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1.
J Neuroendocrinol ; : e13428, 2024 Jun 27.
Article in English | MEDLINE | ID: mdl-38937137

ABSTRACT

Molecular blood biomarkers are lacking for high-grade (HG) gastroenteropancreatic (GEP) neuroendocrine neoplasms (NEN). To histologically distinguish between neuroendocrine carcinoma (NEC), neuroendocrine tumors G3 (NET G3), adenocarcinoma and MINEN is often challenging. The mRNA-based NETest has diagnostic, prognostic and predictive value in neuroendocrine tumors G1-2 but has not been studied in HG GEP-NEN. Patients with advanced HG GEP-NEN were prospectively included in an observational study. A blood sample was collected before the start of chemotherapy and pseudonymised before NETest was performed. NETest results are expressed as an activity index (NETest score) from 0 to 100. The normal score cut-off is 20. Histological sections were pseudonymised before centralized pathological re-evaluation. Samples from 60 patients were evaluable with the NETest. Main primary tumor sites were colon (14), rectum (12), pancreas (11) and esophagus (7). Re-classification: 30 NEC, 12 NET G3, 3 HG-NEN ambiguous morphology, 8 MiNEN, 3 adenocarcinomas with neuroendocrine differentiation (ADNE), 3 adenocarcinomas and 1 NET G2. Elevated NETest (>20) was seen in 38/45 (84%) HG GEP-NEN, all 17 large-cell NEC (100%), 11/13 (85%) small-cell NEC, all ambiguous cases and 7/12 (64%) NET G3. NETest was elevated in 5/8 (63%) MiNEN, 2/3 ADNE, however not in 3 adenocarcinomas. Median survival was 10.2 months (9.6-10.8 95%CI) for evaluable HG GEP-NEN treated with palliative chemotherapy (n = 39), and survival was significantly shorter in patients with NETest >60 with an OS of only 6.5 months. This is the first study to evaluate use of the NETest in advanced HG GEP-NEN. The NETest was almost always elevated in GEP-NEC and in all large-cell NEC. The NETest was also frequently elevated in NET G3 and MiNEN, however cases were limited. Baseline NETest was not predictive for benefit of chemotherapy, however a NETest >60 was prognostic with a shorter survival for patients receiving chemotherapy.

3.
Ann Surg Oncol ; 29(9): 5568-5577, 2022 Sep.
Article in English | MEDLINE | ID: mdl-35583694

ABSTRACT

BACKGROUND: Surgery with radical intent is the only potentially curative option for entero-pancreatic neuroendocrine tumors (EP-NETs) but many patients develop recurrence even after many years. The subset of patients at high risk of disease recurrence has not been clearly defined to date. OBJECTIVE: The aim of this retrospective study was to define, in a series of completely resected EP-NETs, the recurrence-free survival (RFS) rate and a risk score for disease recurrence. PATIENTS AND METHODS: This was a multicenter retrospective analysis of sporadic pancreatic NETs (PanNETs) or small intestine NETs (SiNETs) [G1/G2] that underwent R0/R1 surgery (years 2000-2016) with at least a 24-month follow-up. Survival analysis was performed using the Kaplan-Meier method and risk factor analysis was performed using the Cox regression model. RESULTS: Overall, 441 patients (224 PanNETs and 217 SiNETs) were included, with a median Ki67 of 2% in tumor tissue and 8.2% stage IV disease. Median RFS was 101 months (5-year rate 67.9%). The derived prognostic score defined by multivariable analysis included prognostic parameters, such as TNM stage, lymph node ratio, margin status, and grading. The score distinguished three risk categories with a significantly different RFS (p < 0.01). CONCLUSIONS: Approximately 30% of patients with EP-NETs recurred within 5 years after radical surgery. Risk factors for recurrence were disease stage, lymph node ratio, margin status, and grading. The definition of risk categories may help in selecting patients who might benefit from adjuvant treatments and more intensive follow-up programs.


Subject(s)
Neuroendocrine Tumors , Pancreatic Neoplasms , Humans , Neoplasm Recurrence, Local/pathology , Neuroendocrine Tumors/pathology , Pancreatic Neoplasms/pathology , Prognosis , Retrospective Studies , Risk Factors , Survival Rate
5.
Pathologe ; 41(Suppl 1): 1-8, 2020 Jun.
Article in English | MEDLINE | ID: mdl-31273418

ABSTRACT

Poorly differentiated thyroid carcinomas (PDTCs) are a rare subtype of thyroid carcinomas that are biologically situated between well-differentiated papillary/follicular thyroid carcinomas and anaplastic thyroid carcinomas (ATCs).The diagnosis of conventional as well as oncocytic poorly differentiated thyroid carcinoma is difficult and often missed in daily routine. The current WHO criteria to allow the diagnosis of PDTCs are based on the results of a consensus meeting held in Turin in 2006. Even a minor poorly differentiated component of only 10%of a given carcinoma significantly affects patient prognosis and the oncocytic subtype may even have a worse outcome. Immunohistochemistry is not much help and is mostly used to exclude a medullary thyroid carcinoma with calcitonin and to establish a follicular cell of origin via thyroglobulin staining.Due to the concept of stepwise dedifferentiation, there is a vast overlap of different molecular alterations like BRAF, RAS, CTNNB1, TP53 and others between different thyroid carcinoma subtypes. A distinctive molecular tumor profile is therefore currently not available.PDTCs have a unique miRNA signature, which separates them from other thyroid carcinomas. The average relapse free survival is less than one year and about 50% of patients die of the disease. Modern tyrosine kinase inhibitors offer in conjunction with powerful molecular diagnostic new chances in these difficult to treat carcinomas.


Subject(s)
Carcinoma/pathology , Thyroid Neoplasms/pathology , Humans , Missed Diagnosis , Undiagnosed Diseases
6.
Pathologe ; 40(3): 227-234, 2019 May.
Article in German | MEDLINE | ID: mdl-31093689

ABSTRACT

Poorly differentiated thyroid carcinomas (PDTCs) are a rare subtype of thyroid carcinomas that are biologically situated between well-differentiated papillary/follicular thyroid carcinomas and anaplastic thyroid carcinomas (ATCs).The diagnosis of conventional as well as oncocytic poorly differentiated thyroid carcinoma is difficult and often missed in daily routine. The current WHO criteria to allow the diagnosis of PDTCs are based on the results of a consensus meeting held in Turin in 2006. Even a minor poorly differentiated component of only 10% of a given carcinoma significantly affects patient prognosis and the oncocytic subtype may even have a worse outcome. Immunohistochemistry is not much help and is mostly used to exclude a medullary thyroid carcinoma with calcitonin and to establish a follicular cell of origin via thyroglobulin staining.Due to the concept of stepwise dedifferentiation, there is a vast overlap of different molecular alterations like BRAF, RAS, CTNNB1, TP53 and others between different thyroid carcinoma subtypes. A distinctive molecular tumor profile is therefore currently not available.PDTCs have a unique miRNA signature, which separates them from other thyroid carcinomas.The average relapse free survival is less than one year and about 50% of patients die of the disease. Modern tyrosine kinase inhibitors offer in conjunction with powerful molecular diagnostic new chances in these difficult to treat carcinomas.


Subject(s)
Adenocarcinoma/pathology , Thyroglobulin/physiology , Thyroid Neoplasms , Humans , Neoplasm Recurrence, Local , Prognosis , Thyroid Neoplasms/pathology
7.
CNS Drugs ; 31(12): 1057-1082, 2017 12.
Article in English | MEDLINE | ID: mdl-29260466

ABSTRACT

Over the past few decades, research on Alzheimer's disease (AD) has focused on pathomechanisms linked to two of the major pathological hallmarks of extracellular deposition of beta-amyloid peptides and intra-neuronal formation of neurofibrils. Recently, a third disease component, the neuroinflammatory reaction mediated by cerebral innate immune cells, has entered the spotlight, prompted by findings from genetic, pre-clinical, and clinical studies. Various proteins that arise during neurodegeneration, including beta-amyloid, tau, heat shock proteins, and chromogranin, among others, act as danger-associated molecular patterns, that-upon engagement of pattern recognition receptors-induce inflammatory signaling pathways and ultimately lead to the production and release of immune mediators. These may have beneficial effects but ultimately compromise neuronal function and cause cell death. The current review, assembled by participants of the Chiclana Summer School on Neuroinflammation 2016, provides an overview of our current understanding of AD-related immune processes. We describe the principal cellular and molecular players in inflammation as they pertain to AD, examine modifying factors, and discuss potential future therapeutic targets.


Subject(s)
Alzheimer Disease/drug therapy , Inflammation/drug therapy , Molecular Targeted Therapy , Alzheimer Disease/immunology , Alzheimer Disease/physiopathology , Amyloid beta-Peptides/metabolism , Animals , Humans , Immunity, Innate/immunology , Inflammation/immunology , Inflammation/physiopathology
9.
Eur J Surg Oncol ; 43(9): 1682-1689, 2017 Sep.
Article in English | MEDLINE | ID: mdl-28522174

ABSTRACT

BACKGROUND: Gastroenteropancreatic neuroendocrine carcinomas (GEP-NEC) are generally characterized by synchronous metastases, high aggressiveness and a dismal prognosis. Current international guidelines do not recommend surgical treatment of liver metastases, however the existing data are scarce. The aim of this study was to evaluate the results of curatively intended resection/radiofrequency ablation (RFA) of liver metastases in patients with metastatic GEP-NEC. METHODS: 32 patients with a diagnosis of high-grade gastroenteropancreatic neuroendocrine neoplasm (Ki-67 > 20%) and with intended curative resection/RFA of liver metastases, were identified among 840 patients from two Nordic GEP-NEC registries. Tumor morphology (well vs poor differentiation) was reassessed. Overall survival (OS) and progression-free survival (PFS) was assessed by Kaplan-Meier analyses for the entire cohort and for subgroups. RESULTS: Median OS after resection/RFA of liver metastases was 35.9 months (95%-CI: 20.6-51.3) with a five-year OS of 43%. The median PFS was 8.4 months (95%-CI: 3.9-13). Four patients (13%) were disease-free after 5 years. Two patients had well-differentiated morphology (NET G3) and 20 patients (63%) had Ki-67 ≥ 55%. A Ki-67 < 55% and receiving adjuvant chemotherapy were statistically significant factors of improved OS after liver resection/RFA. CONCLUSION: This study shows a long median and long term survival after liver surgery/RFA for these selected metastatic GEP-NEC patients, particularly for the group with a Ki-67 in the relatively lower G3 range. Our findings indicate a possible role for surgical treatment of liver metastases in the management of this patient population.


Subject(s)
Carcinoma, Neuroendocrine/surgery , Intestinal Neoplasms/pathology , Liver Neoplasms/surgery , Pancreatic Neoplasms/pathology , Stomach Neoplasms/pathology , Adult , Aged , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Carcinoma, Neuroendocrine/drug therapy , Carcinoma, Neuroendocrine/pathology , Carcinoma, Neuroendocrine/secondary , Catheter Ablation/adverse effects , Chemotherapy, Adjuvant , Disease-Free Survival , Female , Hepatectomy/adverse effects , Humans , Ki-67 Antigen/analysis , Liver Neoplasms/drug therapy , Liver Neoplasms/pathology , Liver Neoplasms/secondary , Male , Middle Aged , Neoplasm Grading , Recurrence , Survival Rate
10.
Endocr Relat Cancer ; 24(3): 137-146, 2017 03.
Article in English | MEDLINE | ID: mdl-28115389

ABSTRACT

DAXX and or ATRX loss occur in 40% of pancreatic neuroendocrine tumors (PanNETs). PanNETs negative for DAXX or ATRX show an increased risk of relapse. The tumor-associated pathways activated upon DAXX or ATRX loss and how this event may induce chromosomal instability (CIN) and alternative lengthening telomeres (ALT) are still unknown. Both DAXX and ATRX are involved in DNA methylation regulation. DNA methylation of heterochromatin and of non-coding sequences is extremely important for the maintenance of genomic stability. We analyzed the association of DAXX and/or ATRX loss and CIN with global DNA methylation in human PanNET samples and the effect of DAXX knock-down on methylation and cell proliferation. We assessed LINE1 as well as global DNA methylation in 167 PanNETs, and we found that DAXX and or ATRX-negative tumors and tumors with CIN were hypomethylated. DAXX knock-down in PanNET cell lines blocked cells in G1/G0 phase and seemed to increase CIN in QGP-1 cells. However, no direct changes in DNA methylation were observed after DAXX knock-down in vitro In conclusion, our data indicate that epigenetic changes are crucial steps in the progression of PanNETs loss and suggest that DNA methylation is the mechanism via which CIN is induced, allowing clonal expansion and selection.


Subject(s)
Chromosomal Instability/genetics , DNA Methylation , Neuroendocrine Tumors/genetics , Pancreatic Neoplasms/genetics , Adaptor Proteins, Signal Transducing/genetics , Adaptor Proteins, Signal Transducing/metabolism , Cell Line, Tumor , Cell Survival , Co-Repressor Proteins , Female , Humans , Male , Middle Aged , Molecular Chaperones , Neuroendocrine Tumors/metabolism , Nuclear Proteins/genetics , Nuclear Proteins/metabolism , Pancreatic Neoplasms/metabolism , X-linked Nuclear Protein/genetics , X-linked Nuclear Protein/metabolism
14.
Nature ; 522(7556): 340-4, 2015 Jun 18.
Article in English | MEDLINE | ID: mdl-26061766

ABSTRACT

Misfolded protein aggregates represent a continuum with overlapping features in neurodegenerative diseases, but differences in protein components and affected brain regions. The molecular hallmark of synucleinopathies such as Parkinson's disease, dementia with Lewy bodies and multiple system atrophy are megadalton α-synuclein-rich deposits suggestive of one molecular event causing distinct disease phenotypes. Glial α-synuclein (α-SYN) filamentous deposits are prominent in multiple system atrophy and neuronal α-SYN inclusions are found in Parkinson's disease and dementia with Lewy bodies. The discovery of α-SYN assemblies with different structural characteristics or 'strains' has led to the hypothesis that strains could account for the different clinico-pathological traits within synucleinopathies. In this study we show that α-SYN strain conformation and seeding propensity lead to distinct histopathological and behavioural phenotypes. We assess the properties of structurally well-defined α-SYN assemblies (oligomers, ribbons and fibrils) after injection in rat brain. We prove that α-SYN strains amplify in vivo. Fibrils seem to be the major toxic strain, resulting in progressive motor impairment and cell death, whereas ribbons cause a distinct histopathological phenotype displaying Parkinson's disease and multiple system atrophy traits. Additionally, we show that α-SYN assemblies cross the blood-brain barrier and distribute to the central nervous system after intravenous injection. Our results demonstrate that distinct α-SYN strains display differential seeding capacities, inducing strain-specific pathology and neurotoxic phenotypes.


Subject(s)
Lewy Body Disease/chemically induced , Multiple System Atrophy/chemically induced , Parkinson Disease/pathology , alpha-Synuclein/administration & dosage , alpha-Synuclein/toxicity , Animals , Blood-Brain Barrier , Brain/drug effects , Brain/metabolism , Female , Humans , Lewy Body Disease/metabolism , Lewy Body Disease/pathology , Multiple System Atrophy/metabolism , Multiple System Atrophy/pathology , Parkinson Disease/metabolism , Phenotype , Rats , Rats, Wistar , Substantia Nigra/drug effects , Substantia Nigra/metabolism , Substantia Nigra/pathology , Synapses/metabolism , Synapses/pathology , alpha-Synuclein/chemistry , alpha-Synuclein/classification
15.
Br J Cancer ; 112(12): 1944-50, 2015 Jun 09.
Article in English | MEDLINE | ID: mdl-25989272

ABSTRACT

BACKGROUND: There is evidence that tumour-stroma interactions have a major role in the neoplastic progression of pancreatic ductal adenocarcinoma (PDAC). Tumour budding is thought to reflect the process of epithelial-mesenchymal transition (EMT); however, the relationship between tumour buds and EMT remains unclear. Here we characterize the tumour-budding- and stromal cells in PDAC at protein and mRNA levels concerning factors involved in EMT. METHODS: mRNA in situ hybridisation and immunostaining for E-cadherin, ß-catenin, SNAIL1, ZEB1, ZEB2, N-cadherin and TWIST1 were assessed in the main tumour, tumour buds and tumour stroma on multipunch tissue microarrays from 120 well-characterised PDACs and associated with the clinicopathological features, including peritumoural (PTB) and intratumoural (ITB) budding. RESULTS: Tumour-budding cells showed increased levels of ZEB1 (P<0.0001) and ZEB2 (P=0.0119) and reduced E-cadherin and ß-catenin (P<0.0001, each) compared with the main tumour. Loss of membranous ß-catenin in the main tumour (P=0.0009) and tumour buds (P=0.0053), without nuclear translocation, as well as increased SNAIL1 in tumour and stromal cells (P=0.0002, each) correlated with high PTB. ZEB1 overexpression in the main tumour-budding and stromal cells was associated with high ITB (P=0.0084; 0.0250 and 0.0029, respectively) and high PTB (P=0.0005; 0.0392 and 0.0007, respectively). ZEB2 overexpression in stromal cells correlated with higher pT stage (P=0.03), lymphatic invasion (P=0.0172) and lymph node metastasis (P=0.0152). CONCLUSIONS: In the tumour microenvironment of phenotypically aggressive PDAC, tumour-budding cells express EMT hallmarks at protein and mRNA levels underlining their EMT-type character and are surrounded by stromal cells expressing high levels of the E-cadherin repressors ZEB1, ZEB2 and SNAIL1, this being strongly associated with the tumour-budding phenotype. Moreover, our findings suggest the existence of subtypes of stromal cells in PDAC with phenotypical and functional heterogeneity.


Subject(s)
Carcinoma, Pancreatic Ductal/pathology , Homeodomain Proteins/biosynthesis , Pancreatic Neoplasms/pathology , RNA, Messenger/metabolism , Repressor Proteins/biosynthesis , Stromal Cells/pathology , Transcription Factors/biosynthesis , Cadherins/metabolism , Carcinoma, Pancreatic Ductal/genetics , Carcinoma, Pancreatic Ductal/metabolism , Epithelial-Mesenchymal Transition , Homeodomain Proteins/genetics , Humans , Pancreatic Neoplasms/genetics , Pancreatic Neoplasms/metabolism , Phenotype , RNA, Messenger/genetics , Repressor Proteins/genetics , Snail Family Transcription Factors , Transcription Factors/genetics , Tumor Microenvironment , Zinc Finger E-box Binding Homeobox 2 , Zinc Finger E-box-Binding Homeobox 1
16.
Pathologe ; 36(3): 220-8, 2015 May.
Article in German | MEDLINE | ID: mdl-25941099

ABSTRACT

The diagnostics of pancreatic neuroendocrine tumors (PanNEN) have changed in recent years especially concerning the World Health Organization (WHO) classification, TNM staging and grading. Furthermore, some new prognostic and predictive immunohistochemical markers have been introduced. Most progress, however, has been made in the molecular pathogenesis of these neoplasms. Using next generation sequencing techniques, the mammalian target of rapamycin (mTOR) pathway, hypoxia and epigenetic changes were identified as key players in tumorigenesis. In this article the most important developments of morphological as well as immunohistochemical diagnostics together with the molecular background of PanNEN are summarized.


Subject(s)
Neuroendocrine Tumors/pathology , Pancreatic Neoplasms/pathology , Biomarkers, Tumor/analysis , Biomarkers, Tumor/genetics , Cell Transformation, Neoplastic/genetics , Cell Transformation, Neoplastic/pathology , Humans , Immunohistochemistry , Neoplasm Grading , Neoplasm Staging , Neuroendocrine Tumors/genetics , Pancreas/pathology , Pancreatic Neoplasms/genetics , Prognosis , TOR Serine-Threonine Kinases/genetics
17.
Ann Oncol ; 26(8): 1604-20, 2015 Aug.
Article in English | MEDLINE | ID: mdl-25646366

ABSTRACT

BACKGROUND: Pulmonary carcinoids (PCs) are rare tumors. As there is a paucity of randomized studies, this expert consensus document represents an initiative by the European Neuroendocrine Tumor Society to provide guidance on their management. PATIENTS AND METHODS: Bibliographical searches were carried out in PubMed for the terms 'pulmonary neuroendocrine tumors', 'bronchial neuroendocrine tumors', 'bronchial carcinoid tumors', 'pulmonary carcinoid', 'pulmonary typical/atypical carcinoid', and 'pulmonary carcinoid and diagnosis/treatment/epidemiology/prognosis'. A systematic review of the relevant literature was carried out, followed by expert review. RESULTS: PCs are well-differentiated neuroendocrine tumors and include low- and intermediate-grade malignant tumors, i.e. typical (TC) and atypical carcinoid (AC), respectively. Contrast CT scan is the diagnostic gold standard for PCs, but pathology examination is mandatory for their correct classification. Somatostatin receptor imaging may visualize nearly 80% of the primary tumors and is most sensitive for metastatic disease. Plasma chromogranin A can be increased in PCs. Surgery is the treatment of choice for PCs with the aim of removing the tumor and preserving as much lung tissue as possible. Resection of metastases should be considered whenever possible with curative intent. Somatostatin analogs are the first-line treatment of carcinoid syndrome and may be considered as first-line systemic antiproliferative treatment in unresectable PCs, particularly of low-grade TC and AC. Locoregional or radiotargeted therapies should be considered for metastatic disease. Systemic chemotherapy is used for progressive PCs, although cytotoxic regimens have demonstrated limited effects with etoposide and platinum combination the most commonly used, however, temozolomide has shown most clinical benefit. CONCLUSIONS: PCs are complex tumors which require a multidisciplinary approach and long-term follow-up.


Subject(s)
Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Carcinoid Tumor/therapy , Lung Neoplasms/therapy , Bronchoscopy , Carboplatin/administration & dosage , Carcinoid Heart Disease/diagnostic imaging , Carcinoid Tumor/diagnosis , Cisplatin/administration & dosage , Dacarbazine/administration & dosage , Dacarbazine/analogs & derivatives , Etoposide/administration & dosage , Europe , Humans , Lung Neoplasms/diagnosis , Pneumonectomy , Positron-Emission Tomography , Receptors, Somatostatin/metabolism , Societies, Medical , Temozolomide , Tomography, X-Ray Computed , Ultrasonography
18.
Minerva Anestesiol ; 81(10): 1086-95, 2015 Oct.
Article in English | MEDLINE | ID: mdl-25338282

ABSTRACT

BACKGROUND: Physical restraint is frequently used in the intensive care setting but little is known regarding its clinical scenario and effectiveness in preventing adverse events (AEs), defined as device removal. METHODS: We carried out a prospective observational study in three Intensive Care Units on 120 adult high-risk patients. The effectiveness of physical restraint was evaluated using the propensity score methodology in order to obtain comparable groups. RESULTS: Physical restraint was applied in 1371 of 3256 (43%) nurse shifts accounting for 120 patients. Substantial agitation, the nurse's judgement of insufficient sedation and sedative drug reduction were positively associated with physical restraint, whereas the presence of analgesics at admission, increased disease gravity and the treating hospital as the most substantial variable showed a negative association. Eighty-six AEs were observed in 44 patients. Quiet (SAS=1-4), unrestrained patients accounted for 40 cases, and agitated (SAS≥5) but physically restrained patients for 17 cases. The presence of any type of physical restraint had a protective effect against any type of AE (OR=0.28; CI 0.16-0.51). The observed AEs showed a limited impact on the patients' course of illness. No physical harm related to physical restraint was reported. CONCLUSION: Physical restraint efficiently averts AEs. Its application is mainly driven by local habits. Typically, the almost recovered, apparently calm and hence unrestrained patient is at greatest risk for undesirable device removal. The control/interpretation of the patient's analgo-sedation might be inappropriate.


Subject(s)
Critical Care/methods , Device Removal/adverse effects , Device Removal/methods , Restraint, Physical , Aged , Delirium/complications , Delirium/therapy , Female , Humans , Intensive Care Units , Male , Middle Aged , Propensity Score , Prospective Studies , Psychomotor Agitation/complications , Psychomotor Agitation/therapy
19.
Pathologe ; 35(3): 283-93; quiz 294, 2014 May.
Article in German | MEDLINE | ID: mdl-24671468

ABSTRACT

Neuroendocrine neoplasms (NEN) of the distal jejunum and ileum derive from serotonin-producing enterochromaffin (EC) cells. Due to their low proliferation rate and their infiltrative growth, they are often discovered at an advanced disease stage when metastasis has already occurred. The biology of these tumours is different from other NEN of the digestive tract. In order to standardise and improve diagnosis and therapy, the guidelines for the diagnosis and clinical management of jejuno-ileal NEN as well as for the management of patients with liver and other distant metastases from NEN were revised by the European Neuroendocrine Tumour Society (ENETS) in 2012. This review focuses on aspects relevant for surgical pathology.


Subject(s)
Ileal Neoplasms/pathology , Jejunal Neoplasms/pathology , Neuroendocrine Tumors/pathology , Cell Proliferation , Diagnosis, Differential , Disease Progression , Enterochromaffin Cells/pathology , Humans , Ileal Neoplasms/surgery , Ileum/pathology , Ileum/surgery , Jejunal Neoplasms/surgery , Jejunum/pathology , Jejunum/surgery , Neuroendocrine Tumors/surgery , Practice Guidelines as Topic , Receptors, Somatostatin/analysis
20.
Acta Anaesthesiol Scand ; 58(4): 478-86, 2014 Apr.
Article in English | MEDLINE | ID: mdl-24571536

ABSTRACT

BACKGROUND: The nine equivalents of nursing manpower use score (NEMS) is used to evaluate critical care nursing workload and occasionally to define hospital reimbursements. Little is known about the caregivers' accuracy in scoring, about factors affecting this accuracy and how validity of scoring is assured. METHODS: Accuracy in NEMS scoring of Swiss critical care nurses was assessed using case vignettes. An online survey was performed to assess training and quality control of NEMS scoring and to collect structural and organizational data of participating intensive care units (ICUs). Aggregated structural and procedural data of the Swiss ICU Minimal Data Set were used for matching. RESULTS: Nursing staff from 64 (82%) of the 78 certified adult ICUs participated in this survey. Training and quality control of scoring shows large variability between ICUs. A total of 1378 nurses scored one out of 20 case vignettes: accuracy ranged from 63.7% (intravenous medications) to 99.1% (basic monitoring). Erroneous scoring (8.7% of all items) was more frequent than omitted scoring (3.2%). Mean NEMS per case was 28.0 ± 11.8 points (reference score: 25.7 ± 14.2 points). Mean bias was 2.8 points (95% confidence interval: 1.0-4.7); scores below 37.1 points were generally overestimated. Data from units with a greater nursing management staff showed a higher bias. CONCLUSION: Overall, nurses assess the NEMS score within a clinically acceptable range. Lower scores are generally overestimated. Inaccurate assessment was associated with a greater size of the nursing management staff. Swiss head nurses consider themselves motivated to assure appropriate scoring and its validation.


Subject(s)
Critical Care , Intensive Care Units , Nurses/supply & distribution , Adult , Critical Care/standards , Critical Care/statistics & numerical data , Data Collection , Female , Humans , Intensive Care Units/standards , Intensive Care Units/statistics & numerical data , Linear Models , Male , Middle Aged , Nurses/statistics & numerical data , Nursing Staff, Hospital , Quality Assurance, Health Care , Quality Control , Sex Distribution , Switzerland , Workforce
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