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Protein C Deficiency

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2. Protein C and protein S deficiencies may be related to survival among hemodialysis patients. (PubMed)

Protein C and protein S deficiencies may be related to survival among hemodialysis patients. Thrombophilia due to protein C (PC) and protein S (PS) deficiencies is highly prevalent among patients with stage 5 chronic kidney disease and is reported to arise due to extracorporeal circulation during hemodialysis (HD). This study aimed to evaluate the relationship between HD treatment and thrombophilia.A total of 114 Japanese patients on maintenance HD (62 men, 52 women) were followed during 2008 (...) -2011. Their survival rates were compared against the duration of HD. Prior to each HD, coagulation/fibrinolysis parameters and PC and PS activities were measured using standard techniques. The patients were divided into two groups: Group 1, with PC and/or PS deficiencies (n = 32), and Group 2, without PC and PS deficiencies (n = 82). The influence of such deficiencies and duration of dialysis on survival was examined. Time-to-event analysis was applied using Kaplan-Meier estimates, and the log-rank

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2019 BMC Nephrology

3. Rivaroxaban dose adjustment using thrombin generation in severe congenital protein C deficiency and warfarin-induced skin necrosis (PubMed)

Rivaroxaban dose adjustment using thrombin generation in severe congenital protein C deficiency and warfarin-induced skin necrosis 29365322 2019 01 30 2019 01 30 2473-9537 2 2 2018 01 23 Blood advances Blood Adv Rivaroxaban dose adjustment using thrombin generation in severe congenital protein C deficiency and warfarin-induced skin necrosis. 142-145 10.1182/bloodadvances.2017012047 Menon Neethu N Division of Hematology/Oncology, Department of Pediatrics, and. Sarode Ravi R Department (...) & control Protein C Protein C Deficiency congenital Rivaroxaban administration & dosage Secondary Prevention Skin Diseases chemically induced prevention & control Thrombin biosynthesis metabolism Thrombomodulin metabolism Warfarin adverse effects 2017 08 31 2017 12 13 2018 1 25 6 0 2018 1 25 6 0 2019 1 31 6 0 ppublish 29365322 bloodadvances.2017012047 10.1182/bloodadvances.2017012047 PMC5787863 Ther Drug Monit. 2015 Jun;37(3):375-80 25525760 Ther Drug Monit. 2010 Dec;32(6):673-9 20844464 Thromb Haemost

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2018 Blood advances

5. Vitamin C deficiency

Vitamin C deficiency Vitamin C deficiency - Symptoms, diagnosis and treatment | BMJ Best Practice You'll need a subscription to access all of BMJ Best Practice Search  Vitamin C deficiency Last reviewed: February 2019 Last updated: December 2017 Summary Scurvy is a rare disorder, with epidemics typically affecting populations subject to famine or displacement during wartime. Most key clinical manifestations are related to impaired collagen synthesis. These include bleeding complications (...) (spontaneous petechiae and ecchymoses), friable gingiva and loose teeth, bone pain, and joint effusions. Other complications include heart failure, encephalopathy, and entrapment neuropathies. If not treated promptly, scurvy can be fatal. Complete recovery is anticipated in most patients. Definition Scurvy is a life-threatening condition due to dietary vitamin C deficiency. Those affected are mostly refugees or victims of famine, alcoholics, older people, fad dieters, or children with autism

2017 BMJ Best Practice

6. Endothelial protein C receptor supports hematopoietic stem cell engraftment and expansion in Mpl-deficient mice. (PubMed)

Endothelial protein C receptor supports hematopoietic stem cell engraftment and expansion in Mpl-deficient mice. Thrombopoietin (Thpo)/Mpl signaling controls hematopoietic stem cell (HSC) self-renewal and quiescence, however, how these two seemingly opposing functions are controlled is not well understood. By transplantation of lentiviral transduced hematopoietic cells in the Mpl-deficient mouse model we addressed whether known or predicted Thpo target genes were able to rescue the Mpl (...) -deficient phenotype of the mice. Among the tested genes we identified endothelial protein C receptor (Epcr) to expand HSC with long-term (LT)-HSC surface phenotype in Mpl-/- mice and to enable secondary transplantation of Mpl-deficient BM. Epcr-transduced Mpl-/- HSC enter quiescence earlier after transplantation than control transduced Mpl-/- cells and upregulated expression of the anti-apoptotic gene Bcl-xL. Also in the wildtype background, Epcr expression marked the engrafting population in the BM

2019 Blood

7. Identification of 58 Mutations (26 Novel) in 94 of 109 Symptomatic Spanish Probands with Protein C Deficiency. (PubMed)

Identification of 58 Mutations (26 Novel) in 94 of 109 Symptomatic Spanish Probands with Protein C Deficiency. Presently, no data on the molecular basis of hereditary protein C (PC) deficiency in Spain is available. We analyzed the PC gene (PROC) in 109 patients with symptomatic PC deficiency and in 342 relatives by sequencing the 9 PROC exons and their flanking intron regions. In 93 probands, we found 58 different mutations (26 novel). Thirty-seven consisted of a nucleotide change, mainly (...) missense mutations, 1 was a 6-nucleotide insertion causing the duplication of 2 amino acids, and 4 were deletions of 1, 3, 4, and 16 nucleotides. Nine mutations caused type II deficiencies, with the presence of normal antigen levels but reduced anticoagulant activity. Using a PC level of 70% as lowest normal limit, we found no mutations in 16 probands and 25 relatives with PC levels ≤ 70%. On the contrary, 4 probands and 12 relatives with PC levels > 70% carried the mutation identified in the proband

2019 Thrombosis and haemostasis

8. C-Reactive Protein and Erythrocyte Sedimentation Rate Testing

C-Reactive Protein and Erythrocyte Sedimentation Rate Testing C-Reactive Protein and Erythrocyte Sedimentation Rate Testing - Province of British Columbia theme_3_collection theme_3_frontend theme_3_collection theme_3_frontend Birth, Adoption, Death, Marriage & Divorce theme_1_collection theme_1_frontend theme_1_collection theme_1_frontend British Columbians & Our Governments theme_data_collection data_frontend theme_data_collection data_frontend Data theme_5_collection theme_5_frontend (...) theme_10_collection theme_10_frontend Sports, Recreation, Arts & Culture theme_8_collection theme_8_frontend theme_8_collection theme_8_frontend Taxes & Tax Credits theme_14_collection theme_14_frontend theme_14_collection theme_14_frontend Tourism & Immigration Search default_collection default_frontend Section Navigation C-Reactive Protein and Erythrocyte Sedimentation Rate Testing Effective Date: December 5, 2018 Recommendations and Topics Scope This guideline applies to the clinical use of C-reactive protein

2019 Clinical Practice Guidelines and Protocols in British Columbia

9. Budd–Chiari Syndrome Due to Protein C Deficiency: A Rare Disorder to cause Chronic Liver Disease (PubMed)

Budd–Chiari Syndrome Due to Protein C Deficiency: A Rare Disorder to cause Chronic Liver Disease The Budd-Chiari syndrome (BCS) is a rare disorder due to chronic liver disease (CLD), which is caused by the obstruction of hepatic venous outflow that can be located at any place from the small hepatic venules up to the entrance of the inferior vena cava (IVC) into the right atrium. Among the causes of BCS, the rarer one is coagulation factor deficiencies. Here, we report a case of BCS associated (...) with deficiency of protein C resulting in thrombus in IVC. The patient was a 50-year-old male, who had been suffering from recurrent abdominal and leg swelling for a long period of 7 years. He was evaluated thoroughly, and other causes of liver cirrhosis were excluded.Begum R, Al Mahtab M, Al Mamun A, Moben AL, Hossain SMS, Das DC, Malakar D, Rashid HO, Roy PP, Rahman S. Budd-Chiari Syndrome Due to Protein C Deficiency: A Rare Disorder to cause Chronic Liver Disease. Euroasian J Hepato-Gastroenterol 2016;6(2

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2016 Euroasian journal of hepato-gastroenterology

10. Renal Papillary Necrosis Caused by Protein C Deficiency Leading to Recurrent Hydronephrosis (PubMed)

Renal Papillary Necrosis Caused by Protein C Deficiency Leading to Recurrent Hydronephrosis A patient with history of a solitary functioning kidney and protein C deficiency (PCD) presented with recurrent severe hydronephrosis causing acute kidney injury upon chronic kidney disease. Work-up with endoscopic evaluation revealed renal papillary necrosis (RPN) and sloughed renal papillae to be the true cause of the recurrent obstruction. Pathologic evaluation of the sloughed tissue confirmed

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2016 Journal of endourology case reports

11. Foramen magnum stenosis and midface hypoplasia in C-type natriuretic peptide-deficient rats and restoration by the administration of human C-type natriuretic peptide with 53 amino acids. (PubMed)

Foramen magnum stenosis and midface hypoplasia in C-type natriuretic peptide-deficient rats and restoration by the administration of human C-type natriuretic peptide with 53 amino acids. C-type natriuretic peptide (CNP)-knockout (KO) rats exhibit impaired skeletal growth, with long bones shorter than those in wild-type (WT) rats. This study compared craniofacial morphology in the CNP-KO rat with that in the Spontaneous Dwarf Rat (SDR), a growth hormone (GH)-deficient model. The effects

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2019 PLoS ONE

12. Efficacy and safety of protein C concentrate to treat purpura fulminans and thromboembolic events in severe congenital protein C deficiency. (PubMed)

Efficacy and safety of protein C concentrate to treat purpura fulminans and thromboembolic events in severe congenital protein C deficiency. Severe congenital protein C (PC) deficiency (SCPCD) is associated with disseminated intravascular coagulation (DIC), purpura fulminans (PF), and vascular thromboembolic events (TE), often leading to organ failure and death. PC replacement therapy offers a safe, effective treatment for thromboembolic complications of SCPCD and secondary prophylaxis (...) for recurrent DIC, PF, and TEs. A prospective, multi-centre, open-label, phase 2/3 study was conducted to demonstrate the safety and efficacy of protein C concentrate for treatment of PF and acute TEs. Fifteen enrolled patients with SCPCD received protein C concentrate; 11 received treatment for acute TEs (PF, 18 events; PF and other coumarin-related vascular thromboembolic events [coumarin-induced skin necrosis; CISN], 1 event; venous thrombosis, 5 events). Pre-defined efficacy criteria for treatment

2016 Thrombosis and haemostasis

13. Recurrent cerebellar infarction associated with hereditary heterozygous protein C deficiency in a 35-year-old woman: A case report and genetic study on the pedigree (PubMed)

Recurrent cerebellar infarction associated with hereditary heterozygous protein C deficiency in a 35-year-old woman: A case report and genetic study on the pedigree Deficiency of protein C may cause deep venous thrombosis and pulmonary embolism, leading to ischemic stroke. The present study reports on a case of a young adult with recurrent cerebellar infarction due to hereditary heterozygous protein C deficiency and performs a literature review. A 35-year-old Asian woman was admitted t o (...) intestine thrombosis and was regularly taking hydroxychloroquine sulfate to treat systemic lupus erythematosus. The protein C (PROC) levels were 57.6%, while protein S and antithrombin levels were normal. Gene sequencing analysis of the patient and the patient's pedigree revealed a heterozygous mutation, c.565C>T, on the PROC gene in the patient and the patient's father. In conclusion, the clinical manifestations of hereditary PROC deficiency may vary between individuals. The heterozygous mutation locus

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2018 Experimental and therapeutic medicine

14. Recurrent diffuse lung disease due to surfactant protein C deficiency (PubMed)

Recurrent diffuse lung disease due to surfactant protein C deficiency Surfactant protein C (SP-C) deficiency causes diffuse lung disease with variable prognosis and severity that usually presents in infancy. We present the case of a patient with diffuse lung disease who was successfully treated with hydroxychloroquine and steroids in infancy, who presented again as a young adult with respiratory symptoms. Exome sequencing identified a novel de novo SFTPC mutation (c.397A > C p.S133R). Mutated (...) SP-C accumulates and leads to injury of alveolar type II cells, which normally replenish alveolar type I cells after injury. This may explain the symptom recurrence after lung injury in young adulthood. Although hydroxychloroquine has been hypothesized to interfere with mutated SP-C accumulation, data on long term outcome remains limited.

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2018 Respiratory Medicine Case Reports

15. Predilection of Low Protein C-induced Spontaneous Atherothrombosis for the Right Coronary Sinus in Apolipoprotein E deficient mice (PubMed)

Predilection of Low Protein C-induced Spontaneous Atherothrombosis for the Right Coronary Sinus in Apolipoprotein E deficient mice Silencing of anticoagulant protein C using RNA interference (siProc) evokes low incident but spontaneous atherothrombosis in the aortic root of apolipoprotein E-deficient (Apoe-/-) mice. The aims of the current study were (1) to analyze if plaque characteristics or circulating factors could be linked to atherothrombosis susceptibility, (2) to increase the incidence (...) blood pressure, did not increase atherothrombosis in the aortic root of the Apoe-/- mice nor in the carotid arteries with collars. Plaques in the aortic root with an associated thrombus were lower in collagen and macrophage content, and mice with atherothrombosis had significantly more circulating platelets. Plasma protein C, white blood cell counts, total cholesterol, fibrinogen, serum amyloid A, and IL-6 were not different amongst siProc treated mice with or without thrombosis. Remarkably, our

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2018 Scientific reports

16. Red cell adenylate kinase deficiency in India: identification of two novel missense mutations (c.71A>G and c.413G>A). (PubMed)

Red cell adenylate kinase deficiency in India: identification of two novel missense mutations (c.71A>G and c.413G>A). Adenylate kinase (AK) deficiency is a rare erythroenzymopathy associated with hereditary nonspherocytic haemolytic anaemia along with mental/psychomotor retardation in few cases. Diagnosis of AK deficiency depends on the decreased level of enzyme activity in red cell and identification of a mutation in the AK1 gene. Until, only eight mutations causing AK deficiency have (...) been reported in the literature. We are reporting two novel missense mutation (c.71A > G and c.413G > A) detected in the AK1 gene by next-generation sequencing (NGS) in a 6-year-old male child from India. Red cell AK enzyme activity was found to be 30% normal. We have screened a total of 32 family members of the patient and showed reduced red cell enzyme activity and confirm mutations by Sanger's sequencing. On the basis of Sanger sequencing, we suggest that the proband has inherited a mutation

2019 Journal of Clinical Pathology

17. Comparability of Inflammation-Adjusted Vitamin A Deficiency Estimates and Variance in Retinol Explained by C-Reactive Protein and α<sub>1</sub>-Acid Glycoprotein during Low and High Malaria Transmission Seasons in Rural Zambian Children. (PubMed)

Comparability of Inflammation-Adjusted Vitamin A Deficiency Estimates and Variance in Retinol Explained by C-Reactive Protein and α1-Acid Glycoprotein during Low and High Malaria Transmission Seasons in Rural Zambian Children. Inflammation-induced hyporetinolemia (IIH), a reduction in serum retinol (SR) during inflammation, may bias population estimates of vitamin A deficiency (VAD). The optimal adjustment for IIH depends on the type and extent of inflammation. In rural Zambian (...) children (4-8 years, N = 886), we compared three models for defining inflammation: α-1-acid glycoprotein (AGP) only (inflammation present if > 1 g/L or normal if otherwise), C-reactive protein (CRP) only (moderate inflammation, 5-15 mg/L; high inflammation, > 15 mg/L; or normal if otherwise) and a combined model using both AGP and CRP to delineate stages of infectious episode. Models were compared with respect to 1) the variance in SR explained and 2) comparability of inflammation-adjusted VAD

2017 American Journal of Tropical Medicine & Hygiene

18. Silencing of Anticoagulant Protein C Evokes Low Incident but Spontaneous Atherothrombosis in Apolipoprotein E-Deficient Mice. (PubMed)

Silencing of Anticoagulant Protein C Evokes Low Incident but Spontaneous Atherothrombosis in Apolipoprotein E-Deficient Mice. Murine atherosclerosis models do not spontaneously develop atherothrombotic complications. We investigated whether disruption of natural anticoagulation allows preexisting atherosclerotic plaques to progress toward an atherothrombotic phenotype.On lowering of plasma protein C levels with small interfering RNA (siProc) in 8-week Western-type diet-fed atherosclerotic (...) protein C levels as siProc-treated apolipoprotein E-deficient mice without thrombi. Fibrinogen and thrombin-antithrombin concentrations and blood platelet numbers were also comparable, and plaques in siProc mice with thrombi had a similar composition and size as plaques in siProc mice without thrombi. Seven out of 25 siProc mice featured clots in the left atrium of the heart.Our findings indicate that small interfering RNA-mediated silencing of protein C in apolipoprotein E-deficient mice creates

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2017 Thrombosis and Vascular Biology

19. Protein C deficiency resulting from two mutations in PROC presenting with recurrent venous thromboembolism (PubMed)

Protein C deficiency resulting from two mutations in PROC presenting with recurrent venous thromboembolism Hereditary protein C (PC) deficiency is an autosomal dominant disorder associated with a high risk of venous thromboembolism (VTE). Here we report a case of inherited PC deficiency associated with recurrent deep venous thrombosis. Two mutations were revealed in PROC (c.1152C>G, p.N384K and c.1207G>T, p.G403W) by genetic testing. Results from this case suggest that the inherited PC (...) deficiency due to the PROC mutations may cause recurrent VTE. Long-term anticoagulant therapy may be appropriate for these patients with recurrent VTE and hereditary PC deficiency.

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2017 Journal of Vascular Surgery Cases and Innovative Techniques

20. A delayed presentation of homozygous protein C deficiency in a series of children: a report on two molecular defects (PubMed)

A delayed presentation of homozygous protein C deficiency in a series of children: a report on two molecular defects Pediatric emergency visits with purpura fulminans should raise the suspicion of hereditary homozygous protein C deficiency even beyond the neonatal age. The absence of this classical finding does not role the diagnosis out as atypical presentation with isolated intraocular bleeding was observed. Premarital counseling should be offered when family history suggests.

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2017 Clinical Case Reports

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