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| {{CMG}}; {{AE}}{{RAK}}
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| ==Overview==
| | Cardiac surgery<ref name="pmid23447502">{{cite journal| author=Aya HD, Cecconi M, Hamilton M, Rhodes A| title=Goal-directed therapy in cardiac surgery: a systematic review and meta-analysis. | journal=Br J Anaesth | year= 2013 | volume= 110 | issue= 4 | pages= 510-7 | pmid=23447502 | doi=10.1093/bja/aet020 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23447502 }} </ref> |
| Protein S deficiency is an autosomal dominant thrombophilia, which leads to an increased risk of thromboembolic events. Protein S is a vitamin K-dependent glycoprotein and plays a role in anticoagulation. It is mainly a cofactor to the activated protein C (APC), which inactivates coagulation factors Va and VIIa and thereby controlling the coagulation cascade.
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| ==Historical Perspective==
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| *Protein S was first discovered and purified in Seattle, Washington in 1979, and it was arbitrarily named protein S after the city it was discovered in.
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| *The function of this protein was still unknown; however, it was hypothesized that protein S plays a role in activating protein C.
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| *Protein S deficiency was first discovered in 1984 when two related individuals with recurrent thromboembolic events and normal coagulation tests were studied. At the time, protein C deficiency was usually associated with recurrent familial thrombosis. These individuals were found to have diminished anticoagulation activity with normal coagulation tests (including a normal protein C level), and when purified human protein S was added to their plasma, effective anticoagulation was restored. <ref name="pmid6239877">{{cite journal| author=Comp PC, Nixon RR, Cooper MR, Esmon CT| title=Familial protein S deficiency is associated with recurrent thrombosis. | journal=J Clin Invest | year= 1984 | volume= 74 | issue= 6 | pages= 2082-8 | pmid=6239877 | doi=10.1172/JCI111632 | pmc=425398 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6239877 }} </ref>
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| ==Classification==
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| Protein S deficiency can be subdivided into three types depending on whether the abnormality affects total protein S level, free protein S level, and/or protein S function:<ref name="pmid11127877">{{cite journal| author=Gandrille S, Borgel D, Sala N, Espinosa-Parrilla Y, Simmonds R, Rezende S et al.| title=Protein S deficiency: a database of mutations--summary of the first update. | journal=Thromb Haemost | year= 2000 | volume= 84 | issue= 5 | pages= 918 | pmid=11127877 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11127877 }} </ref>
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| *'''Type I:''' Reduced total protein S, free protein S, and protein S function
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| It is the classic form of hereditary protein S deficiency. Total protein S levels drop to approximately 50% of normal values while free protein S levels collapse to almost 15% of the normal. On a genetic level, type I deficiency usually results from missense or nonsense mutations. On few occasions, microinsertions, microdeletions, and splice site mutations have occurred with this type. <ref name="pmid6238642">{{cite journal| author=Schwarz HP, Fischer M, Hopmeier P, Batard MA, Griffin JH| title=Plasma protein S deficiency in familial thrombotic disease. | journal=Blood | year= 1984 | volume= 64 | issue= 6 | pages= 1297-300 | pmid=6238642 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6238642 }} </ref>
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| *'''Type II:''' Normal total and free protein S, reduced protein S function
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| This form results from a qualitative defect and is very rare. The genetics behind this type isn't certain; however, some reports have linked it to missense mutations affecting the protein S's ability to bind to the activated protein C. <ref name="pmid8943854">{{cite journal| author=Simmonds RE, Ireland H, Kunz G, Lane DA| title=Identification of 19 protein S gene mutations in patients with phenotypic protein S deficiency and thrombosis. Protein S Study Group. | journal=Blood | year= 1996 | volume= 88 | issue= 11 | pages= 4195-204 | pmid=8943854 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8943854 }} </ref> <ref name="pmid7803790">{{cite journal| author=Gandrille S, Borgel D, Eschwege-Gufflet V, Aillaud M, Dreyfus M, Matheron C et al.| title=Identification of 15 different candidate causal point mutations and three polymorphisms in 19 patients with protein S deficiency using a scanning method for the analysis of the protein S active gene. | journal=Blood | year= 1995 | volume= 85 | issue= 1 | pages= 130-8 | pmid=7803790 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7803790 }} </ref>
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| *'''Type III:''' Normal total protein S, reduced free protein S and protein S function
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| This is a quantitative defect.
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| {| class="wikitable sortable"
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| |+
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| !Type
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| !Total Protein S
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| !Free Protein S
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| !Protein S Function
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| |-
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| |I
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| |↓
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| |↓
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| |↓
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| |-
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| |II
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| |↔
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| |↔
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| |↓
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| |-
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| |III
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| |↔
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| |↓
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| |↓
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| |}
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| ==Pathophysiology==
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| {| align="right"
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| [[File:Coagulation cascade.png|thumb|600px|Coagulation cascade - Source: Wikipedia <ref name="urlProtein C - Wikipedia">{{cite web |url=https://en.wikipedia.org/wiki/Protein_C |title=Protein C - Wikipedia |format= |work= |accessdate=}}</ref>]]
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| |}
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| *Protein S is a natural anticoagulant that works with other proteins to regulate coagulation in the body.
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| *After it gets produced by the hepatocytes, endothelial cells, and megakaryocytes, protein S undergoes activation via vitamin K-dependent gamma-carboxylation. <ref name="pmid21239244">{{cite journal| author=Esmon CT| title=Protein S and protein C Biochemistry, physiology, and clinical manifestation of deficiencies. | journal=Trends Cardiovasc Med | year= 1992 | volume= 2 | issue= 6 | pages= 214-9 | pmid=21239244 | doi=10.1016/1050-1738(92)90027-P | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21239244 }} </ref>
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| **The vitamin K-dependent gamma-carboxyalse enzyme acts by modifying the glutamic acid residues in protein S to gamma-carboxyglutamic acid residues.
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| **These gamma-carboxyglutamic acid residues are needed to ensure calcium-dependent binding to membrane surfaces.
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| *The now mature and activated protein S will circulate in the blood in two states:
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| **Free protein S
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| ***This form constitutes 30 to 40 percent of the total protein S in the body.
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| ***It is the only form that will take part in the coagulation cascade.<ref name="pmid12907438">{{cite journal| author=Rezende SM, Simmonds RE, Lane DA| title=Coagulation, inflammation, and apoptosis: different roles for protein S and the protein S-C4b binding protein complex. | journal=Blood | year= 2004 | volume= 103 | issue= 4 | pages= 1192-201 | pmid=12907438 | doi=10.1182/blood-2003-05-1551 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12907438 }} </ref>
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| **C4b-bound protein S
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| ***There is a high affinity interaction between protein S and C4b-binding protein.
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| ***C4b-binding protein is a complement regulator; hence, it is responsible for controlling the activity of protein S.
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| ***Around 70 percent of circulating protein S is in the bound form. <ref name="pmid21805441">{{cite journal| author=Dahlbäck B| title=C4b-binding protein: a forgotten factor in thrombosis and hemostasis. | journal=Semin Thromb Hemost | year= 2011 | volume= 37 | issue= 4 | pages= 355-61 | pmid=21805441 | doi=10.1055/s-0031-1276584 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21805441 }} </ref>
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| *The activated free protein S acts as a cofactor to activated protein C, and with the help of phospholipids and Ca<sup>2+</sup>, it inactivates procoagulant factor Va and factor VIIIa thereby reducing thrombin formation.<ref name="pmid21239244">{{cite journal| author=Esmon CT| title=Protein S and protein C Biochemistry, physiology, and clinical manifestation of deficiencies. | journal=Trends Cardiovasc Med | year= 1992 | volume= 2 | issue= 6 | pages= 214-9 | pmid=21239244 | doi=10.1016/1050-1738(92)90027-P | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21239244 }} </ref>
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| *Protein S deficiency is a hereditary disease that results from mutations in the ''PROS1'' gene, located on chromosome 3.
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| *This disease usually occurs due to heterozygous gene mutations in the ''PROS1'' gene; however, rare cases of homozygous protein S deficiencies have been reported.
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| *Although another gene, ''PROS2,'' has been isolated on the same chromosome 3, it does not seem to have any relevance and has since been classified as a pseudogene.<ref name="pmid2895503">{{cite journal| author=Ploos van Amstel JK, van der Zanden AL, Bakker E, Reitsma PH, Bertina RM| title=Two genes homologous with human protein S cDNA are located on chromosome 3. | journal=Thromb Haemost | year= 1987 | volume= 58 | issue= 4 | pages= 982-7 | pmid=2895503 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2895503 }} </ref><ref name="pmid2148110">{{cite journal| author=Schmidel DK, Tatro AV, Phelps LG, Tomczak JA, Long GL| title=Organization of the human protein S genes. | journal=Biochemistry | year= 1990 | volume= 29 | issue= 34 | pages= 7845-52 | pmid=2148110 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2148110 }} </ref>
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| ==Causes==
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| *In addition to the common hereditary form of protein S deficiency, there are rare circumstances in which acquired causes can result in diminished protein S levels:
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| **Pregnancy<ref name="pmid2944555">{{cite journal| author=Comp PC, Thurnau GR, Welsh J, Esmon CT| title=Functional and immunologic protein S levels are decreased during pregnancy. | journal=Blood | year= 1986 | volume= 68 | issue= 4 | pages= 881-5 | pmid=2944555 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2944555 }} </ref>
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| **Liver disease<ref name="pmid2935211">{{cite journal| author=Comp PC, Doray D, Patton D, Esmon CT| title=An abnormal plasma distribution of protein S occurs in functional protein S deficiency. | journal=Blood | year= 1986 | volume= 67 | issue= 2 | pages= 504-8 | pmid=2935211 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2935211 }} </ref>
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| **Vitamin K deficiency<ref name="pmid8466266">{{cite journal| author=Matsuzaka T, Tanaka H, Fukuda M, Aoki M, Tsuji Y, Kondoh H| title=Relationship between vitamin K dependent coagulation factors and anticoagulants (protein C and protein S) in neonatal vitamin K deficiency. | journal=Arch Dis Child | year= 1993 | volume= 68 | issue= 3 Spec No | pages= 297-302 | pmid=8466266 | doi= | pmc=1590375 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8466266 }} </ref>
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| **Oral hormonal contraceptives<ref name="pmid2966452">{{cite journal| author=Gilabert J, Fernandez JA, España F, Aznar J, Estelles A| title=Physiological coagulation inhibitors (protein S, protein C and antithrombin III) in severe preeclamptic states and in users of oral contraceptives. | journal=Thromb Res | year= 1988 | volume= 49 | issue= 3 | pages= 319-29 | pmid=2966452 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2966452 }} </ref>
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| **Disseminated intravascular disease<ref name="pmid2521800">{{cite journal| author=Heeb MJ, Mosher D, Griffin JH| title=Activation and complexation of protein C and cleavage and decrease of protein S in plasma of patients with intravascular coagulation. | journal=Blood | year= 1989 | volume= 73 | issue= 2 | pages= 455-61 | pmid=2521800 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2521800 }} </ref>
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| **Nephrotic syndrome<ref name="pmid2954500">{{cite journal| author=Vigano-D'Angelo S, D'Angelo A, Kaufman CE, Sholer C, Esmon CT, Comp PC| title=Protein S deficiency occurs in the nephrotic syndrome. | journal=Ann Intern Med | year= 1987 | volume= 107 | issue= 1 | pages= 42-7 | pmid=2954500 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2954500 }} </ref>
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| ==Differentiating Protein S deficiency from Other Diseases==
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| Protein S deficiency must be differentiated from other diseases that cause symptoms of [[DVT]] and [[pulmonary embolism]] such as:
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| *[[Factor V Leiden mutation]]
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| *[[Antithrombin III deficiency]]
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| *[[Protein C deficiency]]
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| *[[Prothrombin gene mutation G20210A|Prothrombin gene mutation]]
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| *[[Disseminated intravascular coagulation|Disseminated intravascular coagulation (DIC)]]
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| *[[Antiphospholipid antibody syndrome]]
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| '''For more information on differentiating protein S deficiency, [[Thrombophilia differential diagnosis|click here.]]'''
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| ==Epidemiology and Demographics==
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| *The prevalence of protein S deficiency in the general population is unknown.
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| *However, its prevalence in individuals with a history of venous thromboembolism is approximately 900 per 100,000 individuals worldwide. <ref name="pmid24014240">{{cite journal| author=Pintao MC, Ribeiro DD, Bezemer ID, Garcia AA, de Visser MC, Doggen CJ et al.| title=Protein S levels and the risk of venous thrombosis: results from the MEGA case-control study. | journal=Blood | year= 2013 | volume= 122 | issue= 18 | pages= 3210-9 | pmid=24014240 | doi=10.1182/blood-2013-04-499335 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24014240 }} </ref>
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| ===Age===
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| *Patients of all age groups may be diagnosed with protein S deficiency.
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| *It is; however, more commonly observed among patients younger than 40 to 50 years old.
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| ===Gender===
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| *There is no difference in the prevalence of the disease between men and women.
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| ===Race===
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| *Protein S deficiency usually affects individuals of the Asian race.
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| *Caucasian individuals are less likely to develop protein S deficiency.
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| ==Risk Factors==
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| *There are no established risk factors for protein S deficiency.
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| *Family history of thrombosis pose increased risk for a mutation.
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| ==Screening==
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| *There is insufficient evidence to recommend routine screening for protein S deficiency in the general population.
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| *A simple positive family history incident of thrombosis is not enough to recommend screening in an asymptomatic low risk individual.<ref name="pmid16173967">{{cite journal| author=Wu O, Robertson L, Twaddle S, Lowe G, Clark P, Walker I et al.| title=Screening for thrombophilia in high-risk situations: a meta-analysis and cost-effectiveness analysis. | journal=Br J Haematol | year= 2005 | volume= 131 | issue= 1 | pages= 80-90 | pmid=16173967 | doi=10.1111/j.1365-2141.2005.05715.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16173967 }} </ref>
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| *High risk patients with a positive family history (first degree relative with protein S deficiency or first degree relative with multiple venous thromboembolic events at an age younger than 50), warrant a screening preferably prior to initiation of the high risk event such as taking oral contraceptives or pregnancy.<ref name="pmid16113779">{{cite journal| author=Wu O, Robertson L, Langhorne P, Twaddle S, Lowe GD, Clark P et al.| title=Oral contraceptives, hormone replacement therapy, thrombophilias and risk of venous thromboembolism: a systematic review. The Thrombosis: Risk and Economic Assessment of Thrombophilia Screening (TREATS) Study. | journal=Thromb Haemost | year= 2005 | volume= 94 | issue= 1 | pages= 17-25 | pmid=16113779 | doi=10.1160/TH04-11-0759 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16113779 }} </ref><ref name="pmid18501222">{{cite journal| author=Dalen JE| title=Should patients with venous thromboembolism be screened for thrombophilia? | journal=Am J Med | year= 2008 | volume= 121 | issue= 6 | pages= 458-63 | pmid=18501222 | doi=10.1016/j.amjmed.2007.10.042 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18501222 }} </ref>
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| *The free protein S antigen assay is the best screening test.
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| ==Natural History, Complications, and Prognosis==
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| If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
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| OR
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| Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
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| OR
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| Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%.
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| ==Diagnosis==
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| ===Diagnostic Study of Choice===
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| The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met: [criterion 1], [criterion 2], [criterion 3], and [criterion 4].
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| OR
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| The diagnosis of [disease name] is based on the [criteria name] criteria, which include [criterion 1], [criterion 2], and [criterion 3].
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| OR
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| The diagnosis of [disease name] is based on the [definition name] definition, which includes [criterion 1], [criterion 2], and [criterion 3].
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| OR
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| There are no established criteria for the diagnosis of [disease name].
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| ===History and Symptoms===
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| The majority of patients with [disease name] are asymptomatic.
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| OR
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| The hallmark of [disease name] is [finding]. A positive history of [finding 1] and [finding 2] is suggestive of [disease name]. The most common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3]. Common symptoms of [disease] include [symptom 1], [symptom 2], and [symptom 3]. Less common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3].
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| ===Physical Examination===
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| Patients with [disease name] usually appear [general appearance]. Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].
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| OR
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| Common physical examination findings of [disease name] include [finding 1], [finding 2], and [finding 3].
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| OR
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| The presence of [finding(s)] on physical examination is diagnostic of [disease name].
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| OR
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| The presence of [finding(s)] on physical examination is highly suggestive of [disease name].
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| ===Laboratory Findings===
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| An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].
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| OR
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| Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
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| OR
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| [Test] is usually normal among patients with [disease name].
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| OR
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| Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].
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| OR
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| There are no diagnostic laboratory findings associated with [disease name].
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| ===Electrocardiogram===
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| There are no ECG findings associated with [disease name].
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| OR
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| An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
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| ===X-ray===
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| There are no x-ray findings associated with [disease name].
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| OR
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| An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
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| OR
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| There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
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| ===Echocardiography or Ultrasound===
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| There are no echocardiography/ultrasound findings associated with [disease name].
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| OR
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| Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
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| OR
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| There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
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| ===CT scan===
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| There are no CT scan findings associated with [disease name].
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| OR
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| [Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
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| OR
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| There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
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| ===MRI===
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| There are no MRI findings associated with [disease name].
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| OR
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| [Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
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| | |
| OR
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| There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
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| ===Other Imaging Findings===
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| There are no other imaging findings associated with [disease name].
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| OR
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| [Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
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| ===Other Diagnostic Studies===
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| There are no other diagnostic studies associated with [disease name].
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| OR
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| [Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
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| OR
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| Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].
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| ==Treatment==
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| ===Medical Therapy===
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| There is no treatment for [disease name]; the mainstay of therapy is supportive care.
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| OR
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| | |
| Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].
| |
| | |
| OR
| |
| | |
| The majority of cases of [disease name] are self-limited and require only supportive care.
| |
| | |
| OR
| |
| | |
| [Disease name] is a medical emergency and requires prompt treatment.
| |
| | |
| OR
| |
| | |
| The mainstay of treatment for [disease name] is [therapy].
| |
| | |
| OR
| |
|
| |
| The optimal therapy for [malignancy name] depends on the stage at diagnosis.
| |
| | |
| OR
| |
| | |
| [Therapy] is recommended among all patients who develop [disease name].
| |
| | |
| OR
| |
| | |
| Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].
| |
| | |
| OR
| |
| | |
| Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].
| |
| | |
| OR
| |
| | |
| Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].
| |
| | |
| OR
| |
| | |
| Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].
| |
| | |
| ===Surgery===
| |
| Surgical intervention is not recommended for the management of [disease name].
| |
| | |
| OR
| |
| | |
| Surgery is not the first-line treatment option for patients with [disease name]. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]
| |
| | |
| OR
| |
| | |
| The mainstay of treatment for [disease name] is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].
| |
| | |
| OR
| |
| | |
| The feasibility of surgery depends on the stage of [malignancy] at diagnosis.
| |
| | |
| OR
| |
| | |
| Surgery is the mainstay of treatment for [disease or malignancy].
| |
| | |
| ===Primary Prevention===
| |
| There are no established measures for the primary prevention of [disease name].
| |
| | |
| OR
| |
| | |
| There are no available vaccines against [disease name].
| |
| | |
| OR
| |
| | |
| Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
| |
| | |
| OR
| |
| | |
| [Vaccine name] vaccine is recommended for [patient population] to prevent [disease name]. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].
| |
| | |
| ===Secondary Prevention===
| |
| There are no established measures for the secondary prevention of [disease name].
| |
| | |
| | |
| ==References==
| |
| {{Reflist|2}}
| |