with diabetes-related complications have an elevated risk of pancreatic cancer. Identifying diabetes-related complications may help identify high-risk groups who can be studied for development of early markers for this fatal cancer.

Resolution of Clostridium difficile–Associated Diarrhea in Patients With Cancer Treated With Fidaxomicin or Vancomycin

2013 ◽  
Vol 31 (19) ◽  
pp. 2493-2499 ◽  
Author(s):  
Oliver A. Cornely ◽  
Mark A. Miller ◽  
Bruno Fantin ◽  
Kathleen Mullane ◽  
Yin Kean ◽  
...  
Keyword(s):  
Clostridium Difficile ◽  
Cancer Recurrence ◽  
Patient Characteristics ◽  
Sustained Response ◽  
Recurrence Rates ◽  
Double Blind ◽  
Patients With Cancer ◽  
Increased Risk ◽  
Intent To Treat ◽  
Clostridium Difficile Associated Diarrhea

Purpose Patients with cancer are at increased risk for Clostridium difficile–associated diarrhea (CDAD). Little is known about treatment response. Patients and Methods Two double-blind trials randomly allocated 1,105 patients with CDAD to fidaxomicin or vancomycin treatment (modified intent-to-treat [mITT]), and 183 of these had cancer. Univariate and multivariate post hoc analyses compared effects of treatment and patient characteristics on cure, recurrence, and sustained response after 4 weeks. Time to resolution of diarrhea (TTROD) was also evaluated. Results Patients with cancer had a lower cure rate and longer TTROD than patients without cancer. Recurrence rates were similar. Cure was more likely with fidaxomicin than vancomycin (odds ratio [OR] 2.0; P = .065), recurrence was less likely (OR = 0.37; P = .018), and sustained response more frequent (OR = 2.56; P = .003). Under vancomycin, median TTROD was longer in patients with cancer than in those without (123 v 58 hours; log-rank P < .001). With fidaxomicin, median TTROD was not significantly affected by presence of cancer (74 v 54 hours; log-rank P = .145). In the full mITT population, age, hypoalbuminemia, and cancer were inversely associated with clinical cure by multivariate analysis. Study treatment with vancomycin was a significant predictor of recurrence (P < .001). Within the cancer population, low albumin was negatively and fidaxomicin was positively associated with improved cure. Conclusion For patients with cancer, fidaxomicin treatment was superior to vancomycin, resulting in higher cure and sustained response rates, shorter TTROD, and fewer recurrences.

scholarly journals Developing a preoperative serum metabolome-based recurrence-predicting nomogram for patients with resected pancreatic ductal adenocarcinoma

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Seoung Yoon Rho ◽  
Sang-Guk Lee ◽  
Minsu Park ◽  
Jinae Lee ◽  
Sung Hwan Lee ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Area Under The Curve ◽  
Pancreatic Head ◽  
Cancer Recurrence ◽  
Disease Free Survival ◽  
Early Recurrence ◽  
Ductal Adenocarcinoma ◽  
Free Survival ◽  
Preoperative Serum

AbstractWe investigated the potential application of preoperative serum metabolomes in predicting recurrence in patients with resected pancreatic cancer. From November 2012 to June 2014, patients who underwent potentially curative pancreatectomy for pancreatic ductal adenocarcinoma were examined. Among 57 patients, 32 were men; 42 had pancreatic head cancers. The 57 patients could be clearly categorized into two main clusters using 178 preoperative serum metabolomes. Patients within cluster 2 showed earlier tumor recurrence, compared with those within cluster 1 (p = 0.034). A nomogram was developed for predicting the probability of early disease-free survival in patients with resected pancreatic cancer. Preoperative cancer antigen (CA) 19–9 levels and serum metabolomes PC.aa.C38_4, PC.ae.C42_5, and PC.ae.C38_6 were the most powerful preoperative clinical variables with which to predict 6-month and 1-year cancer recurrence-free survival after radical pancreatectomy, with a Harrell’s concordance index of 0.823 (95% CI: 0.750–0.891) and integrated area under the curve of 0.816 (95% CI: 0.736–0.893). Patients with resected pancreatic cancer could be categorized according to their different metabolomes to predict early cancer recurrence. Preoperative detectable parameters, serum CA 19–9, PC.aa.C38_4, PC.ae.C42_5, and PC.ae.C38_6 were the most powerful predictors of early recurrence of pancreatic cancer.

Thrombosis of the dorsal vein of the penis as first clinical presentation of pancreatic cancer metastatic to the penis

2019 ◽  
Vol 105 (6) ◽  
pp. NP43-NP47 ◽  
Author(s):  
Matteo Virdis ◽  
Cristiana Bonifacio ◽  
Tatiana Brambilla ◽  
Giovanni Capretti ◽  
Pasquale De Nittis ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Rare Event ◽  
Standard Of Care ◽  
Ductal Adenocarcinoma ◽  
Complete Replacement ◽  
Dorsal Vein ◽  
Excellent Control ◽  
Total Body ◽  
Penile Metastases ◽  
Tomography Scan

Introduction: Though metastatic disease is a common presentation of pancreatic adenocarcinoma, localization to the penis is an extremely rare event despite its abundant vascularization. Primary cancers responsible for penile metastases usually occur in prostate and rectum and are often associated with disseminated malignancy and poor prognosis. Case description: A 66-year-old man was diagnosed with adenocarcinoma of the tail of the pancreas after the onset of thrombosis of the dorsal vein of the penis; pubis ultrasound and total body computed tomography scan were negative for metastases at other sites. The patient was submitted to distal pancreatectomy with splenectomy for a pT3 N1 G4 pancreatic ductal adenocarcinoma. Three weeks after discharge, the patient returned to the outpatient clinic complaining of a painful permanent turgidity of the penis shaft. Ultrasound revealed a complete replacement of the cavernosal bodies by multiple nodular masses and a penile biopsy confirmed metastases from the primary pancreatic cancer. The patient started chemotherapy with NAB-paclitaxel and gemcitabine, with excellent control of symptoms. However, the disease progressed to bone and liver and the patient died 9 months after surgery. Conclusions: Penile localization is an extremely rare event and a standard of care has not been elaborated. Treatments are palliative and mainly aimed at pain relief and can comprise chemotherapy, radiotherapy, and surgery. Identification of venous thrombosis as an early sign of involvement could potentially offer patients an earlier diagnosis and a better treatment option.

scholarly journals What Should Guide the Performance of Venous Resection During Pancreaticoduodenectomy for Pancreatic Ductal Adenocarcinoma with Venous Contact?

2021 ◽  
Author(s):  
Julie Navez ◽  
Christelle Bouchart ◽  
Diane Lorenzo ◽  
Maria Antonietta Bali ◽  
Jean Closset ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Surgical Resection ◽  
Tumor Biology ◽  
Surgical Techniques ◽  
Surgical Margin ◽  
Ductal Adenocarcinoma ◽  
Pancreatic Tumors ◽  
R0 Resection ◽  
Venous Resection ◽  
Increased Risk

AbstractComplete surgical resection, most often associated with perioperative chemotherapy, is the only way to offer a chance of cure for patients with pancreatic cancer. One of the most important factors in determining survival outcome that can be influenced by the surgeon is the R0 resection. However, the proximity of mesenteric vessels in cephalic pancreatic tumors, especially the mesenterico-portal venous axis, results in an increased risk of vein involvement and/or the presence of malignant cells in the venous bed margin. A concomitant venous resection can be performed to decrease the risk of a positive margin. Given the additional technical difficulty that this implies, many surgeons seek a path between the tumor and the vein, hoping for the absence of tumor infiltration into the perivascular tissue on pathologic analysis, particularly in cases with administration of neoadjuvant therapy. The definition of optimal surgical margin remains a subject of debate, but at least 1 mm is an independent predictor of survival after pancreatic cancer surgical resection. Although preoperative radiologic assessment is essential for accurate planning of a pancreatic resection, intraoperative decision-making with regard to resection of the mesenterico-portal vein in tumors with a venous contact remains unclear and variable. Although venous histologic involvement and perivascular infiltration are not accurately predictable preoperatively, clinicians must examine the existing criteria and normograms to guide their surgical management according to the integration of new imaging techniques, preoperative chemotherapy use, tumor biology and molecular histopathology, and surgical techniques.

scholarly journals The role of insulin and IGF system in pancreatic cancer

2013 ◽  
Vol 50 (3) ◽  
pp. R67-R74 ◽  
Author(s):  
Marija Trajkovic-Arsic ◽  
Evdokia Kalideris ◽  
Jens T Siveke
Keyword(s):  
Pancreatic Cancer ◽  
Insulin Receptors ◽  
Ductal Adenocarcinoma ◽  
Igf System ◽  
Increased Risk ◽  
Igf1 Receptor ◽  
Risk Of Cancer ◽  
Circulating Levels ◽  
Insulin Like Growth Factors

The importance of the IGF system in carcinogenesis has been established for many solid cancers. It is well known that individuals with higher circulating levels of the IGF1 ligand present an increased risk of cancer. However, therapies with monoclonal antibodies targeting the IGF1 receptor (IGF1R) have been largely unsuccessful. One of the potential reasons for this failure is the existence of the highly homologous insulin receptor (IR), which appears to be at least equally efficient as the IGF1R in the transition of mitogenic signals to the nucleus and promotion of cell growth. Furthermore, IGF1 and insulin receptors can form hybrid receptors sensitive to stimulation of all three ligands of the system: insulin, IGF1, and IGF2. Although the connection between insulin, diabetes, and cancer has been established for years now, clear evidence that demonstrate the redundancy of insulin and insulin receptors and insulin-like growth factors and their receptors in cancer is missing. In this review, we focus on the contribution of insulin and IGFs to carcinogenesis in the insulin-producing organ, the pancreas. We give a short summary on the complexity of insulin and the IGF system in the pancreas and their potential roles in pancreatic cancer, especially pancreatic ductal adenocarcinoma. Finally, we discuss drug-targeting options of this system and the rationale of simultaneous targeting of both the insulin and the IGF systems.

scholarly journals Diabetes and Pancreatic Cancer—A Dangerous Liaison Relying on Carbonyl Stress

Cancers ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 313 ◽  
Author(s):  
Stefano Menini ◽  
Carla Iacobini ◽  
Martina Vitale ◽  
Carlo Pesce ◽  
Giuseppe Pugliese
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Development ◽  
Experimental Models ◽  
Ductal Adenocarcinoma ◽  
Carbonyl Stress ◽  
Common Mechanism ◽  
Promoting Effect ◽  
Reactive Carbonyl Species ◽  
Oncogenic Pathways ◽  
Increased Risk

Both type 2 (T2DM) and type 1 (T1DM) diabetes mellitus confer an increased risk of pancreatic cancer in humans. The magnitude and temporal trajectory of the risk conferred by the two forms of diabetes are similar, suggesting a common mechanism. Carbonyl stress is a hallmark of hyperglycemia and dyslipidemia, which accompanies T2DM, prediabetes, and obesity. Accumulating evidence demonstrates that diabetes promotes pancreatic ductal adenocarcinoma (PDAC) in experimental models of T2DM, a finding recently confirmed in a T1DM model. The carbonyl stress markers advanced glycation end-products (AGEs), the levels of which are increased in diabetes, were shown to markedly accelerate tumor development in a mouse model of Kras-driven PDAC. Consistently, inhibition of AGE formation by trapping their carbonyl precursors (i.e., reactive carbonyl species, RCS) prevented the PDAC-promoting effect of diabetes. Considering the growing attention on carbonyl stress in the onset and progression of several cancers, including breast, lung and colorectal cancer, this review discusses the mechanisms by which glucose and lipid imbalances induce a status of carbonyl stress, the oncogenic pathways activated by AGEs and their precursors RCS, and the potential use of carbonyl-scavenging agents and AGE inhibitors in PDAC prevention and treatment, particularly in high-risk diabetic individuals.

scholarly journals Hereditary vs Familial Pancreatic Cancer: Associated Genetic Syndromes and Clinical Perspective

ONCOLOGY ◽  
2020 ◽  
Author(s):  
Mehmet Sitki Copur ◽  
Geoffrey Talmon ◽  
Jonathan Hart ◽  
Shaheed Merani ◽  
Luciano Vargas
Keyword(s):  
Pancreatic Cancer ◽  
Genetic Testing ◽  
Ductal Adenocarcinoma ◽  
Rapid Progression ◽  
Familial Pancreatic Cancer ◽  
Genetic Syndromes ◽  
Causative Gene ◽  
Increased Risk ◽  
American Society ◽  
Cancer Network

Pancreatic ductal adenocarcinoma (PDAC) is a disease marked by high rates of mortality; it is mostly incurable at the time of diagnosis. Only about 7% of patients survive 5 years after diagnosis. Diagnosis at a late stage and rapid progression with minimal response to available treatments are the main reasons for this poor outcome. It is crucial to identify individuals at high risk of developing PDAC so preventive and early detection measures can be employed. Approximately 10% to 15% of PDAC cases have a hereditary or familial basis. In the majority of PDAC cases, no main causative gene has been identified, but several known germline pathogenic mutations have been shown to be related to an increased risk of this cancer. The presence of 2 or more patients with pancreatic cancer within the circle of first-degree relatives, without the presence of a causative germline mutation, is defined as familial pancreatic cancer; this accounts for 4% to 10% of PDAC. Based on the growing evidence supporting the benefit of germline genetic testing in patients with PDAC, both the American Society of Clinical Oncology and the National Comprehensive Cancer Network recently updated their guidelines to include recommendations around genetic testing for patients with pancreatic cancer. However, there is no general consensus on the group of patients and individuals who should be studied and screened. We present a demonstrative case and review the available data on hereditary and familial PDAC.

Efficacy and tolerability of adjuvant gemcitabine and capecitabine in patients with resected pancreatic cancer in US population: A single network experience.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e15789-e15789
Author(s):  
Gurveen Kaur ◽  
Vida Jahangiri ◽  
Seon Jo Park ◽  
Rodney E Wegner ◽  
Dulabh K. Monga
Keyword(s):  
Pancreatic Cancer ◽  
Progression Free Survival ◽  
Ductal Adenocarcinoma ◽  
Combination Regimen ◽  
Kaplan Meier ◽  
The Us ◽  
Collect Patient Data ◽  
Grade 3 ◽  
Adenocarcinoma Of The Pancreas ◽  
Dose Reductions

e15789 Background: Adjuvant chemotherapy with combination of gemcitabine and capecitabine improved overall survival (OS) with an acceptable toxicity profile in the European patient population. However, limited data is available for tolerability and efficacy of the combination regimen in the adjuvant setting in the US population. Herein, we report a single network experience with the combination regimen. Methods: We retrospectively evaluated 45 patients with pancreatic cancer who were treated at our institution from 1/1/2017 – 12/31/2018. Eligible patients were aged 18 years or older and had undergone complete macroscopic resection for ductal adenocarcinoma of the pancreas. These patients received adjuvant combination chemotherapy with gemcitabine (1000 mg/m2) and capecitabine (1660 mg/m2). Electronic medical record was reviewed to collect patient data. Medcalc software was used for statistical analysis including Kaplan Meier analyses. Results: Median age of patients was 64.6 years (range 47-87). Majority of patients had stage II disease (73.5%). Seventy-one percent of patients were able to receive 6 cycles of chemotherapy. Median OS for all patients was 20.2 months (95% CI 11.7-22.7). Median OS for patients who received < 6 vs 6 cycles was 14.9 months (95% CI 6.6-14.9) vs 21.5 months (95% CI 11.9-22.9) (p = 0.21). Median progression free survival (PFS) for all patients was 19.3months (95% CI 13.1-25.7). Median PFS for patients with < 6 vs 6 cycles was 7.3 months versus 22.2 months (p = 0.0002). Overall, 31.1% of patients developed disease progression. Of note, 33.3% and 71.1% of patients required dose reductions for gemcitabine and capecitabine respectively. Fifteen grade 3-4 adverse events were reported of which 11 were hematologic and 4 non-hematologic. Conclusions: This single institution analysis shows a trend in improvement for PFS for patients able to complete adjuvant therapy with gemcitabine and capecitabine following pancreatic resection. It is worth noting, however, that dose reductions were required in the majority of patients. Therefore, we propose investigating a modified regimen of gemcitabine and capecitabine in the US population.

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