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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. These situations arise due to different mechanisms:<ref name="pmid21523802">{{cite journal| author=Marlar RA, Gausman JN| title=Protein S abnormalities: a diagnostic nightmare. | journal=Am J Hematol | year= 2011 | volume= 86 | issue= 5 | pages= 418-21 | pmid=21523802 | doi=10.1002/ajh.21992 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21523802 }} </ref>
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| **Protein S consumption
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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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| ***Surgery
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| **Decreased synthesis of protein S
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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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| **Redistribution of complexed protein S
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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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| ***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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| ***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 protein S deficiency is the toughest out of all the hereditary thrombophilias.
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| *Getting the correct diagnosis of protein S deficiency is difficult due to several factors:
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| *1 protein S's interaction with other proteins
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| *2 its complex genetic regulation
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| *3
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| The accurate and correct diagnosis of PS deficiency is just plain difficult! A result artifact for a PS assay can be due to: (1) complex genetic regulation, (2) interaction of PS with other proteins, (3) biological variation, (4) preanalytical variables, and (5) assay performance (analytical). These complicating conditions make the results of PS assays difficult to interpret.
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| Three basic assay types are utilized for assessing PS in plasma [7, 9]. The “activity” assay is based on the ability of PS to function as a cofactor for APC, however it is fraught with the most problems [9, 10]. Free PS antigen assay is an immunologic measure of the unbound PS fraction and in most cases can be used as a surrogate marker for PS activity [9, 10]. Finally, the Total PS antigen assay determines both free and bound fractions of PS in plasma [7, 9]. Each method has its own drawbacks and must be interpreted carefully together to accurately diagnose true deficiencies of PS
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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 protein S deficiency.
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| ===X-ray===
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| * There are no x-ray findings associated with protein S deficiency.
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| ===Echocardiography or Ultrasound===
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| * There are no echocardiography/ultrasound findings associated with protein S deficiency.
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| ===CT scan===
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| * There are no CT scan findings associated with protein S deficiency.
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| ===MRI===
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| * There are no MRI findings associated with protein S deficiency.
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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 protein S deficiency.
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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].
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| OR
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| The majority of cases of [disease name] are self-limited and require only supportive care.
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| OR
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| [Disease name] is a medical emergency and requires prompt treatment.
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| OR
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| The mainstay of treatment for [disease name] is [therapy].
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| OR
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|
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| The optimal therapy for [malignancy name] depends on the stage at diagnosis.
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| OR
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| [Therapy] is recommended among all patients who develop [disease name].
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| OR
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| Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].
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| OR
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| Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].
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| OR
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| Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].
| |
| | |
| OR
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| | |
| Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].
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| | |
| ===Surgery===
| |
| * Surgical intervention is not recommended for the management of protein S deficiency.
| |
| | |
| ===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}}
| |