Background: Chronic pancreatitis (CP) often leads to recurrent pain as well as exocrine and/or endocrine pancreatic insufficiency. This study aimed to investigate the effect of pancreatic head resections on glucose metabolism in patients with CP. Methods: Patients who underwent pylorus-preserving pancreaticoduodenectomy (PPPD), Whipple procedure (cPD), or duodenum-preserving pancreatic head resection (DPPHR) for CP between January 2011 and December 2020 were retrospectively analyzed with regard to markers of pancreatic endocrine function including steady-state beta cell function (%B), insulin resistance (IR), and insulin sensitivity (%S) according to the updated Homeostasis Model Assessment (HOMA2). Results: Out of 141 pancreatic resections for CP, 43 cases including 31 PPPD, 2 cPD and 10 DPPHR, met the inclusion criteria. Preoperatively, six patients (14%) were normoglycemic (NG), 10 patients (23.2%) had impaired glucose tolerance (IGT) and 27 patients (62.8%) had diabetes mellitus (DM). In each subgroup, no significant changes were observed for HOMA2-%B (NG: p = 0.57; IGT: p = 0.38; DM: p = 0.1), HOMA2-IR (NG: p = 0.41; IGT: p = 0.61; DM: p = 0.18) or HOMA2-%S (NG: p = 0.44; IGT: p = 0.52; DM: p = 0.51) 3 and 12 months after surgery, respectively. Conclusion: Pancreatic head resections for CP, including DPPHR and pancreatoduodenectomies, do not significantly affect glucose metabolism within a follow-up period of 12 months.

ZusammenfassungDer offen-chirurgische thorakale und thorakoabdominelle Aortenersatz (open repair, OR) bei Aneurysmen oder Dissektionen hat in der aktuellen Versorgungsrealität im Vergleich zur endovaskulären Versorgung mit einfachen und speziellen Stentprothesen (fenestrated/branched [thoracic] endovascular aortic repair, f/b[T]EVAR) eine deutlich untergeordnete Rolle. Zudem besteht die Notwendigkeit einer hohen technischen Expertise und eines umfangreichen operativen Settings, um ein OR sicher anbieten zu können.Zu Reduktion der spezifischen Komplikationen, wie z. B. perioperative Mortalität, permanente Dialysepflichtigkeit, spinale Ischämie, Schlaganfall oder Mesenterialischämie, ist ein hohes Maß an intraoperativer Protektion, z. B. mittels Liquordrainage, Point-of-Care-Gerinnungstherapie, distaler oder selektiver Aortenperfusion im Sinne eines temporären Linksherzbypasses und sequenziellem Clamping der Aorta erforderlich. Trotz der Dominanz der endovaskulären Therapie ist diese Expertise aber weiterhin nötig, um spezifische Indikationen, wie beispielsweise junges Patientenalter oder Bindegewebserkrankungen bzw. Protheseninfektionen, sicher versorgen zu können. Zusätzlich ist nicht jedes Aneurysma oder jede Dissektion anatomisch langfristig sicher mit einer endovaskulären Behandlung zu therapieren.Die aktuelle Evidenzlage sieht einen geringen, meist nicht statistisch signifikanten Vorteil von TEVAR und f/bEVAR versus OR bei den wichtigsten kurz- und mittelfristigen Ergebnisparametern, bei deutlich geringerer Invasivität und verkürzter Krankenhausliegedauer. Im langfristigen Verlauf sind die Ergebnisse bezüglich Gesamtüberleben und Re-Interventionsraten bzw. sekundärer Komplikationen bei OR deutlich besser.Der offene thorakoabdominelle Aortenersatz ist also nach wie vor mehr als ein exklusives Hobby, sondern vielmehr eine absolute Notwendigkeit im Gesamtspektrum der aortalen Chirurgie, dessen Bedeutung in den nächsten Jahren mutmaßlich wieder zunimmt.

Sarcomas are rare malignant tumors originating from various mesenchymal tissue types and are hence extremely heterogeneous in the histomorphology, radiological presentation, clinical and oncological behavior as well as location. Curative treatment requires as a rule radical surgical tumor resection in the sense of a compartmental resection or wide excision. The surgical resection and defect reconstruction can be technically demanding depending on the anatomical proximity to neighboring essential neurovascular structures. This situation must be planned and solved in an interdisciplinary approach. Advances in multimodal treatment concepts as well as biological reconstruction or endoprosthetic replacement for large peripheral osseous defects, often enable extremity-preserving operations; however, in sarcomas showing circumferential encasement of vascular structures, vascular resection and reconstruction is an absolute prerequisite for attainment of clean surgical margins (RO). Meanwhile, modern osteosynthetic, arthroplasty or vertebral body replacement systems allow reconstruction of multiple vertebral segments, pelvic or large joints. This article presents and discusses aspects of the contribution of vascular surgery for the treatment of mediastinal, retroperitoneal and peripheral sarcomas. In addition to vascular replacement procedures for extremity or organ salvage, the establishment of an adequate ventral access route, e.g. in spinal and pelvic tumors, can also make it necessary to include a vascular surgeon in the interdisciplinary team.

Sarkome sind seltene maligne Tumoren, die aus verschiedenen mesenchymalen Geweben entstehen und dementsprechend in Histomorphologie, radiologischem Erscheinungsbild, klinischem und onkologischem Verhalten sowie der Lokalisation ausgesprochen heterogen sind. Die Behandlung von Sarkomen mit kurativer Zielsetzung erfordert in der Regel eine radikale Tumorexstirpation im Sinne einer „Kompartmentresektion“ oder „wide excision“. In Abhängigkeit der anatomischen Lagebeziehungen des Tumors zu Umgebungsstrukturen können sich bei der Resektion und Defektrekonstruktion komplexe chirurgisch-technische Anforderungen ergeben, die interdisziplinär geplant und gelöst werden müssen. Die Fortschritte bei multimodalen Therapieansätzen sowie bei der biologischen Rekonstruktion oder prothetischen Versorgung von großen peripheren Skelettdefekten machen häufig extremitätenerhaltende Operationen möglich. Dabei können im Falle eines zirkumferenten Tumorwachstums onkologisch suffiziente Resektionsgrenzen (R0) manchmal nur durch segmentale Gefäßresektion und -rekonstruktion erreicht werden. Weiterhin können zwischenzeitlich am Stammskelett entweder ganze Beckensegmente und/oder mehrere Wirbelsäulensegmente osteosynthetisch oder mittels Wirbelkörperersatz rekonstruiert werden. In diesem Artikel sollen Aspekte des gefäßchirurgischen Beitrags zur Behandlung von mediastinalen, retroperitonealen und peripheren Sarkomen dargelegt und diskutiert werden. Neben Gefäßersatzverfahren zum Extremitäten- bzw. Organerhalt kann auch die Schaffung eines adäquaten ventralen Zugangswegs – z. B. bei spinalen oder pelvinen Tumoren – die gefäßchirurgische Beteiligung im interdisziplinären Team notwendig machen.

Purpose Visceral and renal artery aneurysms (VAA, RAA) are very rare pathologies. Both surgical and endovascular therapies are discussed as therapeutic options for ruptured and non-ruptured aneurysm repair; we describe our experience in the open and endovascular management of these entities. Methods Retrospective database analysis of 60 treated VAA and RAA in 59 patients between 1994 and 2020. Outcome data was descriptively analyzed. Results Thirty-seven aneurysms were surgically treated and 23 interventionally. In the total study cohort, we observed a mortality of 1.7% and a morbidity of 18.6%. One major complication occurred. The morbidity was higher after surgical repair in ruptured and non-ruptured cases. The mean aneurysm diameter was 30.5 ± 15.6 mm. Patients with hepatic or pancreaticoduodenal artery aneurysms presented more often in the stage of rupture, without differences in aneurysm size. The length of hospital stay after endovascular repair was significantly shorter compared to open surgical treatment (7.2 ± 6.9 days versus 11.8 ± 6.7 days, p = 0.014), but only in elective cases. Primary technical success was significantly better in patients that underwent surgical repair in an intention to treat analysis (100% versus 79.3%). The mean follow-up of the cohort was 53.5 months (range 3–207 months). Conclusion Elective endovascular therapy and open surgery of VAA and RAA are safe procedures with a good periprocedural and long-term outcome. Surgical revascularization showed a better primary technical success but was associated with longer length of hospital stays.

The classical approach of open repair (OR) for thoracic and thoracoabdominal aortic pathologies, including aneurysms and dissection, has been outnumbered by the use of fenestrated/branched (thoracic) endovascular aortic repair (f/b[T]EVAR) in recent years. Providing OR for complex cases in an aortic service requires a dedicated surgical setup and a huge body of expertise in this particular field. In order to reduce specific complications, such as perioperative mortality, kidney failure, spinal cord ischemia, stroke or bowel ischemia, it is necessary to apply cerebrospinal-spinal fluid drainage, point-of-care coagulation therapy, distal and retrograde aortic perfusion and sequential clamping. Despite the predominance of endovascular solutions, the specific OR expertise is still needed for specific indications, such as young patients, connective tissue disorder or aortic graft infections. Currently, the short and mid term results for f/b(T)EVAR outweigh those for OR, including the shorter hospital stay and less invasive procedures. However, OR provides better long-term results for overall mortality, re-intervention rates and secondary complications. In conclusion, in our opinion OR is a service that is still necessary for dedicated aortic centres, but will most likely become more frequent again in the years to come.

Type 2 diabetes is characterized by peripheral insulin resistance and insufficient insulin release from pancreatic islet β cells. However, the role and sequence of β cell dysfunction and mass loss for reduced insulin levels in type 2 diabetes pathogenesis are unclear. Here, we exploit freshly explanted pancreas specimens from metabolically phenotyped surgical patients using an in situ tissue slice technology. This approach allows assessment of β cell volume and function within pancreas samples of metabolically stratified individuals. We show that, in tissue of pre-diabetic, impaired glucose-tolerant subjects, β cell volume is unchanged, but function significantly deteriorates, exhibiting increased basal release and loss of first-phase insulin secretion. In individuals with type 2 diabetes, function within the sustained β cell volume further declines. These results indicate that dysfunction of persisting β cells is a key factor in the early development and progression of type 2 diabetes, representing a major target for diabetes prevention and therapy.

Objective: Genome wide association studies (GWAS) for type 2 diabetes (T2D) have identified genetic loci that often localise in non-coding regions of the genome, suggesting gene regulation effects. We combined genetic and transcriptomic analysis from human islets obtained from brain-dead organ donors or surgical patients to detect expression quantitative trait loci (eQTLs) and shed light into the regulatory mechanisms of these genes. Methods: Pancreatic islets were isolated either by laser capture microdissection (LCM) from surgical specimens of 103 metabolically phenotyped pancreatectomized patients (PPP) or by collagenase digestion of pancreas from 100 brain-dead organ donors (OD). Genotyping (> 8.7 million single nucleotide polymorphisms) and expression (> 47,000 transcripts and splice variants) analyses were combined to generate cis-eQTLs. Results: After applying genome-wide false discovery rate significance thresholds, we identified 1,173 and 1,021 eQTLs in samples of OD and PPP, respectively. Among the strongest eQTLs shared between OD and PPP were CHURC1 (OD p-value=1.71 x 10(-24); PPP p-value = 3.64 x 10(-24)) and PSPH (OD p-value = 3.92 x 10(-26); PPP p-value = 3.64 x 10(-24)). We identified eQTLs in linkage-disequilibrium with GWAS loci T2D and associated traits, including TTLL6, MLXand KIF9 loci, which do not implicate the nearest gene. We found in the PPP datasets 11 eQTL genes, which were differentially expressed in T2D and two genes (CYP4V2 and TSEN2) associated with HbA1c but none in the OD samples. Conclusions: eQTL analysis of LCM islets from PPP led us to identify novel genes which had not been previously linked to islet biology and T2D. The understanding gained from eQTL approaches, especially using surgical samples of living patients, provides a more accurate 3-dimensional representation than those from genetic studies alone. (C) 2019 The Authors. Published by Elsevier GmbH.

Ampullary cancer represents approximately 6% of the malignant periampullary tumors. An early occurrence of symptoms leads to a 5-year survival rate after curative surgery of 30 to 67%. In addition to the tumor stage, the immunohistological subtypes appear to be important for postoperative prognosis. The aim of this study was to analyze the different subtypes regarding their prognostic relevance. A total of 170 patients with ampullary cancer were retrospectively analyzed between 1999 until 2016 after pancreatic resection. Patients were grouped according to their pathohistological subtype of ampullary cancer (pancreatobiliary, intestinal, mixed). Characteristics among the groups were analyzed using univariate and multivariate models. Survival probability was analyzed by the Kaplan-Meier method. An exact subtyping was possible in 119 patients. A pancreatobiliary subtype was diagnosed in 69 patients (58%), intestinal in 41 patients (34.5%), and a mixed subtype in 9 patients (7.6%). Survival analysis showed a significantly worse 5-year survival rate for the pancreatobiliary subtype compared with the intestinal subtype (27.5% versus 61%, p < 0.001). The mean overall survival of patients with pancreatobiliary, intestinal, and mixed subtype was 52.5, 115 and 94.7 months, respectively (p < 0.001). The pathohistological subtypes of ampullary cancer allows a prediction of the postoperative prognosis.

Aims/hypothesis Pancreatic islet beta cell failure causes type 2 diabetes in humans. To identify transcriptomic changes in type 2 diabetic islets, the Innovative Medicines Initiative for Diabetes: Improving beta-cell function and identification of diagnostic biomarkers for treatment monitoring in Diabetes (IMIDIA) consortium ( www.imidia.org ) established a comprehensive, unique multicentre biobank of human islets and pancreas tissues from organ donors and metabolically phenotyped pancreatectomised patients (PPP). Methods Affymetrix microarrays were used to assess the islet transcriptome of islets isolated either by enzymatic digestion from 103 organ donors (OD), including 84 non-diabetic and 19 type 2 diabetic individuals, or by laser capture microdissection (LCM) from surgical specimens of 103 PPP, including 32 non-diabetic, 36 with type 2 diabetes, 15 with impaired glucose tolerance (IGT) and 20 with recent-onset diabetes (<1 year), conceivably secondary to the pancreatic disorder leading to surgery (type 3c diabetes). Bioinformatics tools were used to (1) compare the islet transcriptome of type 2 diabetic vs non-diabetic OD and PPP as well as vs IGT and type 3c diabetes within the PPP group; and (2) identify transcription factors driving gene co-expression modules correlated with insulin secretion ex vivo and glucose tolerance in vivo. Selected genes of interest were validated for their expression and function in beta cells. Results Comparative transcriptomic analysis identified 19 genes differentially expressed (false discovery rate ≤0.05, fold change ≥1.5) in type 2 diabetic vs non-diabetic islets from OD and PPP. Nine out of these 19 dysregulated genes were not previously reported to be dysregulated in type 2 diabetic islets. Signature genes included TMEM37 , which inhibited Ca 2+ -influx and insulin secretion in beta cells, and ARG2 and PPP1R1A , which promoted insulin secretion. Systems biology approaches identified HNF1A , PDX1 and REST as drivers of gene co-expression modules correlated with impaired insulin secretion or glucose tolerance, and 14 out of 19 differentially expressed type 2 diabetic islet signature genes were enriched in these modules. None of these signature genes was significantly dysregulated in islets of PPP with impaired glucose tolerance or type 3c diabetes. Conclusions/interpretation These studies enabled the stringent definition of a novel transcriptomic signature of type 2 diabetic islets, regardless of islet source and isolation procedure. Lack of this signature in islets from PPP with IGT or type 3c diabetes indicates differences possibly due to peculiarities of these hyperglycaemic conditions and/or a role for duration and severity of hyperglycaemia. Alternatively, these transcriptomic changes capture, but may not precede, beta cell failure.

Das Papillenkarzinom ist selten und macht ca. 6% der malignen periampullären Tumore aus. Eine frühe Symptomatik und Diagnosesicherung führt zu einer 5-Jahres Überlebensrate nach kurativer Operation von 30 – 67%. Prognostisch entscheidend scheinen neben dem Tumorstadium auch die immunhistologischen Subtypen (intestinal-, pankreatobiliär-) zu sein. Ziel dieser Arbeit war die Analyse der verschiedenen Subtypen hinsichtlich der prognostischen Bedeutung.

ZUSAMMENFASSUNGDie Sammlung humanen Gewebes in Form einer Biobank birgt einen großen Informationsgehalt für verschiedenste wissenschaftliche Fragestellungen. Die „DZD Human Islet Biobank“ enthält pankreatisches Gewebe von metabolisch charakterisierten Patienten, die einer kompletten oder teilweisen Pankreatektomie unterzogen wurden. Um das Diabetesrisiko bzw. den Diabetesrisikostatus eines Patienten abzuschätzen, ermitteln die Forscher mit spezifischen Voruntersuchungen den individuellen Glukosetoleranzstatus. Zudem untersuchen sie die genetischen und funktionellen Eigenschaften der pankreatischen Inselzellen, welche Hormone ausschütten, die im direkten Zusammenhang mit der Blutglukoseregulation stehen. Direkte vergleichende Analysen humaner Proben nicht diabetischer, prädiabetischer und diabetischer Probanden können dazu beitragen, Biomarker zu identifizieren, die mit der Anfälligkeit für die Entwicklung sowie dem Fortschreiten des Diabetes korrelieren, wodurch sie für die Früherkennung oder die Entwicklung neuer blutglukosesenkender Therapien nutzbar wären.

BACKGROUND AND AIM:Partial pancreatic resection is accompanied not only by a reduction in the islet cell mass but also by a variety of other factors that are likely to interfere with glucose metabolism. The aim of this work was to characterize the patient dynamics of blood glucose homeostasis during the course of partial pancreatic resection and to specify the associated clinico-pathological variables.METHODS:In total, 84 individuals undergoing elective partial pancreatic resection were consecutively recruited into this observational trial. The individuals were assigned based on their fasting glucose or oral glucose tolerance testing results into one of the following groups: (I) deteriorated, (II) stable or (III) improved glucose homeostasis three months after surgery. Co-variables associated with blood glucose dynamics were identified.RESULTS:Of the 84 participants, 25 (30%) displayed a normal oGTT, 17 (20%) showed impaired glucose tolerance, and 10 (12%) exhibited pathological glucose tolerance. Elevated fasting glucose was present in 32 (38%) individuals before partial pancreatic resection. Three months after partial pancreatic resection, 14 (17%) patients deteriorated, 16 (19%) improved, and 54 (64%) retained stable glucose homeostasis. Stability and improvement was associated with tumor resection and postoperative normalization of recently diagnosed glucose dysregulation, preoperatively elevated tumor markers and markers for common bile duct obstruction, acute pancreatitis and liver cell damage. Improvement was linked to preoperatively elevated insulin resistance, which normalized after resection and was accompanied by a decrease in fasting- and glucose-stimulated insulin secretion.CONCLUSIONS:Surgically reversible blood glucose dysregulation diagnosed concomitantly with a (peri-) pancreatic tumor appears secondary to compromised liver function due to tumor compression of the common bile duct and the subsequent increase in insulin resistance. It can be categorized as "cholestasis-induced diabetes" and thereby distinguished from other forms of hyperglycemic disorders.

Studies on islet of Langerhans physiology are crucial to understand the role of the endocrine pancreas in diabetes pathogenesis and the development of new therapeutic approaches. However, so far most research addressing islet of Langerhans biology relies on islets obtained via enzymatic isolation from the pancreas, which is known to cause mechanical and chemical stress, thus having a major impact on islet cell physiology. To circumvent the limitations of islet isolation, we have pioneered a platform for the study of islet physiology using the pancreas tissue slice technique. This approach allows to explore the detailed three-dimensional morphology of intact pancreatic tissue at a cellular level and to investigate islet cell function under near-physiological conditions. The described procedure is less damaging and faster than alternative approaches and particularly advantageous for studying infiltrated and structurally damaged islets. Furthermore, pancreas tissue slices have proven valuable for acute studies of endocrine as well as exocrine cell physiology in their conserved natural environment. We here provide a detailed protocol for the preparation of mouse pancreas tissue slices, the assessment of slice viability, and the study of pancreas cell physiology by hormone secretion and immunofluorescence staining.

Einleitung: Papillen-Karzinome werden entsprechend ihres epithelialen Ursprungs in pankreato-biliäre und intestinale Subtypen eingeteilt.

European Journal of HaematologyVolume 92, Issue 1 p. 88-89 Clinical Picture Macroglossia as the only presenting feature of amyloidosis due to MGUS Elena Tsourdi, Elena Tsourdi Department of Medicine III, Dresden Technical University Medical Center, DresdenThese authors contributed equally to this work.Search for more papers by this authorRoland Därr, Roland Därr Department of Medicine III, Dresden Technical University Medical Center, DresdenThese authors contributed equally to this work.Search for more papers by this authorKathrin Wieczorek, Kathrin Wieczorek Institute of Pathology, Dresden Technical University Medical Center, DresdenSearch for more papers by this authorChristoph Röcken, Christoph Röcken Institute of Pathology, University Hospital Kiel, KielSearch for more papers by this authorFlorian Ehehalt, Florian Ehehalt Department of Surgery, Dresden Technical University Medical Center, DresdenSearch for more papers by this authorKarsten Conrad, Karsten Conrad Institute of Immunology, Dresden Technical University Medical Center, DresdenSearch for more papers by this authorUwe Platzbecker, Uwe Platzbecker Department of Medicine I, Dresden Technical University Medical Center, DresdenSearch for more papers by this authorLorenz C Hofbauer, Corresponding Author Lorenz C Hofbauer Department of Medicine III, Dresden Technical University Medical Center, DresdenCorrespondence Lorenz C. Hofbauer, MD, Division of Endocrinology, Diabetes, and Bone Diseases, Department of Medicine III, Dresden Technical University Medical Center, Fetscherstr 74, 01307 Dresden, Germany. Tel: +49 351 458 3173; Fax: +49 351 458 5801; e-mail: lorenz.hofbauer@uniklinikum-dresden.deSearch for more papers by this author Elena Tsourdi, Elena Tsourdi Department of Medicine III, Dresden Technical University Medical Center, DresdenThese authors contributed equally to this work.Search for more papers by this authorRoland Därr, Roland Därr Department of Medicine III, Dresden Technical University Medical Center, DresdenThese authors contributed equally to this work.Search for more papers by this authorKathrin Wieczorek, Kathrin Wieczorek Institute of Pathology, Dresden Technical University Medical Center, DresdenSearch for more papers by this authorChristoph Röcken, Christoph Röcken Institute of Pathology, University Hospital Kiel, KielSearch for more papers by this authorFlorian Ehehalt, Florian Ehehalt Department of Surgery, Dresden Technical University Medical Center, DresdenSearch for more papers by this authorKarsten Conrad, Karsten Conrad Institute of Immunology, Dresden Technical University Medical Center, DresdenSearch for more papers by this authorUwe Platzbecker, Uwe Platzbecker Department of Medicine I, Dresden Technical University Medical Center, DresdenSearch for more papers by this authorLorenz C Hofbauer, Corresponding Author Lorenz C Hofbauer Department of Medicine III, Dresden Technical University Medical Center, DresdenCorrespondence Lorenz C. Hofbauer, MD, Division of Endocrinology, Diabetes, and Bone Diseases, Department of Medicine III, Dresden Technical University Medical Center, Fetscherstr 74, 01307 Dresden, Germany. Tel: +49 351 458 3173; Fax: +49 351 458 5801; e-mail: lorenz.hofbauer@uniklinikum-dresden.deSearch for more papers by this author First published: 26 June 2013 https://doi.org/10.1111/ejh.12163Citations: 5 Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume92, Issue1January 2014Pages 88-89 RelatedInformation

Background: Hepatic recurrence is seen in approximately 40% of patients undergoing hepatectomy for colorectal metastases. The authors assessed the benefit and the main prognostic factors for a second liver resection of recurrent colorectal metastases. Methods: This study reports the experience with second liver resections for recurrent liver metastases at a German University Hospital. A total of 39 parameters from 60 patients were identified from a prospective database and analysed as to their influence on recurrence-free survival and overall survival. Results: At a median follow-up of 26 months (range: 2-173 months) after second hepatic resection, recurrence-free survival at 3 and 5 years were 50% and 37%, respectively. The overall survival at three and five years were 61% and 52%, respectively. Recurrence was identified in 58.3% of the patients. Recurrences involved exclusively the liver in 19 patients (31.6%). By multivariate analysis (Cox proportional hazard model), a time interval between diagnosis of the liver metastases of less than 24 months after operation for colorectal primary carcinoma (HR: 6.47, p = 0.002), a CEA level of 4.0 ng/mL or more (HR: 3.48, p = 0.004) at the time of first liver metastases and a size of second liver metastases of 80 mm or more (HR: 4.73, p = 0.007) were independent prognostic factors for a reduced recurrence-free survival. A repeat recurrence of liver metastases without the option of curative resection was the only risk factor for overall survival after second hepatic resection (p = 0.009). In these cases, mortality risk was 4.51-fold, however, when the second liver recurrence was resectable, the mortality risk increased only 1.4-fold. Conclusions: Technically resectable recurrent colorectal hepatic metastases should be resected the same as the first metastases. Characteristics of the primary metastasis as well as parameters of the hepatic recurrence are shown to influence the prognosis of patients after resection of recurrent liver metastases. Repeat resection of colorectal liver metastases allows for improved survival in patients even after two previous liver operations.

Hepatic recurrence is seen in approximately 40 % of patients undergoing hepatectomy for colorectal metastases. The authors assessed the benefit and the main prognostic factors for a second liver resection of recurrent colorectal metastases.This study reports the experience with second liver resections for recurrent liver metastases at a German University Hospital. A total of 39 parameters from 60 patients were identified from a prospective database and analysed as to their influence on recurrence-free survival and overall survival.At a median follow-up of 26 months (range: 2-173 months) after second hepatic resection, recurrence-free survival at 3 and 5 years were 50 % and 37 %, respectively. The overall survival at three and five years were 61 % and 52 %, respectively. Recurrence was identified in 58.3 % of the patients. Recurrences involved exclusively the liver in 19 patients (31.6 %). By multivariate analysis (Cox proportional hazard model), a time interval between diagnosis of the liver metastases of less than 24 months after operation for colorectal primary carcinoma (HR: 6.47, p = 0.002), a CEA level of 4.0 ng/mL or more (HR: 3.48, p = 0.004) at the time of first liver metastases and a size of second liver metastases of 80 mm or more (HR: 4.73, p = 0.007) were independent prognostic factors for a reduced recurrence-free survival. A repeat recurrence of liver metastases without the option of curative resection was the only risk factor for overall survival after second hepatic resection (p = 0.009). In these cases, mortality risk was 4.51-fold, however, when the second liver recurrence was resectable, the mortality risk increased only 1.4-fold.Technically resectable recurrent colorectal hepatic metastases should be resected the same as the first metastases. Characteristics of the primary metastasis as well as parameters of the hepatic recurrence are shown to influence the prognosis of patients after resection of recurrent liver metastases. Repeat resection of colorectal liver metastases allows for improved survival in patients even after two previous liver operations.