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Article ; Online: Severe extra-glandular involvement and pleural effusions complicating primary Sjogren's syndrome: a case report.

Abou Ziki, Maen D / Taoutel, Roy / Hong, Julian C / Podell, David N

2022 Volume 16, Issue 1, Page(s) 374

Abstract: Background: Sjogren's syndrome, an autoimmune disease of the exocrine glands, results in keratoconjunctivitis sicca, xerostomia, and dental caries. It is often overlooked, considered by clinicians to be a benign disease. However, it can cause life- ... ...

Abstract	Background: Sjogren's syndrome, an autoimmune disease of the exocrine glands, results in keratoconjunctivitis sicca, xerostomia, and dental caries. It is often overlooked, considered by clinicians to be a benign disease. However, it can cause life-threatening extra-glandular complications that affect multiple organ systems. Case presentation: Here we present a 78-year-old Caucasian woman with a history of primary Sjogren's syndrome (pSS) whose symptoms of keratoconjunctivitis sicca were managed managed conservatively. She was evaluated for sub-acute shortness of breath. Imaging showed severe bronchiectasis with features of lymphocytic interstitial pneumonia. She also had exudative bilateral pleural effusions and skin ulcers, likely vasculitic in origin. The workup was significant for anti-Ro antibody, pancytopenia, hypocomplementia, cryoglobulinemia and monoclonal gammopathy, all of which reflect disease severity. Although there was no evidence of malignancy, she developed B-cell non-Hodgkin lymphoma during follow-up. Conclusions: Primary Sjogren's syndrome can result in severe multi-organ disease. Pleural effusions are a rare complication of pSS, with only ten cases reported in the literature over the last 30 years, and tend to respond well to steroids. Prognostic biomarkers for disease severity include hypocomplementia, cryoglobulinemia, monoclonal gammopathy, and hypergammaglobulinemia. In this report we review the literature and the management of the disease.
MeSH term(s)	Aged ; Biomarkers ; Cryoglobulinemia/complications ; Dental Caries/complications ; Female ; Humans ; Keratoconjunctivitis Sicca/complications ; Pleural Effusion/complications ; Pleural Effusion/etiology ; Sjogren's Syndrome/complications ; Sjogren's Syndrome/diagnosis
Chemical Substances	Biomarkers
Language	English
Publishing date	2022-10-18
Publishing country	England
Document type	Case Reports ; Journal Article ; Review
ZDB-ID	2269805-X
ISSN	1752-1947 ; 1752-1947
ISSN (online)	1752-1947
ISSN	1752-1947
DOI	10.1186/s13256-022-03557-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: The interplay of canonical and noncanonical Wnt signaling in metabolic syndrome

Abou Ziki, Maen D / Mani, Arya

Nutrition research. 2019 Oct., v. 70

2019

Abstract: Metabolic syndrome is a cluster of inherited metabolic traits, which centers around obesity and insulin resistance and is a major contributor to the growing prevalence of cardiovascular disease. The factors that underlie the association of metabolic ... ...

Abstract	Metabolic syndrome is a cluster of inherited metabolic traits, which centers around obesity and insulin resistance and is a major contributor to the growing prevalence of cardiovascular disease. The factors that underlie the association of metabolic traits in this syndrome are poorly understood due to disease heterogeneity and complexity. Genetic studies of kindreds with severe manifestation of metabolic syndrome have led to the identification of casual rare mutations in the LDL receptor-related protein 6, which serves as a co-receptor with frizzled protein receptors for Wnt signaling ligands. Extensive investigations have since unraveled the significance of the Wnt pathways in regulating body mass, glucose metabolism, de novo lipogenesis, low-density lipoprotein clearance, vascular smooth muscle plasticity, liver fat, and liver inflammation. The impaired canonical Wnt signaling observed in the R611C mutation carriers and the ensuing activation of noncanonical Wnt signaling constitute the underlying mechanism for these cardiometabolic abnormalities. Transcription factor 7-like 2 is a key transcription factor activated through LDL receptor-related protein 6 canonical Wnt and reciprocally inhibited by the noncanonical pathway. TC7L2 increases insulin receptor expression, decreases low-density lipoprotein and triglyceride synthesis, and inhibits vascular smooth muscle proliferation. Canonical Wnt also inhibits noncanonical protein kinase C, Ras homolog gene family member A, and Rho associated coiled-coil containing protein kinase 2 activation, thus inhibiting steatohepatitis and transforming growth factor β–mediated extracellular matrix deposition and hepatic fibrosis. Therefore, dysregulation of the highly conserved Wnt signaling pathway underlies the pleiotropy of metabolic traits of the metabolic syndrome and the subsequent end-organ complications.
Keywords	cardiovascular diseases ; extracellular matrix ; genes ; glucose ; inflammation ; insulin receptors ; insulin resistance ; ligands ; lipogenesis ; liver ; liver cirrhosis ; low density lipoprotein ; metabolic syndrome ; mutation ; obesity ; plasticity ; pleiotropy ; protein kinase C ; signal transduction ; smooth muscle ; transcription factors ; transforming growth factor beta ; triacylglycerols
Language	English
Dates of publication	2019-10
Size	p. 18-25.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	582432-1
ISSN	1879-0739 ; 0271-5317
ISSN (online)	1879-0739
ISSN	0271-5317
DOI	10.1016/j.nutres.2018.06.009
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Article ; Online: The interplay of canonical and noncanonical Wnt signaling in metabolic syndrome.

Abou Ziki, Maen D / Mani, Arya

Nutrition research (New York, N.Y.)

2018 Volume 70, Page(s) 18–25

Abstract	Metabolic syndrome is a cluster of inherited metabolic traits, which centers around obesity and insulin resistance and is a major contributor to the growing prevalence of cardiovascular disease. The factors that underlie the association of metabolic traits in this syndrome are poorly understood due to disease heterogeneity and complexity. Genetic studies of kindreds with severe manifestation of metabolic syndrome have led to the identification of casual rare mutations in the LDL receptor-related protein 6, which serves as a co-receptor with frizzled protein receptors for Wnt signaling ligands. Extensive investigations have since unraveled the significance of the Wnt pathways in regulating body mass, glucose metabolism, de novo lipogenesis, low-density lipoprotein clearance, vascular smooth muscle plasticity, liver fat, and liver inflammation. The impaired canonical Wnt signaling observed in the R611C mutation carriers and the ensuing activation of noncanonical Wnt signaling constitute the underlying mechanism for these cardiometabolic abnormalities. Transcription factor 7-like 2 is a key transcription factor activated through LDL receptor-related protein 6 canonical Wnt and reciprocally inhibited by the noncanonical pathway. TC7L2 increases insulin receptor expression, decreases low-density lipoprotein and triglyceride synthesis, and inhibits vascular smooth muscle proliferation. Canonical Wnt also inhibits noncanonical protein kinase C, Ras homolog gene family member A, and Rho associated coiled-coil containing protein kinase 2 activation, thus inhibiting steatohepatitis and transforming growth factor β-mediated extracellular matrix deposition and hepatic fibrosis. Therefore, dysregulation of the highly conserved Wnt signaling pathway underlies the pleiotropy of metabolic traits of the metabolic syndrome and the subsequent end-organ complications.
MeSH term(s)	Animals ; Fatty Liver/genetics ; Fatty Liver/metabolism ; Humans ; Lipid Metabolism/physiology ; Liver/metabolism ; Liver/pathology ; Liver Cirrhosis/genetics ; Liver Cirrhosis/metabolism ; Low Density Lipoprotein Receptor-Related Protein-6/metabolism ; Metabolic Syndrome/genetics ; Metabolic Syndrome/metabolism ; Muscle, Smooth, Vascular/physiology ; Receptor, Insulin/metabolism ; Receptors, LDL/genetics ; Receptors, LDL/metabolism ; Transcription Factor 7-Like 2 Protein/metabolism ; Wnt Signaling Pathway/physiology
Chemical Substances	Low Density Lipoprotein Receptor-Related Protein-6 ; Receptors, LDL ; Transcription Factor 7-Like 2 Protein ; Receptor, Insulin (EC 2.7.10.1)
Language	English
Publishing date	2018-07-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	582432-1
ISSN	1879-0739 ; 0271-5317
ISSN (online)	1879-0739
ISSN	0271-5317
DOI	10.1016/j.nutres.2018.06.009
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Zs.A 1686: Show issues

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Article ; Online: Beware of Limb Lead Reversal-Reply.

Abou Ziki, Maen D / Rosenfeld, Lynda E

JAMA internal medicine

2018 Volume 178, Issue 3, Page(s) 435

Language	English
Publishing date	2018-03-06
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2699338-7
ISSN	2168-6114 ; 2168-6106
ISSN (online)	2168-6114
ISSN	2168-6106
DOI	10.1001/jamainternmed.2017.8639
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Article ; Online: Wnt signaling, a novel pathway regulating blood pressure? State of the art review.

Abou Ziki, Maen D / Mani, Arya

Atherosclerosis

2017 Volume 262, Page(s) 171–178

Abstract: Recent antihypertensive trials show conflicting results on blood pressure (BP) targets in patient populations with different metabolic profiles, with lowest benefit from tight BP control observed in patients with type 2 diabetes mellitus. This paradox ... ...

Abstract	Recent antihypertensive trials show conflicting results on blood pressure (BP) targets in patient populations with different metabolic profiles, with lowest benefit from tight BP control observed in patients with type 2 diabetes mellitus. This paradox could arise from the heterogeneity of study populations and underscores the importance of precision medicine initiatives towards understanding and treating hypertension. Wnt signaling pathways and genetic variations in its signaling peptides have been recently associated with metabolic syndrome, hypertension and diabetes, generating a breakthrough for advancement of precision medicine in the field of hypertension. We performed a review of PubMed for publications addressing the contributions of Wnt to BP regulation and hypertension. In addition, we performed a manual search of the reference lists for relevant articles, and included unpublished observations from our laboratory. There is emerging evidence for Wnt's role in BP regulation and its involvement in the pathogenesis of hypertension. Wnt signaling has pleiotropic effects on distinct pathways that involve vascular smooth muscle plasticity, and cardiac, renal, and neural physiology. Hypertension is a heterogeneous disease with unique molecular pathways regulating its response to therapy. Recognition of these pathways is a prerequisite to identify novel targets for drug development and personalizing medicine. A review of Wnt signaling reveals its emerging role in BP regulation and as a target for novel drug development that has the potential to transform the therapy of hypertension in specific populations.
MeSH term(s)	Animals ; Antihypertensive Agents/therapeutic use ; Blood Pressure/drug effects ; Blood Pressure/genetics ; Humans ; Hypertension/drug therapy ; Hypertension/genetics ; Hypertension/metabolism ; Hypertension/physiopathology ; Molecular Targeted Therapy ; Wnt Proteins/antagonists & inhibitors ; Wnt Proteins/genetics ; Wnt Proteins/metabolism ; Wnt Signaling Pathway/drug effects ; Wnt Signaling Pathway/genetics
Chemical Substances	Antihypertensive Agents ; Wnt Proteins
Language	English
Publishing date	2017-05-04
Publishing country	Ireland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2017.05.001
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Zs.A 226: Show issues

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Article ; Online: Tachyarrhythmia Onset Captured on Telemetry Deciphers the Diagnosis.

Abou Ziki, Maen D / Rosenfeld, Lynda E

JAMA internal medicine

2017 Volume 177, Issue 11, Page(s) 1673–1675

MeSH term(s)	Aged ; Diagnosis, Differential ; Electrocardiography/methods ; Humans ; Male ; Tachycardia, Atrioventricular Nodal Reentry/diagnosis ; Telemetry/methods
Language	English
Publishing date	2017-09-04
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	2699338-7
ISSN	2168-6114 ; 2168-6106
ISSN (online)	2168-6114
ISSN	2168-6106
DOI	10.1001/jamainternmed.2017.3328
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Article ; Online: Dyrk1b promotes autophagy during skeletal muscle differentiation by upregulating 4e-bp1.

Bhat, Neha / Narayanan, Anand / Fathzadeh, Mohsen / Shah, Kanan / Dianatpour, Mehdi / Abou Ziki, Maen D / Mani, Arya

Cellular signalling

2021 Volume 90, Page(s) 110186

Abstract: Rare gain of function mutations in the gene encoding Dyrk1b, a key regulator of skeletal muscle differentiation, have been associated with sarcopenic obesity (SO) and metabolic syndrome (MetS) in humans. So far, the global gene networks regulated by ... ...

Abstract	Rare gain of function mutations in the gene encoding Dyrk1b, a key regulator of skeletal muscle differentiation, have been associated with sarcopenic obesity (SO) and metabolic syndrome (MetS) in humans. So far, the global gene networks regulated by Dyrk1b during myofiber differentiation have remained elusive. Here, we have performed untargeted proteomics to determine Dyrk1b-dependent gene-network in differentiated C2C12 myofibers. This analysis led to identification of translational inhibitor, 4e-bp1 as a post-transcriptional target of Dyrk1b in C2C12 cells. Accordingly, CRISPR/Cas9 mediated knockout of Dyrk1b in zebrafish identified 4e-bp1 as a downstream target of Dyrk1b in-vivo. The Dyrk1b knockout zebrafish embryos exhibited markedly reduced myosin heavy chain 1 expression in poorly developed myotomes and were embryonic lethal. Using knockdown and overexpression approaches in C2C12 cells, we found that 4e-bp1 enhances autophagy and mediates the effects of Dyrk1b on skeletal muscle differentiation. Dyrk1b
MeSH term(s)	Animals ; Autophagy/genetics ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Muscle Development ; Muscle, Skeletal/metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/genetics ; Protein-Tyrosine Kinases/metabolism ; Zebrafish/metabolism ; Zebrafish Proteins ; Dyrk Kinases
Chemical Substances	Cell Cycle Proteins ; Phosphoproteins ; Zebrafish Proteins ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2021-11-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2021.110186
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Zs.A 2579: Show issues

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Article ; Online: Metabolic syndrome: genetic insights into disease pathogenesis.

Abou Ziki, Maen D / Mani, Arya

Current opinion in lipidology

2016 Volume 27, Issue 2, Page(s) 162–171

Abstract: Purpose of review: Metabolic syndrome (MetS) is a cluster of interrelated and heritable metabolic traits, which collectively impart unsurpassed risk for atherosclerotic cardiovascular disease and type 2 diabetes. Considerable work has been done to ... ...

Abstract	Purpose of review: Metabolic syndrome (MetS) is a cluster of interrelated and heritable metabolic traits, which collectively impart unsurpassed risk for atherosclerotic cardiovascular disease and type 2 diabetes. Considerable work has been done to understand the underlying disease mechanisms by elucidating its genetic cause. Recent findings: Genome-wide association studies have been widely utilized albeit with modest success in identifying variants that are associated with more than two metabolic traits. Another limitation of this approach is the inherent small effect of the common variants, a major barrier for dissecting their cognate pathways. Modest advances in this venue have been also made by genetic studies of kindreds at the extreme ends of quantitative distributions. These efforts have led to the discovery of a number of disease genes with large effects that underlie the association of diverse traits of this syndrome. Summary: Substantial progress has been made over the last decade in identification of genetic risk factors associated with the various traits of MetS. The heterogeneity and multifactorial heritability of MetS, however, has been a challenge toward understanding the factors underlying the association of these traits. Genetic investigations of outlier kindreds or homogenous populations with high prevalence for the disease can potentially improve our knowledge of the disease pathophysiology.
MeSH term(s)	Animals ; Genetic Linkage ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Metabolic Syndrome/genetics
Language	English
Publishing date	2016
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1045394-5
ISSN	1473-6535 ; 0957-9672
ISSN (online)	1473-6535
ISSN	0957-9672
DOI	10.1097/MOL.0000000000000276
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Zs.A 3010: Show issues

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Article ; Online: Pulmonary Embolism and Atrial Fibrillation: Two Sides of the Same Coin? A Systematic Review.

Bikdeli, Behnood / Abou Ziki, Maen D / Lip, Gregory Y H

Seminars in thrombosis and hemostasis

2017 Volume 43, Issue 8, Page(s) 849–863

Abstract: Pulmonary embolism (PE) is a common, potentially fatal thrombotic disease. Atrial fibrillation (AF), the most common arrhythmia, may also lead to thromboembolic complications. Although initially appearing as distinct entities, PE and AF may coexist. The ... ...

Abstract	Pulmonary embolism (PE) is a common, potentially fatal thrombotic disease. Atrial fibrillation (AF), the most common arrhythmia, may also lead to thromboembolic complications. Although initially appearing as distinct entities, PE and AF may coexist. The direction and extent of this association has not been well characterized. We performed a search of PubMed, Scopus, and the Cochrane Database of Systematic Reviews for publications that reported coexisting AF in patients with PE, or vice versa, to provide a systematic overview of pathophysiological and epidemiological aspects of this association (last search: October 13, 2016). We screened 650 articles following the PubMed search, and 697 through Scopus. PE and AF share many common risk factors, including old age, obesity, heart failure, and inflammatory states. In addition, PE may lead to AF through right-sided pressure overload or inflammatory cytokines. AF, in turn, might lead to right atrial appendage clot formation and thereby PE. Epidemiological studies indicate that AF can be seen as a presenting sign, during the early phase, or later in the course of recovery from PE. Patients with AF are also at increased risk of developing PE, a risk that correlates with the CHA
MeSH term(s)	Age Factors ; Animals ; Atrial Fibrillation/complications ; Atrial Fibrillation/drug therapy ; Atrial Fibrillation/epidemiology ; Atrial Fibrillation/metabolism ; Cytokines/metabolism ; Fibrinolytic Agents/adverse effects ; Fibrinolytic Agents/therapeutic use ; Heart Failure/complications ; Heart Failure/drug therapy ; Heart Failure/epidemiology ; Humans ; Inflammation ; Obesity/complications ; Obesity/drug therapy ; Obesity/epidemiology ; Pulmonary Embolism/drug therapy ; Pulmonary Embolism/epidemiology ; Pulmonary Embolism/etiology ; Pulmonary Embolism/metabolism ; Risk Factors
Chemical Substances	Cytokines ; Fibrinolytic Agents
Language	English
Publishing date	2017-02-14
Publishing country	United States
Document type	Journal Article ; Review ; Systematic Review
ZDB-ID	196901-8
ISSN	1098-9064 ; 0094-6176
ISSN (online)	1098-9064
ISSN	0094-6176
DOI	10.1055/s-0036-1598005
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Zs.A 1259: Show issues

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Article ; Online: Rare mutation in the SLC26A3 transporter causes life-long diarrhoea with metabolic alkalosis.

Abou Ziki, Maen D / Verjee, Mohamud A

BMJ case reports

2015 Volume 2015

Abstract: SLC26A3, a chloride/bicarbonate transporter mainly expressed in the intestines, plays a pivotal role in chloride absorption. We present a 23-year-old woman with a history of congenital chloride diarrhoea (CCD) and renal transplant who was admitted for ... ...

Abstract	SLC26A3, a chloride/bicarbonate transporter mainly expressed in the intestines, plays a pivotal role in chloride absorption. We present a 23-year-old woman with a history of congenital chloride diarrhoea (CCD) and renal transplant who was admitted for rehydration and treatment of acute kidney injury after she presented with an acute diarrhoeal episode. Laboratory investigations confirmed metabolic alkalosis and severe hypochloraemia, consistent with her underlying CCD. This contrasts with most other forms of diarrhoea, which are normally associated with metabolic acidosis. Genetic testing was offered and revealed a homozygous non-sense mutation in SLC26A3 (Gly-187-Stop). This loss-of-function mutation results in bicarbonate retention in the blood and chloride loss into the intestinal lumen. Symptomatic management with daily NaCl and KCl oral syrups was supplemented with omeprazole therapy. The loss of her own kidneys is most likely due to crystal-induced nephropathy secondary to chronic volume contraction and chloride depletion. This case summarises the pathophysiology and management of CCD.
MeSH term(s)	Adult ; Alkalosis/blood ; Alkalosis/drug therapy ; Alkalosis/etiology ; Alkalosis/genetics ; Bicarbonates/blood ; Chloride-Bicarbonate Antiporters/genetics ; Chlorides/metabolism ; Chlorides/therapeutic use ; Diarrhea/congenital ; Diarrhea/drug therapy ; Diarrhea/genetics ; Female ; Humans ; Kidney/metabolism ; Kidney/surgery ; Kidney Diseases/etiology ; Kidney Diseases/genetics ; Kidney Diseases/surgery ; Kidney Transplantation ; Metabolism, Inborn Errors/drug therapy ; Metabolism, Inborn Errors/genetics ; Mutation ; Omeprazole/therapeutic use ; Proton Pump Inhibitors/therapeutic use ; Young Adult
Chemical Substances	Bicarbonates ; Chloride-Bicarbonate Antiporters ; Chlorides ; Proton Pump Inhibitors ; SLC26A3 protein, human ; Omeprazole (KG60484QX9)
Language	English
Publishing date	2015-01-07
Publishing country	England
Document type	Case Reports ; Journal Article
ISSN	1757-790X
ISSN (online)	1757-790X
DOI	10.1136/bcr-2014-206849
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