Database : MEDLINE
Search on : Caroli and Disease [Words]
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[PMID]: 25763333
[Au] Autor:Monteiro JM; Monteiro GM; Caroli-Bottino A; Pannain VL
[Ad] Address:Postgraduate Program, Department of Pathology, University Hospital, Faculty of Medicine, Federal University of Rio de Janeiro, Avenida Prof. Rodolpho Paulo Rocco 255, Cidade Universitária, 21941-913 Rio de Janeiro, RJ, Brazil....
[Ti] Title:Nonalcoholic fatty liver disease: different classifications concordance and relationship between degrees of morphological features and spectrum of the disease.
[So] Source:Anal Cell Pathol (Amst);2014:526979, 2014.
[Is] ISSN:2210-7185
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The morphological features of nonalcoholic fatty liver disease (NAFLD) range from steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis. Liver biopsy remains the main tool for NASH diagnosis and many histological systems to diagnose and grade NAFLD were proposed. We evaluated the relationship among NAFLD activity score (NAS), histological diagnoses (non-NASH, possible NASH, and definite NASH), and histological algorithm proposed by Bedossa et al.; additionally the degrees of morphological features were semiquantified and correlated with non-NASH and NASH. Seventy-one liver biopsies were studied. The agreement among the three systems considering NASH and non-NASH was excellent (Κ = 0.96). Among the 22 biopsies with NAS 3-4, 72.7% showed to be NASH according to Bedossa's algorithm. The degree of steatosis, ballooning, lobular inflammation, and fibrosis stage were correlated with NASH (P < 0.001). Fibrosis stage 1 was also found in non-NASH. Over the spectrum of NAFLD, no association was observed between intensity of steatosis and fibrosis grade. The degrees of lobular inflammation showed association with fibrosis stage (P < 0.0001). In conclusion, there is agreement among different NAFLD classifications and NAS > 4 may be a better cutoff from which to consider NASH diagnosis; besides the highest degrees of steatosis, ballooning, inflammation, and fibrosis are associated with NASH.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Cu] Class update date: 150317
[Lr] Last revision date:150317
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1155/2014/526979

  2 / 1228 MEDLINE  
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[PMID]: 25689455
[Au] Autor:Hoyer PF
[Ad] Address:Zentrum für Kinder- und Jugendmedizin, Klinik für Kinderheilkunde 2, Universitätsklinikum Essen, Universität Duisburg Essen, Essen, Germany.
[Ti] Title:Clinical manifestations of autosomal recessive polycystic kidney disease.
[So] Source:Curr Opin Pediatr;27(2):186-92, 2015 Apr.
[Is] ISSN:1531-698X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE OF REVIEW: To describe the recent increase in the understanding of the clinical manifestation of autosomal recessive polycystic kidney disease (ARPKD), which is caused by mutations in the PKHD1 gene. The change in nomenclature reflects the genetic contribution to the understanding of pleiotropic disease manifestations. The term 'hepatorenal fibrocystic disorder' or 'ARPKD-congenital hepatic fibrosis (CHF)' addresses the major organ manifestations of the disease. RECENT FINDINGS: More than 300 different mutations in the PKHD1 gene have been described; however, there is no genotype-phenotype correlation. Cystic phenotype in the kidneys is highly variable. Renal oligohydramnios before 28 weeks of gestation may be lethal, whereas perinatal manifestations have a better prognosis. More than 60% of neonates with pulmonary hypoplasia may survive; about 25% need postnatal dialysis. After 10 years, 60% require renal replacement therapy. Liver fibrosis is always found and cholangiodysplasia is common. The Caroli phenotype is seen in up to 80% with perinatal manifestation. Recurrent cholangitis and cirrhosis may require liver transplantation in about 10% of patients. Neurocognitive development is in the usual range of children with moderate renal failure, but deserves further research. SUMMARY: The pleiotropic manifestations of ARPKD-CHF require multidisciplinary efforts to anticipate organ complications and to improve a possible good prognosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1097/MOP.0000000000000196

  3 / 1228 MEDLINE  
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[PMID]: 25758310
[Au] Autor:Marikar D; Gaafer D
[Ad] Address:Department of Paediatrics, Lister Hospital, Stevenage, UK.
[Ti] Title:What is this sign? The 'central dot sign', associated with Caroli's disease and Caroli's syndrome.
[So] Source:J Paediatr Child Health;51(3):347-8, 2015 Mar.
[Is] ISSN:1440-1754
[Cp] Country of publication:Australia
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1111/jpc.12575

  4 / 1228 MEDLINE  
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[PMID]: 25907884
[Au] Autor:Lorenzo AJ; Noone D
[Ad] Address:Toronto, ON, Canada.
[Ti] Title:Renal cystic disease and liver abnormalities: polycystic kidney and hepatic disease and the association with caroli disease.
[So] Source:J Am Coll Surg;220(5):976-7, 2015 May.
[Is] ISSN:1879-1190
[Cp] Country of publication:United States
[La] Language:eng
[Pt] Publication type:LETTER
[Em] Entry month:1504
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review

  5 / 1228 MEDLINE  
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[PMID]: 25884923
[Au] Autor:Ballotari P; Caroli S; Ferrari F; Romani G; Marina G; Chiarenza A; Manicardi V; Giorgi Rossi P
[Ad] Address:Servizio Interaziendale di Epidemiologia, Local Health Authority, Via Amendola 2, Reggio Emilia, Italy. paola.ballotari@ausl.re.it....
[Ti] Title:Differences in diabetes prevalence and inequalities in disease management and glycaemic control by immigrant status: a population-based study (Italy).
[So] Source:BMC Public Health;15:87, 2015.
[Is] ISSN:1471-2458
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: The diabetes prevalence increases at an alarming rate around the world and understanding disparities in occurrence, care management, and health outcomes may be a starting point towards achieving more effective strategies to prevent and manage it. The aims of this study are to compare immigrants and Italians in terms of the differences in diabetes prevalence and to evaluate inequalities in disease management and glycaemic control by using information included in Reggio Emilia diabetes register. METHODS: We retrieved from the diabetes register subjects aged 20-74 on December 31(st), 2009. Using citizenship, we created three main groups: Italy, High Developed Countries (HDC), and High Migration Pressure Countries (HMPC). These were split into sub-regions of origin. We calculated age-adjusted prevalence by gender and sub-region. Using logistic regression model, we analyzed the association between area of origin and following indicators: 1) not being in care of diabetes clinics; 2) not having glycated haemoglobin (HbA1c) test in 2010; 3) among those tested, having a HbA1c value > = 9% (75 mmol/mol). RESULTS: We found 15,889 Italian and 1,295 HMPC citizens with diabetes. HMPC citizens had higher age-adjusted prevalence of diabetes than Italians (females 5.0% vs 3.6%; males 6.5% vs 5.5%). The excess was mostly due to a strong excess in immigrants from Southern Asia (females 9.7%, males 10.2%) and Northern Africa (females 9.3%, males 5.9%). HMPC citizens were cared for by diabetes clinics in a similar proportion than Italians (OR: 1.08; 95% CI: 0.93-1.25), but had a greater odds of not being tested for HbA1c (OR: 1.51; 95% CI: 1.34-1.71), as well as of having HbA1c values equal to or over 9% (OR: 2.06; 95% CI: 1.80-3.14). The outcomes were poorer in HMPC females for the first two outcomes, while there was no difference for the HbA1c values (Wald test for heterogeneity p = 0.0850; p = 0.0156; p = 0.6635, respectively). CONCLUSIONS: Our findings highlight the need for gender-oriented actions for prevention and early diagnosis of the diabetes to contrast the higher risk in Northern Africans and Southern Asians. Further studies are required to determine whether the protocols in use are adequate for different immigrant groups.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Cu] Class update date: 150420
[Lr] Last revision date:150420
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1186/s12889-015-1403-4

  6 / 1228 MEDLINE  
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[PMID]: 25600951
[Au] Autor:Zhao L; Hosseini M; Wilcox R; Liu Q; Crook T; Taxy JB; Ferrell L; Hart J
[Ad] Address:Department of Pathology, University of Chicago, Chicago, IL 60637. Electronic address: lei.zhao@uchospitals.edu....
[Ti] Title:Segmental cholangiectasia clinically worrisome for cholangiocarcinoma: comparison with recurrent pyogenic cholangitis.
[So] Source:Hum Pathol;46(3):426-33, 2015 Mar.
[Is] ISSN:1532-8392
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The aim of this study was to review the clinical, radiographic, and pathologic features of cases of benign segmental cholangiectasia in non-Asian US patients with clinical concern for cholangiocarcinoma and compare these features with cases of recurrent pyogenic cholangitis (RPC) in Asian patients. A total of 10 non-Asian US patients with benign segmental cholangiectasia were included in this study. Nine of them underwent partial hepatic resection due to cholangiographic findings of segmental cholangiectasia with mural thickening and/or proximal biliary stricture. One was found to have markedly dilated and thickened intrahepatic bile ducts at the time of autopsy. Clinical and radiographic findings were reviewed. Elastin stains and immunostains for immunoglobulin G4, cluster of differentiation (CD1a), and Langerin were performed. Six comparison cases of RPC in Asian US patients were also examined. Histologic examination of resection specimens revealed markedly dilated large intrahepatic bile ducts with variable degrees of mural fibrosis, periductal gland hyperplasia, inflammation, and liver parenchymal atrophy. These changes were not associated with a ductular reaction. There was no evidence of biliary dysplasia or biliary cirrhosis in any cases. No gross or microscopic feature definitively separated the Asian from non-Asian patients. The etiology of this disorder in non-Asian US patients is unclear. It does not appear to represent a localized variant of Caroli disease or primary sclerosing cholangitis. The high degree of similarity shared by these cases and classic RPC suggests a common pathogenic mechanism, although the pathologic features tend to be less well developed in the cases from the non-Asian US patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Js] Journal subset:IM
[St] Status:In-Process

  7 / 1228 MEDLINE  
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[PMID]: 23884666
[Au] Autor:Caroli G; Dolci G; Dell'Amore A; Asadi N; Greco D; Chadi A; Bini A; Stella F
[Ad] Address:Thoracic Surgery Operative Unit, S.Orsola Malpighi Hospital, University of Bologna, Via Massarenti 9, Bologna, Italy.
[Ti] Title:Video-assisted thoracoscopic lobectomy for non-small cell lung cancer: a morbidity limiting approach in a patient on chronic hemodialysis and double agent antiplatelet therapy.
[So] Source:Gen Thorac Cardiovasc Surg;63(3):177-80, 2015 Mar.
[Is] ISSN:1863-6713
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:Patients with end-stage renal disease on hemodialysis undergoing surgery for lung cancer represent a high-risk group because of electrolyte imbalance, anemia, hemodynamic instability, bleeding tendency, and immunocompromised state. We describe a patient on hemodialysis with three lung adenocarcinoma of the right lower lobe as an incidental finding during the clinical course of a myocardial infarction treated with drug-eluting stent implantation and double-agent antiplatelet therapy. Considering patient comorbidities, we decided to perform a right lower lobectomy and complete lymph node dissection by a minimally invasive technique. In our experience, the thoracoscopic approach allowed us to perform lobectomy with complete lymph nodes dissection without morbidity. The use of ultrasound scalpel permits a complete lymph node dissection minimizing bleeding even in a double antiplatelet therapy patient.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1007/s11748-013-0294-5

  8 / 1228 MEDLINE  
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[PMID]: 25501066
[Au] Autor:Marzano AV; Ceccherini I; Gattorno M; Fanoni D; Caroli F; Rusmini M; Grossi A; De Simone C; Borghi OM; Meroni PL; Crosti C; Cugno M
[Ad] Address:From the Dipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti (AVM, DF, CC), Università degli Studi di Milano, Unità Operativa di Dermatologia, IRCCS Fondazione Ca' Granda, Ospedale Maggiore Policlinico, Milano; UOC Genetica Medica (IC, FC, MR, AG), Istituto Giannina Gaslini; Pediatria II (MG), Istituto Giannina Gaslini, Genova; Dipartimento di Dermatologia (CDS), Università Cattolica del Sacro Cuore, Roma; Dipartimento di Scienze Cliniche e di Comunità (OMB, PLM), Università degli Studi di Milano, Cattedra di Reumatologia, Istituto G. Pini, Milano; and Dipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti (MC), Università degli Studi di Milano, Unità Operativa di Medicina Interna, IRCCS Fondazione Ca' Granda, Ospedale Maggiore Policlinico, Milano, Italy.
[Ti] Title:Association of pyoderma gangrenosum, acne, and suppurative hidradenitis (PASH) shares genetic and cytokine profiles with other autoinflammatory diseases.
[So] Source:Medicine (Baltimore);93(27):e187, 2014 Dec.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The association of pyoderma gangrenosum, acne, and suppurative hidradenitis (PASH) has recently been described and suggested to be a new entity within the spectrum of autoinflammatory syndromes, which are characterized by recurrent episodes of sterile inflammation, without circulating autoantibodies and autoreactive T-cells. We conducted an observational study on 5 patients with PASH syndrome, analyzing their clinical features, genetic profile of 10 genes already known to be involved in autoinflammatory diseases (AIDs), and cytokine expression pattern both in lesional skin and serum. In tissue skin samples, the expressions of interleukin (IL)-1ß and its receptors I and II were significantly higher in PASH (P = 0.028, 0.047, and 0.050, respectively) than in controls. In PASH patients, chemokines such as IL-8 (P = 0.004), C-X-C motif ligand (CXCL) 1/2/3 (P = 0.028), CXCL 16 (P = 0.008), and regulated on activation, normal T cell expressed and secreted (RANTES) (P = 0.005) were overexpressed. Fas/Fas ligand and cluster of differentiation (CD)40/CD40 ligand systems were also overexpressed (P = 0.016 for Fas, P = 0.006 for Fas ligand, P = 0.005 for CD40, and P = 0.004 for CD40 ligand), contributing to tissue damage and inflammation. In peripheral blood, serum levels of the main proinflammatory cytokines, that is, IL-1ß, tumor necrosis factor-α, and IL-17, were within the normal range, suggesting that in PASH syndrome, the inflammatory process is mainly localized into the skin. Four out of our 5 PASH patients presented genetic alterations typical of well-known AIDs, including inflammatory bowel diseases, and the only patient lacking genetic changes had clinically evident Crohn disease. In conclusion, overexpression of cytokines/chemokines and molecules amplifying the inflammatory network, along with the genetic changes, supports the view that PASH syndrome is autoinflammatory in origin.
[Mh] MeSH terms primary: Acne Vulgaris/complications
Autoimmune Diseases/genetics
Cytokines/blood
Hidradenitis Suppurativa/complications
Pyoderma Gangrenosum/complications
[Mh] MeSH terms secundary: Acne Vulgaris/blood
Acne Vulgaris/genetics
Adolescent
Adult
Antigens, CD40/metabolism
Antigens, CD95/metabolism
Autoimmune Diseases/blood
E-Selectin/metabolism
Female
Hidradenitis Suppurativa/blood
Hidradenitis Suppurativa/genetics
Humans
L-Selectin/metabolism
Male
Matrix Metalloproteinases/metabolism
Middle Aged
Pyoderma Gangrenosum/blood
Pyoderma Gangrenosum/genetics
Sialic Acid Binding Immunoglobulin-like Lectins/metabolism
Skin/metabolism
Tissue Inhibitor of Metalloproteinases/metabolism
Young Adult
[Pt] Publication type:JOURNAL ARTICLE; OBSERVATIONAL STUDY; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Antigens, CD40); 0 (Antigens, CD95); 0 (Cytokines); 0 (E-Selectin); 0 (Sialic Acid Binding Immunoglobulin-like Lectins); 0 (Tissue Inhibitor of Metalloproteinases); 126880-86-2 (L-Selectin); EC 3.4.24.- (Matrix Metalloproteinases)
[Em] Entry month:1502
[Cu] Class update date: 150416
[Lr] Last revision date:150416
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:141216
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000000187

  9 / 1228 MEDLINE  
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[PMID]: 24621061
[Au] Autor:Mezzelani A; Landini M; Facchiano F; Raggi ME; Villa L; Molteni M; De Santis B; Brera C; Caroli AM; Milanesi L; Marabotti A
[Ti] Title:Environment, dysbiosis, immunity and sex-specific susceptibility: A translational hypothesis for regressive autism pathogenesis.
[So] Source:Nutr Neurosci;18(4):145-61, 2015 May.
[Is] ISSN:1476-8305
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Background Autism is an increasing neurodevelopmental disease that appears by 3 years of age, has genetic and/or environmental etiology, and often shows comorbid situations, such as gastrointestinal (GI) disorders. Autism has also a striking sex-bias, not fully genetically explainable. Objective Our goal was to explain how and in which predisposing conditions some compounds can impair neurodevelopment, why this occurs in the first years of age, and, primarily, why more in males than females. Methods We reviewed articles regarding the genetic and environmental etiology of autism and toxins effects on animal models selected from PubMed and databases about autism and toxicology. Discussion Our hypothesis proposes that in the first year of life, the decreasing of maternal immune protection and child immune-system immaturity create an immune vulnerability to infection diseases that, especially if treated with antibiotics, could facilitate dysbiosis and GI disorders. This condition triggers a vicious circle between immune system impairment and increasing dysbiosis that leads to leaky gut and neurochemical compounds and/or neurotoxic xenobiotics production and absorption. This alteration affects the 'gut-brain axis' communication that connects gut with central nervous system via immune system. Thus, metabolic pathways impaired in autistic children can be affected by genetic alterations or by environment-xenobiotics interference. In addition, in animal models many xenobiotics exert their neurotoxicity in a sex-dependent manner. Conclusions We integrate fragmented and multi-disciplinary information in a unique hypothesis and first disclose a possible environmental origin for the imbalance of male:female distribution of autism, reinforcing the idea that exogenous factors are related to the recent rise of this disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1179/1476830513Y.0000000108

  10 / 1228 MEDLINE  
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[PMID]: 25568301
[Au] Autor:Caroli A; Prestia A; Galluzzi S; Ferrari C; van der Flier WM; Ossenkoppele R; Van Berckel B; Barkhof F; Teunissen C; Wall AE; Carter SF; Schöll M; Choo IH; Grimmer T; Redolfi A; Nordberg A; Scheltens P; Drzezga A; Frisoni GB; Alzheimer's Disease Neuroimaging Initiative
[Ad] Address:From the Medical Imaging Unit (A.C.), Biomedical Engineering Department, IRCCS Istituto di Ricerche Farmacologiche Mario Negri, Bergamo; LENITEM-Laboratory of Epidemiology Neuroimaging and Telemedicine (A.P., S.G., C.F., A.R., G.B.F.), IRCCS Centro San Giovanni di Dio Fatebenefratelli, Brescia, Ital...
[Ti] Title:Mild cognitive impairment with suspected nonamyloid pathology (SNAP): Prediction of progression.
[So] Source:Neurology;84(5):508-15, 2015 Feb 3.
[Is] ISSN:1526-632X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVES: The aim of this study was to investigate predictors of progressive cognitive deterioration in patients with suspected non-Alzheimer disease pathology (SNAP) and mild cognitive impairment (MCI). METHODS: We measured markers of amyloid pathology (CSF ß-amyloid 42) and neurodegeneration (hippocampal volume on MRI and cortical metabolism on [(18)F]-fluorodeoxyglucose-PET) in 201 patients with MCI clinically followed for up to 6 years to detect progressive cognitive deterioration. We categorized patients with MCI as A+/A- and N+/N- based on presence/absence of amyloid pathology and neurodegeneration. SNAPs were A-N+ cases. RESULTS: The proportion of progressors was 11% (8/41), 34% (14/41), 56% (19/34), and 71% (60/85) in A-N-, A+N-, SNAP, and A+N+, respectively; the proportion of APOE ε4 carriers was 29%, 70%, 31%, and 71%, respectively, with the SNAP group featuring a significantly different proportion than both A+N- and A+N+ groups (p ≤ 0.005). Hypometabolism in SNAP patients was comparable to A+N+ patients (p = 0.154), while hippocampal atrophy was more severe in SNAP patients (p = 0.002). Compared with A-N-, SNAP and A+N+ patients had significant risk of progressive cognitive deterioration (hazard ratio = 2.7 and 3.8, p = 0.016 and p < 0.001), while A+N- patients did not (hazard ratio = 1.13, p = 0.771). In A+N- and A+N+ groups, none of the biomarkers predicted time to progression. In the SNAP group, lower time to progression was correlated with greater hypometabolism (r = 0.42, p = 0.073). CONCLUSIONS: Our findings support the notion that patients with SNAP MCI feature a specific risk progression profile.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Em] Entry month:1502
[Cu] Class update date: 150407
[Lr] Last revision date:150407
[Js] Journal subset:AIM; IM
[St] Status:In-Process
[do] DOI:10.1212/WNL.0000000000001209


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