Database : MEDLINE
Search on : Factor and V and Deficiency [Words]
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[PMID]: 29512880
[Au] Autor:Zhai HJ; Li R; You XR; Wang K
[Ad] Address:Shanxi University, Institute of Molecular Science, 92 Wucheng Road, 030006, Taiyuan, CHINA.
[Ti] Title:Nature of Bonding in Bowl-Like B36 Cluster Revisited. Concentric (6 pi Plus 18 pi) Double Aromaticity and Reason for the Preference of Hexagonal Hole in Central Location.
[So] Source:Chem Asian J;, 2018 Mar 07.
[Is] ISSN:1861-471X
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Bowl-shaped C6v B36 cluster with a central hexagon hole is considered an ideal molecular model for low-dimensional boron-based nanosystems. Owing to electron-deficiency of boron, chemical bonding in B36 cluster is intriguing and complicated and has remained elusive despite a couple of papers in literature. Herein we shall offer an in-depth bonding analysis via canonical molecular orbitals (CMOs) and adaptive natural density partitioning (AdNDP), further aided with natural bond orbital (NBO) analysis and orbital composition calculations. The concerted computational data establish the idea of concentric double pi aromaticity for B36 cluster, with inner 6 pi and outer 18 pi electron-counting, which both conform to the (4n + 2) Hückel rule. The updated bonding picture differs from existing knowledge of the system. A refined bonding model is also proposed for coronene, of which B36 cluster is an inorganic analogue. It is further shown that concentric double pi aromaticity in B36 cluster is retained and spatially fixed, irrespective of migration of the hexagonal hole; the latter process varies the system energetically. Hexagonal hole is found to be a destabilization factor for sigma/pi CMOs. The central hexagon hole affects substantially fewer CMOs, thus making bowl-shaped C6v B36 cluster the global minimum.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.1002/asia.201800174

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[PMID]: 29369791
[Au] Autor:Souza LC; Jesse CR; Del Fabbro L; de Gomes MG; Gomes NS; Filho CB; Goes ATR; Wilhelm EA; Luchese C; Roman SS; Boeira SP
[Ad] Address:Laboratório de Avaliações Farmacológicas e Toxicológicas Aplicadas às Moléculas Bioativas, LaftamBio Pampa, Universidade Federal do Pampa, Itaqui, RS, Brazil. Electronic address: leandrosouza@unipampa.edu.br.
[Ti] Title:Aging exacerbates cognitive and anxiety alterations induced by an intracerebroventricular injection of amyloid-ß peptide in mice.
[So] Source:Mol Cell Neurosci;88:93-106, 2018 Feb 02.
[Is] ISSN:1095-9327
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:An increasing body of evidence indicates that the activation of indoleamine-2,3-dyoxigenase (IDO), a first and rate-limiting enzyme in the kynurenine (KYN) pathway, is involved in Aß -neurotoxicity and AD pathogenesis. We have reported for the first time that brain IDO activation is related to Aß exposure in young mice. Because aging is characterized by a brain dyshomeostasis and because it remains the most dominant risk factor for AD, the purpose of this study was to determine whether aging is associated with a higher sensitivity to behavioural and neurochemical alterations elicited by an intracerebroventricular (i.c.v.) injection of Aß (400 pmol/mice), and whether KYN pathway is involved in these effects. We confirmed that aged mice displayed higher cognitive deficit in the object recognition test and higher anxiety-like behaviour in the elevated plus-maze and open field tests after the Aß administration. Aged mice also responded to Aß with a higher deficiency of brain-derived neurotrophic factor, glutathione levels and total radical-trapping antioxidant capacity, a higher IDO activity, and a higher KYN and KYN/tryptophan ratio in the prefrontal cortex and hippocampus. These effects of Aß were associated with a higher proinflammatory status, as measured by higher levels of interleukin-6, lower levels of interleukin-10 and higher expression of glial fibrillary acidic protein (GFAP) and allograft inflammatory factor 1 (Iba1) in the brain of aged mice. These results represent primary evidence suggesting that age-associated inflammatory signature and down-regulation of neuroprotectants in the brain render aged mice more vulnerable to Aß -induced memory loss, anxiety symptoms and KYN pathway dysregulation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher

  3 / 12396 MEDLINE  
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[PMID]: 29369598
[Au] Autor:Li X; Lin W; Zhu L; Wang Y; Liu S; Liu J; Du H; Fang S
[Ad] Address:Department of Neurology, Neuroscience Centre, the First Teaching Hospital of Jilin University, No 71 Xinmin Street, Changchun, Jilin, 130021, China.
[Ti] Title:A case of hereditary thrombophilia in a Chinese Han patient with both antithrombin deficiency and Factor V Leiden: A case report and literature review.
[So] Source:Neuro Endocrinol Lett;38(7):479-483, 2017 Dec.
[Is] ISSN:0172-780X
[Cp] Country of publication:Sweden
[La] Language:eng
[Ab] Abstract:Hereditary thrombophilia is a blood coagulation disorder that increases the risk of venous thromboembolism, due to several genetic risk factors. Factor V Leiden(FVL) is the most common contributing factor to thrombophilia in the Caucasian population but very rare in Asian population and concurrent occurrence of antithrombin(AT) deficiency and FVL in Chinese Han population is even more rare. We report the case of a 22-year-old female who experienced recurrent intracranial venous thromboses, furthermore, color Doppler ultrasound showed multiple extracranial thromboses. Thrombophilia was suspected and screening tests indicated decreased AT activity and activated protein C sensitivity ratio, then further sequencing analysis identified missense mutations in SERPINC1 and F5. The patient's condition slightly improved after treatment with low molecular heparin during hospitalization followed by oral warfarin after discharge. The present report highlights a very rare case of thrombophilia with concurrent occurrence of AT deficiency and FVL in a Chinese Han patient, and our findings suggest that genetic testing is a reliable approach for identifying different risk factors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:In-Data-Review

  4 / 12396 MEDLINE  
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[PMID]: 29506241
[Au] Autor:Hendee KE; Sorokina EA; Muheisen SS; Reis LM; Tyler RC; Markovic V; Cuturilo G; Link BA; Semina EV
[Ad] Address:Department of Pediatrics and Children's Research Institute.
[Ti] Title:PITX2 deficiency and associated human disease: insights from the zebrafish model.
[So] Source:Hum Mol Genet;, 2018 Mar 01.
[Is] ISSN:1460-2083
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The PITX2 (paired-like homeodomain 2) gene encodes a bicoid-like homeodomain transcription factor linked with several human disorders. The main associated congenital phenotype is Axenfeld-Rieger syndrome, type 1 (ARS), an autosomal dominant condition characterized by variable defects in the anterior segment of the eye, an increased risk of glaucoma, craniofacial dysmorphism and dental and umbilical anomalies; in addition to this, one report implicated PITX2 in ring dermoid of the cornea and a few others described cardiac phenotypes. We report three novel PITX2 mutations- c.271C>T, p.(Arg91Trp); c.259T>C, p.(Phe87Leu); and c.356delA, p.(Gln119Argfs*36)- identified in independent families with typical ARS characteristics and some unusual features such as corneal guttata, Wolf-Parkinson-White syndrome, and hyperextensibility. To gain further insight into the diverse roles of PITX2/pitx2 in vertebrate development, we generated various genetic lesions in the pitx2 gene via TALEN-mediated genome editing. Affected homozygous zebrafish demonstrated congenital defects consistent with the range of PITX2-associated human phenotypes: abnormal development of the cornea, iris, and iridocorneal angle; corneal dermoids; and craniofacial dysmorphism. In addition, via comparison of pitx2M64*and wild-type embryonic ocular transcriptomes we defined molecular changes associated with pitx2 deficiency, thereby implicating processes potentially underlying disease pathology. This analysis identified numerous affected factors including several members of the Wnt pathway and collagen type I and V gene families. These data further support the link between PITX2 and the WNT pathway and suggest a new role in regulation of collagen gene expression during development.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:Publisher
[do] DOI:10.1093/hmg/ddy074

  5 / 12396 MEDLINE  
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[PMID]: 29390379
[Au] Autor:Choi S; Song M
[Ti] Title:Successful coronary stenting in a patient with factor V deficiency in the absence of fresh frozen plasma transfusion: Case report.
[So] Source:Medicine (Baltimore);96(50):e9274, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: Drug-eluting stent (DES) implantation in a patient with factor V deficiency (F5D) is very complex. No antithrombotic therapy study has been reported for F5D patients who undergo a coronary stenting procedure. PATIENT CONCERNS: A 73-year-old woman presented with chest discomfort and exertional dyspnea. Coronary stenting was performed successfully using DES stents. DIAGNOSES: The D-dimer, prothrombin time, and partial thromboplastin time prolongation persisted from admission until 24 hours after coronary stenting. Epistaxis and blood-tinged sputum occurred on day 3. The antiplatelet therapy measured using a Multiplate Analyzer was adequate, and other laboratory findings except factor V activity (14%) were within normal ranges; she was diagnosed with F5D based on low factor V activity. INTERVENTIONS: While taking 90 mg of ticagrelor and 100 mg of aspirin daily, the patient revisited due to recurrent epistaxis, hemoptysis, and coughing on day 26. Epistaxis and hemoptysis stopped after the aspirin was discontinued. Finally, the daily maintenance dose was reduced to 90 mg of ticagrelor once. OUTCOMES: She led healthy life for 9 months without any recurrent symptoms and the test results also were stabilized. LESSONS: We report a case of an F5D patient who underwent coronary stenting in the absence of frozen fresh plasma transfusion who received successful maintenance therapy using a single antiplatelet agent (90 mg of ticagrelor/day) with recurrent multiple mucosal bleeding events after coronary stenting.
[Mh] MeSH terms primary: Adenosine/analogs & derivatives
Coronary Stenosis/drug therapy
Drug-Eluting Stents
Factor V Deficiency/complications
Purinergic P2Y Receptor Antagonists/therapeutic use
[Mh] MeSH terms secundary: Adenosine/therapeutic use
Aged
Blood Coagulation Tests
Coronary Stenosis/diagnosis
Female
Humans
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:0 (Purinergic P2Y Receptor Antagonists); GLH0314RVC (Ticagrelor); K72T3FS567 (Adenosine)
[Em] Entry month:1802
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009274

  6 / 12396 MEDLINE  
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[PMID]: 29235020
[Au] Autor:Ghorbel R; Ben Salah G; Ghorbel R; Ben Mahmoud A; Chamkha I; Mkaouar-Rebai E; Ammar-Keskes L; Fakhfakh F
[Ad] Address:Laboratory of Human Molecular Genetics, Faculty of Medicine of Sfax, University of Sfax, Sfax, Tunisia. raouiaghorbel@yahoo.fr.
[Ti] Title:Do GSTM1 and GSTT1 polymorphisms influence the risk of developing mitochondrial diseases in a Tunisian population?
[So] Source:Environ Sci Pollut Res Int;25(6):5779-5787, 2018 Feb.
[Is] ISSN:1614-7499
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Mitochondria play an essential role to supply the cell with metabolic energy in the form of adenosine triphosphate (ATP) through oxidative phosphorylation (OXPHOS). As a consequence, they are also the primary source of cellular reactive oxygen species (ROS) which can cause oxidative damage of individual respiratory chain complexes. Indeed, affected OXPHOS subunits result in decreases in ATP production and increases in ROS formation which generate oxidative phosphorylation deficiency leading to mitochondrial dysfunctions. It has been suggested that ROS play a vital role in the pathogenesis of mitochondrial diseases. To the best of our knowledge, this is the first study which aimed to investigate the genetic variant effect of the antioxidant enzymes GSTM1 and GSTT1 on mitochondrial disease among a Tunisian population. In this report, 109 patients with mitochondrial disease and 154 healthy controls were genotyped by multiplex PCR amplification, and data were analyzed by SPSS v20 software. The results showed that GSTM1 null genotype was found to be associated with mitochondrial disease with a protective effect; however, no significant association of GSTT1 polymorphism with mitochondrial disease risk was revealed. But, interestingly, our findings highlight that GSTM1 active and GSTT1 null genotype combination increased by three fold the risk of developing mitochondrial disease with p = 0.020, notably mitochondrial myopathy with p = 0.046 and Leigh syndrome with p = 0.042. In conclusion, this study suggests that GSTM1 active and GSTT1 null genotype combination might be a risk factor in developing mitochondrial disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180225
[Lr] Last revision date:180225
[St] Status:In-Process
[do] DOI:10.1007/s11356-017-0775-7

  7 / 12396 MEDLINE  
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[PMID]: 29237838
[Au] Autor:Yoshida A; Kawabata R; Honda T; Sakai K; Ami Y; Sakaguchi T; Irie T
[Ad] Address:Department of Virology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
[Ti] Title:A Single Amino Acid Substitution within the Paramyxovirus Sendai Virus Nucleoprotein Is a Critical Determinant for Production of Interferon-Beta-Inducing Copyback-Type Defective Interfering Genomes.
[So] Source:J Virol;92(5), 2018 Mar 01.
[Is] ISSN:1098-5514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:One of the first defenses against infecting pathogens is the innate immune system activated by cellular recognition of pathogen-associated molecular patterns (PAMPs). Although virus-derived RNA species, especially copyback (cb)-type defective interfering (DI) genomes, have been shown to serve as real PAMPs, which strongly induce interferon-beta (IFN-ß) during mononegavirus infection, the mechanisms underlying DI generation remain unclear. Here, for the first time, we identified a single amino acid substitution causing production of cbDI genomes by successful isolation of two distinct types of viral clones with cbDI-producing and cbDI-nonproducing phenotypes from the stock Sendai virus (SeV) strain Cantell, which has been widely used in a number of studies on antiviral innate immunity as a representative IFN-ß-inducing virus. IFN-ß induction was totally dependent on the presence of a significant amount of cbDI genome-containing viral particles (DI particles) in the viral stock, but not on deficiency of the IFN-antagonistic viral accessory proteins C and V. Comparison of the isolates indicated that a single amino acid substitution found within the N protein of the cbDI-producing clone was enough to cause the emergence of DI genomes. The mutated N protein of the cbDI-producing clone resulted in a lower density of nucleocapsids than that of the DI-nonproducing clone, probably causing both production of the DI genomes and their formation of a stem-loop structure, which serves as an ideal ligand for RIG-I. These results suggested that the integrity of mononegaviral nucleocapsids might be a critical factor in avoiding the undesirable recognition of infection by host cells. The type I interferon (IFN) system is a pivotal defense against infecting RNA viruses that is activated by sensing viral RNA species. RIG-I is a major sensor for infection with most mononegaviruses, and copyback (cb)-type defective interfering (DI) genomes have been shown to serve as strong RIG-I ligands in real infections. However, the mechanism underlying production of cbDI genomes remains unclear, although DI genomes emerge as the result of an error during viral replication with high doses of viruses. Sendai virus has been extensively studied and is unique in that its interaction with innate immunity reveals opposing characteristics, such as high-level IFN-ß induction and strong inhibition of type I IFN pathways. Our findings provide novel insights into the mechanism of production of mononegaviral cbDI genomes, as well as virus-host interactions during innate immunity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180222
[Lr] Last revision date:180222
[St] Status:In-Data-Review

  8 / 12396 MEDLINE  
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[PMID]: 29452885
[Au] Autor:Bermea KC; Rodríguez-García A; Tsin A; Barrera-Saldaña HA
[Ad] Address:Department of Biomedical Sciences, School of Medicine, The University of Texas Rio Grande Valley, 1210 W Schunior St., Edinburg, TX 78541, United States.
[Ti] Title:Somatolactogens and diabetic retinopathy.
[So] Source:Growth Horm IGF Res;, 2018 Feb 06.
[Is] ISSN:1532-2238
[Cp] Country of publication:Scotland
[La] Language:eng
[Ab] Abstract:IMPORTANCE: Diabetic retinopathy (DR) is one of the most common of all diabetic complications. The number of people with DR in the United States is expected to increase to 16 million by 2050. DR is the leading cause of blindness among working-age adults in many different countries, including the United States. In later DR stages, neovascularization is associated with extensive retinal capillary non-perfusion and vitreo-proliferation leading to retinal detachment. This neovascularization is orchestrated by an imbalance of growth factors in the retina from which somatolactogens (pituitary growth hormone, GH-N; placental growth hormone, GH-V; prolactin, PRL; and placental lactogen, PL, also referred as chorionic somatomammotropin, CSH), may play an important role. OBSERVATIONS: Somatolactogens are a group of hormones that share many structural and functional features. They are important for physiological changes in pregnancy, for adequate development of the fetus, and in the case of GH-N, for promoting growth after birth. GH-N is synthesized by the anterior pituitary, GH-V and PL are secreted by the placenta, whereas, PRL is synthesized by the anterior pituitary and uterine decidua. However, in recent years the expression of GH-N and PRL and their receptors have been detected in other tissues including the retina, acting as neuroprotective and pro-angiogenic agents. The relationship of GH-N and diabetic retinopathy (DR) was established many years ago when it was observed that its deficiency was related to regression of DR while an increase in serum levels of GH-N, GH-V, and PL promoted DR. While more studies are needed to define the potential implications of GH-V and PL in DR pathogenesis, it has been demonstrated that GH-N and PRL participate in DR by enhancing neovascularization. Some PRL isoforms, however, have shown an anti-angiogenic activity rather than pro-angiogenesis and appears to be PRL's main role in the regulation of retinal vasculature. CONCLUSIONS: Somatolactogens are a group of hormones with a significant role in neuroprotection and angiogenesis regulation in the eye. Understanding the mechanisms of angiogenesis regulation by somatolactogens will potentially lead to the development of new drugs for DR.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180217
[Lr] Last revision date:180217
[St] Status:Publisher

  9 / 12396 MEDLINE  
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[PMID]: 29371650
[Au] Autor:Sheikhbahaei S; Turovsky EA; Hosford PS; Hadjihambi A; Theparambil SM; Liu B; Marina N; Teschemacher AG; Kasparov S; Smith JC; Gourine AV
[Ad] Address:Centre for Cardiovascular and Metabolic Neuroscience, Department of Neuroscience, Physiology and Pharmacology, University College London, London, WC1E 6BT, UK.
[Ti] Title:Astrocytes modulate brainstem respiratory rhythm-generating circuits and determine exercise capacity.
[So] Source:Nat Commun;9(1):370, 2018 01 25.
[Is] ISSN:2041-1723
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Astrocytes are implicated in modulation of neuronal excitability and synaptic function, but it remains unknown if these glial cells can directly control activities of motor circuits to influence complex behaviors in vivo. This study focused on the vital respiratory rhythm-generating circuits of the preBötzinger complex (preBötC) and determined how compromised function of local astrocytes affects breathing in conscious experimental animals (rats). Vesicular release mechanisms in astrocytes were disrupted by virally driven expression of either the dominant-negative SNARE protein or light chain of tetanus toxin. We show that blockade of vesicular release in preBötC astrocytes reduces the resting breathing rate and frequency of periodic sighs, decreases rhythm variability, impairs respiratory responses to hypoxia and hypercapnia, and dramatically reduces the exercise capacity. These findings indicate that astrocytes modulate the activity of CNS circuits generating the respiratory rhythm, critically contribute to adaptive respiratory responses in conditions of increased metabolic demand and determine the exercise capacity.
[Mh] MeSH terms primary: Astrocytes/physiology
Brain Stem/physiology
Periodicity
Physical Conditioning, Animal/physiology
Respiration
[Mh] MeSH terms secundary: Action Potentials/physiology
Adenoviridae/genetics
Adenoviridae/metabolism
Animals
Animals, Newborn
Astrocytes/cytology
Brain Stem/cytology
Calcium/metabolism
Female
Gene Expression Regulation
Genetic Vectors/chemistry
Genetic Vectors/metabolism
Hypercapnia/metabolism
Hypercapnia/physiopathology
Hypoxia/metabolism
Hypoxia/physiopathology
Male
Medulla Oblongata/cytology
Medulla Oblongata/physiology
Primary Cell Culture
Rats
Rats, Sprague-Dawley
SNARE Proteins/antagonists & inhibitors
SNARE Proteins/genetics
SNARE Proteins/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (SNARE Proteins); SY7Q814VUP (Calcium)
[Em] Entry month:1802
[Cu] Class update date: 180215
[Lr] Last revision date:180215
[Js] Journal subset:IM
[Da] Date of entry for processing:180127
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02723-6

  10 / 12396 MEDLINE  
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[PMID]: 29238798
[Au] Autor:Dobry AS; Ko LN; St John J; Sloan JM; Nigwekar S; Kroshinsky D
[Ad] Address:Department of Dermatology, Massachusetts General Hospital, and Harvard Medical School, Boston.
[Ti] Title:Association Between Hypercoagulable Conditions and Calciphylaxis in Patients With Renal Disease: A Case-Control Study.
[So] Source:JAMA Dermatol;154(2):182-187, 2018 Feb 01.
[Is] ISSN:2168-6084
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Importance: Calciphylaxis is a rare skin disease with high morbidity and mortality that frequently affects patients with renal disease. Hypercoagulable conditions are frequently observed in both patients with calciphylaxis and those with chronic kidney disease (CKD), complicating our understanding of which hypercoagulable conditions are specific to calciphylaxis. Objective: To identify hypercoagulable conditions that are risk factors for developing calciphylaxis while controlling for CKD. Design, Setting, and Participants: This was a case-control study, comparing the hypercoagulability status of patients with calciphylaxis and with renal disease with that of a matched control population at 2 large urban academic hospitals in Boston, Massachusetts. Retrospective medical record review of laboratory values was performed to identify patients with hypercoagulable conditions. Case and control patients were further stratified based on both severity of CKD and warfarin. Patients with a dermatologic diagnosis of calciphylaxis between 2006 and 2014 and concomitant CKD were included as cases (n = 38). Three controls (n = 114) per case patient with CKD were included, and were matched by age, sex, and race. Main Outcomes and Measures: The rate of various hypercoagulable states (ie, antithrombin III [ATIII] deficiency, protein C and S deficiency, factor V Leiden mutation, prothrombin gene mutation [G20210A], elevated factor VIII level, lupus anticoagulant, anti-IgG or IgM cardiolipin antibodies, heparin-induced thrombocytopenia antibodies, and elevation of homocysteine) in patients with calciphylaxis compared with their matched controls. Results: Of the calciphylaxis cohort, 28 (58%) were female and 18 (55%) were non-Hispanic white. Among all patients, lupus anticoagulant (13 [48%] positive in cases vs 1 [5%] in controls; P = .001), protein C deficiency (9 [50%] vs 1 [8%]; P = .02), and combined thrombophilias (18 [62%] vs 10 [31%]; P = .02) were found to be significantly associated with calciphylaxis. In a subanalysis of patients with stage 5 CKD, only lupus anticoagulant (12 [53%] vs 9 [0%]; P = .01) and combined thrombophilia (15 [63%] vs 1 [8%]; P = .004) remained significantly associated with calciphylaxis. In a separate subanalysis of warfarin-unexposed patients, only lupus anticoagulant (7 [50%] vs 1 [6%]; P = .01) and protein C deficiency (5 [46%] vs 10 [0%]; P = .04) remained significantly associated with calciphylaxis. Conclusions and Relevance: Presence of lupus anticoagulant and combined thrombophilias are risk factors for the development of calciphylaxis in patients with late-stage renal disease. Clinicians should be aware of these associations in patients with impaired kidney function and may consider increased screening and appropriate anticoagulation treatment to reduce the risk of calciphylaxis development.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180216
[Lr] Last revision date:180216
[St] Status:In-Data-Review
[do] DOI:10.1001/jamadermatol.2017.4920


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