Database : MEDLINE
Search on : Wasting and Syndrome [Words]
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[PMID]: 29457962
[Au] Autor:Ding S; Huang W; Qin Q; Tang J; Liu H
[Ti] Title:Genotype Identification and Phylogenetic Analysis of Enterocytozoon Bieneusi Isolates from Stool Samples of Diarrheic Children.
[So] Source:J Parasitol;, 2018 Mar 09.
[Is] ISSN:1937-2345
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Among approximately 14 human-pathogenic microsporidian species, Enterocytozoon bieneusi is the most common. It can inhabit the small intestines, causing chronic diarrhea and wasting syndrome. Until now, determining prevalence and the corresponding genotypes of E. bieneusi in humans have been performed only in a few provinces of China. Herein, 93 fecal specimens were collected from diarrheic children in Chongqing. By PCR and sequencing of the internal transcribed spacer (ITS) region of the E. bieneusi rDNA sequence, we found 11 (11.83%) positive specimens. Among them, 8 (8.60%) are from patients with ages ranging from 2 months to 6 years old, and 3 (3.23%) positive specimens from patients 7 to 11 years old. In total, 6 genotypes (4 novel genotypes and 2 known genotypes) have been identified in this study. Phylogenetic analysis showed that all the genotypes identified in present study belong to group 1, which previously has been described as a zoonotic group. This could mean these infections were acquired zoonotically. It may be prudent to warn of this potential risk to those people having close contact with animals.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1645/17-108

  2 / 8639 MEDLINE  
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[PMID]: 29358615
[Au] Autor:Castiglioni C; Fattori F; Udd B; de Los Angeles Avaria M; Suarez B; D'Amico A; Malandrini A; Carrozzo R; Verrigni D; Bertini E; Tasca G
[Ad] Address:Department of Pediatric Neurology, Clinica Las Condes, Santiago, Chile.
[Ti] Title:Neuromyopathy with congenital cataracts and glaucoma: a distinct syndrome caused by POLG variants.
[So] Source:Eur J Hum Genet;26(3):367-373, 2018 Mar.
[Is] ISSN:1476-5438
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:We identified three non-related patients manifesting a childhood-onset progressive neuromyopathy with congenital cataracts, delayed walking, distal weakness and wasting, glaucoma and swallowing difficulties. Electrophysiology and nerve biopsies showed a mixed axonal and demyelinating neuropathy, while muscle biopsy disclosed both neurogenic and myopathic changes with ragged red fibers, and muscle MRI showed consistent features across patients, with a peculiar concentric disto-proximal gradient of fatty replacement. We used targeted next generation sequencing and candidate gene approach to study these families. Compound biallelic heterozygous variants, p.[(Pro648Arg)]; [(His932Tyr)] and p.[(Thr251Ile),(Pro587Leu)]; [(Arg943Cys)], were found in the three patients causing this homogeneous phenotype. Our report on a subset of unrelated patients, that showed a distinct autosomal recessive childhood-onset neuromyopathy with congenital cataracts and glaucoma, expands the clinical spectrum of POLG-related disorders. It also confirms the association between cataracts and neuropathy with variants in POLG. Early onset cataract is otherwise rare in POLG-related disorders and so far reported only in a few patients with the clinical pattern of distal myopathy or neuromyopathy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1038/s41431-017-0003-4

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[PMID]: 29489032
[Au] Autor:Khatib MN; Shankar AH; Kirubakaran R; Gaidhane A; Gaidhane S; Simkhada P; Quazi Syed Z
[Ad] Address:Division of Evidence Synthesis; School of Epidemiology and Public Health & Department of Physiology, Datta Meghe Institute of Medical Sciences, Sawangi Meghe, Wardha, Maharashtra, India, 442004.
[Ti] Title:Ghrelin for the management of cachexia associated with cancer.
[So] Source:Cochrane Database Syst Rev;2:CD012229, 2018 02 28.
[Is] ISSN:1469-493X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Cancer sufferers are amongst the most malnourished of all the patient groups. Studies have shown that ghrelin, a gut hormone can be a potential therapeutic agent for cachexia (wasting syndrome) associated with cancer. A variety of mechanisms of action of ghrelin in people with cancer cachexia have been proposed. However, safety and efficacy of ghrelin for cancer-associated cachexia have not been systematically reviewed. The aim of this review was to assess whether ghrelin is associated with better food intake, body composition and survival than other options for adults with cancer cachexia. OBJECTIVES: To assess the efficacy and safety of ghrelin in improving food intake, body composition and survival in people with cachexia associated with cancer. SEARCH METHODS: We searched CENTRAL, MEDLINE and Embase without language restrictions up to July 2017. We also searched for ongoing studies in trials registers, performed handsearching, checked bibliographic references of relevant articles and contacted authors and experts in the field to seek potentially relevant research. We applied no restrictions on language, date, or publication status. SELECTION CRITERIA: We included randomised controlled (parallel-group or cross-over) trials comparing ghrelin (any formulation or route of administration) with placebo or an active comparator in adults (aged 18 years and over) who met any of the international criteria for cancer cachexia. DATA COLLECTION AND ANALYSIS: Two review authors independently assessed studies for eligibility. Two review authors then extracted data and assessed the risk of bias for individual studies using standard Cochrane methodology. For dichotomous variables, we planned to calculate risk ratio with 95% confidence intervals (CI) and for continuous data, we planned to calculate mean differences (MD) with 95% CI. We assessed the evidence using GRADE and created 'Summary of findings' tables. MAIN RESULTS: We screened 926 individual references and identified three studies that satisfied the inclusion criteria. Fifty-nine participants (37 men and 22 women) aged between 54 and 78 years were randomised initially, 47 participants completed the treatment. One study had a parallel design and two had a cross-over design. The studies included people with a variety of cancers and also differed in the dosage, route of administration, frequency and duration of treatment.One trial, which compared ghrelin with placebo, found that ghrelin improved food intake (very low-quality evidence) and had no adverse events (very low-quality evidence). Due to unavailability of data we were unable to report on comparisons for ghrelin versus no treatment or alternative experimental treatment modalities, or ghrelin in combination with other treatments or ghrelin analogues/ghrelin mimetics/ghrelin potentiators. Two studies compared a higher dose of ghrelin with a lower dose of ghrelin, however due to differences in study designs and great diversity in the treatment provided we did not pool the results. In both trials, food intake did not differ between participants on higher-dose and lower-dose ghrelin. None of the included studies assessed data on body weight. One study reported higher adverse events with a higher dose as compared to a lower dose of ghrelin.All studies were at high risk of attrition bias and bias for size of the study. Risk of bias in other domains was unclear or low.We rated the overall quality of the evidence for primary outcomes (food intake, body weight, adverse events) as very low. We downgraded the quality of the evidence due to lack of data, high or unclear risk of bias of the studies and small study size. AUTHORS' CONCLUSIONS: There is insufficient evidence to be able to support or refute the use of ghrelin in people with cancer cachexia. Adequately powered randomised controlled trials focusing on evaluation of safety and efficacy of ghrelin in people with cancer cachexia is warranted.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Process
[do] DOI:10.1002/14651858.CD012229.pub2

  4 / 8639 MEDLINE  
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[PMID]: 28460445
[Au] Autor:Lv W; Fan Z; Huang F; Xu N; Xuan L; GuopanYu; Jiang Q; Zhou H; Lin R; Zhang X; Sun J; Liu Q
[Ad] Address:Department of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou 510515 China.
[Ti] Title:Autoimmune hematological diseases following haploidentical donor hematopoietic stem cell Transplant compared with matched sibling and unrelated donor.
[So] Source:Oncotarget;8(16):26505-26514, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Autoimmune hematological diseases (AHDs) occur more frequently than other autoimmune complications after allogeneic hematopoietic stem cell transplantation (allo-HSCT) and are often refractory to treatment. This study was to analyze the incidence and risk factors of AHDs as well as their response to treatment . Four hundred and forty-five adult malignant hematopoietic disorders underwent allo-HSCT were enrolled in this retrospective study, including 124 haploidentical donor (HRD), 140 unrelated donor (MUD) and 181 HLA-matched sibling donor (MSD) transplants. Twelve patients developed AHDs, including 6 autoimmune hemolytic anemia and 6 Evans syndrome. Evans syndrome all occurred in HRD transplants. The 3-year cumulative incidence of AHDs was 4.0 ± 1.3%, and HRD had higher incidence than MUD (8.7 ± 3.0% vs 1.8 ± 1.2%, P = 0.012) and MSD (8.7 ± 3.0% vs 3.5 ± 2.6%, P = 0.004 ). The steroids combined with Cyclosporine A were acted as the first line treatment, and the response rate was 73%. No patients experienced recurrence at a median follow up of 313 days after stopping treatment. HRD transplants (vs MUD: HR, 5.87; CI, 1.24 to 27.73; p = 0.026 and vs MSD: HR, 7.70; CI, 1.63 to 36.44; P = 0.010) and concurrent chronic graft versus host disease (HR, 3.76; CI, 1.18 to 11.92; P = 0.025) were risk factors for AHDs.
[Mh] MeSH terms primary: Autoimmune Diseases/therapy
Hematologic Diseases/therapy
Hematopoietic Stem Cell Transplantation
Siblings
Unrelated Donors
[Mh] MeSH terms secundary: Adolescent
Adult
Autoimmune Diseases/diagnosis
Autoimmune Diseases/mortality
Female
Graft vs Host Disease/diagnosis
Graft vs Host Disease/etiology
HLA Antigens/genetics
HLA Antigens/immunology
Hematologic Diseases/diagnosis
Hematologic Diseases/mortality
Hematopoietic Stem Cell Transplantation/adverse effects
Hematopoietic Stem Cell Transplantation/methods
Histocompatibility Testing
Humans
Incidence
Male
Middle Aged
Transplantation, Homologous
Treatment Outcome
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (HLA Antigens)
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:IM
[Da] Date of entry for processing:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15710

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[PMID]: 29501408
[Au] Autor:Gowda VK; Udhayabanu T; Varalakshmi P; Srinivasan VM; Ashokkumar B
[Ad] Address:Department of Pediatric Neurology, Indira Gandhi Institute of Child Health, Bangalore, India. Electronic address: drknvraju@hotmail.com.
[Ti] Title:Fazio-Londe syndrome in siblings from India with different phenotypes.
[So] Source:Brain Dev;, 2018 Feb 28.
[Is] ISSN:1872-7131
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Fazio-Londe syndrome also called progressive bulbar palsy of childhood is a very rare motor neuron disease of pediatric age group characterized by progressive paralysis of lower cranial nerves. OBJECTIVE: To describe Fazio-Londe syndrome in sibling with different phenotype. METHODS: A 6 years old female child presented with inability to close eyes, difficulty in swallowing, respiratory muscle weakness and voice change since 5 yr of age. Examination showed lower motor neuron facial nerve palsy, absent gag reflex, tongue atrophy, fasciculation, limb wasting and exaggerated deep tendon reflexes. An 11 year old boy, elder sibling of the above child presented with similar complaints at 10 years of age, other than later onset and lack of respiratory problem. Genetic testing in both cases confirmed the diagnosis of Fazio-Londe Syndrome. CONCLUSION: In any child who presents with progressive bulbar palsy with lower motor neuron facial palsy a diagnosis of Fazio-Londe Syndrome should be considered and family members should also be screened.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:Publisher

  6 / 8639 MEDLINE  
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[PMID]: 29483623
[Au] Autor:Chan KS; Mourtzakis M; Aronson Friedman L; Dinglas VD; Hough CL; Ely EW; Morris PE; Hopkins RO; Needham DM; with the National Institutes of Health NHLBI ARDS Network
[Ad] Address:Department of Health Policy and Management, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. kchan10@jhu.edu.
[Ti] Title:Upper arm anthropometrics versus DXA scan in survivors of acute respiratory distress syndrome.
[So] Source:Eur J Clin Nutr;, 2018 Feb 26.
[Is] ISSN:1476-5640
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Survivors of acute respiratory distress syndrome (ARDS) experience severe muscle wasting. Upper arm anthropometrics can provide a quick, non-invasive estimate of muscle status, but its accuracy is unknown. This study examines the accuracy of upper arm percent muscle area (UAMA) with reference measures of lean mass from dual energy X-ray absorptiometry (DXA). Data are from 120 ARDS survivors participating in a multicenter national study. Receiver operating characteristic (ROC) curves, by patient sex, demonstrated that UAMA did no better than chance in discriminating low appendicular skeletal muscle mass identified using DXA findings (c-statistics, 6 months: 0.50-0.59, 12 months: 0.54-0.57). Modest correlations of UAMA with DXA measures (whole-body: r = 0.46-0.49, arm-specific: r = 0.50-0.51, p < 0.001) and Bland-Altman plots indicate poor precision. UAMA is not an appropriate screening measure for estimating muscle mass when compared to a DXA reference standard. Alternate screening measures should be evaluated in ARDS survivors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:Publisher
[do] DOI:10.1038/s41430-018-0106-1

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[PMID]: 29371419
[Au] Autor:Boscardin E; Perrier R; Sergi C; Maillard MP; Loffing J; Loffing-Cueni D; Koesters R; Rossier BC; Hummler E
[Ad] Address:Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland.
[Ti] Title:Plasma Potassium Determines NCC Abundance in Adult Kidney-Specific ENaC Knockout.
[So] Source:J Am Soc Nephrol;29(3):977-990, 2018 Mar.
[Is] ISSN:1533-3450
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The amiloride-sensitive epithelial sodium channel (ENaC) and the thiazide-sensitive sodium chloride cotransporter (NCC) are key regulators of sodium and potassium and colocalize in the late distal convoluted tubule of the kidney. Loss of the ENaC subunit leads to a perinatal lethal phenotype characterized by sodium loss and hyperkalemia resembling the human syndrome pseudohypoaldosteronism type 1 (PHA-I). In adulthood, inducible nephron-specific deletion of ENaC in mice mimics the lethal phenotype observed in neonates, and as in humans, this phenotype is prevented by a high sodium (HNa )/low potassium (LK ) rescue diet. Rescue reflects activation of NCC, which is suppressed at baseline by elevated plasma potassium concentration. In this study, we investigated the role of the ENaC subunit in the PHA-I phenotype. Nephron-specific ENaC knockout mice also presented with salt-wasting syndrome and severe hyperkalemia. Unlike mice lacking ENaC or ΕΝaC, an HNa /LK diet did not normalize plasma potassium (K ) concentration or increase NCC activation. However, when K was eliminated from the diet at the time that ENaC was deleted, plasma K concentration and NCC activity remained normal, and progressive weight loss was prevented. Loss of the late distal convoluted tubule, as well as overall reduced ENaC subunit expression, may be responsible for the more severe hyperkalemia. We conclude that plasma K concentration becomes the determining and limiting factor in regulating NCC activity, regardless of Na balance in ENaC-deficient mice.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:In-Data-Review
[do] DOI:10.1681/ASN.2017030345

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[PMID]: 28459069
[Au] Autor:Esposito P; La Porta E; Calatroni M; Grignano MA; Milanesi S; Verzola D; Battaglia Y; Gregorini M; Libetta C; Garibotto G; Rampino T
[Ad] Address:Department of Nephrology, Dialysis and Transplantation, Fondazione IRCCS Policlinico San Matteo and University of Pavia, Pavia, Italy.
[Ti] Title:Modulation of Myostatin/Hepatocyte Growth Factor Balance by Different Hemodialysis Modalities.
[So] Source:Biomed Res Int;2017:7635459, 2017.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In this study we investigated the relevance of myostatin and Hepatocyte Growth Factor (HGF) in patients undergoing hemodialysis HD and the influence of different HD modalities on their levels. We performed a prospective crossover study in which HD patients were randomized to undergo 3-month treatment periods with bicarbonate hemodialysis (BHD) followed by online hemodiafiltration (HDF). Clinical data, laboratory parameters, and myostatin and HGF serum levels were collected and compared. Ten patients and six controls (C) were evaluated. In any experimental condition myostatin and HGF levels were higher in HD than in C. At enrollment and after BHD there were not significant correlations, whereas at the end of the HDF treatment period myostatin and HGF were inversely correlated ( -0.65, < 0.05), myostatin serum levels inversely correlated with transferrin ( -0.73, < 0.05), and HGF levels that resulted positively correlated with BMI ( 0.67, < 0.05). Moving from BHD to HDF, clinical and laboratory parameters were unchanged, as well as serum HGF, whereas myostatin levels significantly decreased (6.3 ± 4.1 versus 4.3 ± 3.1 ng/ml, < 0.05). Modulation of myostatin levels and myostatin/HGF balance by the use of different HD modalities might represent a novel approach to the prevention and treatment of HD-related muscle wasting syndrome.
[Mh] MeSH terms primary: Hemodiafiltration/methods
Hemodiafiltration/statistics & numerical data
Hepatocyte Growth Factor/metabolism
Myostatin/metabolism
[Mh] MeSH terms secundary: Aged
Bicarbonates
Cross-Over Studies
Female
Hepatocyte Growth Factor/blood
Humans
Male
Middle Aged
Myostatin/blood
Prospective Studies
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Bicarbonates); 0 (HGF protein, human); 0 (MSTN protein, human); 0 (Myostatin); 67256-21-7 (Hepatocyte Growth Factor)
[Em] Entry month:1802
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[Js] Journal subset:IM
[Da] Date of entry for processing:170502
[St] Status:MEDLINE
[do] DOI:10.1155/2017/7635459

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[PMID]: 29470902
[Au] Autor:Marutyan ZG; Kartavenko VI; Petrikov SS; Kilaseva ON; Khovrin DV; Barmina TG
[Ti] Title:[AQUATIC AND ELECTROLYTE DISORDERS AT THE PATIENT WITH SEVERE TRAUMATIC BRAIN INJURY.]
[So] Source:Anesteziol Reanimatol;61(4):300-304, 2016 Jul.
[Is] ISSN:0201-7563
[Cp] Country of publication:Russia (Federation)
[La] Language:rus
[Ab] Abstract:This article is dedicated to the problem ofwater and electrolyte disturbances in patient with acute severe head trauma. We present the case study of patient with severe head injury who consistently developed diabetes insipidus and cerebral salt wasting syndrome. His water and electrolyte disorders were successfully corrected by target-oriented intensive care. Constant tight monitoring and of intensive care allowed to avoid secondary ischemic injuries till the water and electrolytic homeostasis regulation mechanisms restoration.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[St] Status:In-Process

  10 / 8639 MEDLINE  
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[PMID]: 29477186
[Au] Autor:Willig A; Wright L; Galvin TA
[Ti] Title:Practice Paper of the Academy of Nutrition and Dietetics: Nutrition Intervention and Human Immunodeficiency Virus Infection.
[So] Source:J Acad Nutr Diet;118(3):486-498, 2018 Mar.
[Is] ISSN:2212-2672
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Nutrition is an integral component of medical care for people living with human immunodeficiency virus (HIV)/autoimmune deficiency syndrome (AIDS) (PLWHA). The Academy of Nutrition and Dietetics supports integration of medical nutrition therapy into routine care for this population. Fewer PLWHA experience wasting and undernutrition, while the prevalence of obesity and other chronic diseases has increased significantly. Improved understanding of HIV infection's impact on metabolism and chronic inflammation has only increased the complexity of managing chronic HIV infection. Nutrition assessment should encompass food insecurity risk, changes in body composition, biochemical indices, and clinical indicators of comorbid disease. Side effects from current antiretroviral therapy regimens are less prevalent than with previous generations of therapy. However, micronutrient deficiencies and chronic anemia also remain significant nutritional risks for PLWHA, making vitamin and mineral supplementation necessary in cases of acute deficiency or food insecurity. Additional factors can impact HIV-related nutrition care among the pediatric population, older adults, minority groups, those co-infected with tuberculosis or hepatitis, and PLWHA in rural or underserved areas. Registered dietitian nutritionists and nutrition and dietetic technicians, registered should participate in multidisciplinary care to incorporate nutrition into the medical management of PLWHA.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180225
[Lr] Last revision date:180225
[St] Status:In-Data-Review


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