U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination

Short telomere length

MedGen UID:
1627435
Concept ID:
C4531138
Anatomical Abnormality
HPO: HP:0031413

Definition

An abnormal reduction in telomere length. Telomeres are non-coding, repetitive sequences of DNA at the ends of the chromosomes of eukaryotic cells which become shorter as cells divide, and when telomere attrition reaches its limit, cell proliferation arrest, senescence, and apoptosis can occur. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • Short telomere length

Conditions with this feature

Revesz syndrome
MedGen UID:
231230
Concept ID:
C1327916
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Dyskeratosis congenita, autosomal recessive 3
MedGen UID:
462792
Concept ID:
C3151442
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Dyskeratosis congenita, autosomal dominant 3
MedGen UID:
462795
Concept ID:
C3151445
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Pulmonary fibrosis and/or bone marrow failure, Telomere-related, 1
MedGen UID:
766531
Concept ID:
C3553617
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Dyskeratosis congenita, autosomal dominant 6
MedGen UID:
904824
Concept ID:
C4225284
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Pulmonary fibrosis and/or bone marrow failure, Telomere-related, 3
MedGen UID:
901644
Concept ID:
C4225346
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Pulmonary fibrosis and/or bone marrow failure, Telomere-related, 4
MedGen UID:
903928
Concept ID:
C4225347
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Dyskeratosis congenita, autosomal recessive 6
MedGen UID:
905452
Concept ID:
C4225356
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Bone marrow failure syndrome 3
MedGen UID:
934711
Concept ID:
C4310744
Disease or Syndrome
Bone marrow failure syndrome-3 is an autosomal recessive disorder characterized by onset of pancytopenia in early childhood. Patients may have additional variable nonspecific somatic abnormalities, including poor growth, microcephaly, and skin anomalies (summary by Tummala et al., 2016). BMFS3 has a distinct phenotype and may include features that overlap with Shwachman-Diamond syndrome (SDS1; 260400), such as pancreatic insufficiency and short stature, and with dyskeratosis congenita (see, e.g., DKCA1, 127550), such as dental and hair abnormalities and shortened telomeres. In addition, some patients may have joint and skeletal abnormalities, impaired development, and retinal dysplasia (summary by D'Amours et al., 2018). For a discussion of genetic heterogeneity of BMFS, see BMFS1 (614675).
Bone marrow failure syndrome 5
MedGen UID:
1648380
Concept ID:
C4748488
Disease or Syndrome
Bone marrow failure syndrome-5 (BMFS5) is a hematologic disorder characterized by infantile onset of severe red cell anemia requiring transfusion. Additional features include hypogammaglobulinemia, poor growth with microcephaly, developmental delay, and seizures (summary by Toki et al., 2018) For a discussion of genetic heterogeneity of BMFS, see BMFS1 (614675).
Pulmonary fibrosis and/or bone marrow failure, telomere-related, 5
MedGen UID:
1684878
Concept ID:
C5231457
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Bone marrow failure syndrome 6
MedGen UID:
1717739
Concept ID:
C5394274
Disease or Syndrome
Pulmonary fibrosis and/or bone marrow failure, telomere-related, 6
MedGen UID:
1805650
Concept ID:
C5676927
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
Dyskeratosis congenita, digenic
MedGen UID:
1823990
Concept ID:
C5774217
Disease or Syndrome
Digenic dyskeratosis congenita (DKCD) is characterized clinically by a combination of mucocutaneous features including abnormal skin pigmentation, nail dystrophy, thin hair, and oral leukoplakia. Some patients may have evidence of bone marrow failure, manifest as immune defects such as recurrent infections or hypogammaglobulinemia. Telomeres are shortened in patient cells. Individuals with DKCD may show severe adverse reactions to treatment with 5-FU (Tummala et al., 2022). For a discussion of genetic heterogeneity of dyskeratosis congenita, see DKCA1 (127550).
Pulmonary fibrosis and/or bone marrow failure syndrome, telomere-related, 8
MedGen UID:
1841132
Concept ID:
C5830496
Disease or Syndrome
Telomere-related pulmonary fibrosis and/or bone marrow failure syndrome-8 (PFBMFT8) is an autosomal dominant disorder characterized by the onset of progressive pulmonary fibrosis in adulthood. Some affected individuals have signs of bone marrow failure, such as thrombocytopenia, or liver dysfunction, including hepatopulmonary syndrome. Other features of dyskeratosis congenita, including premature graying of the hair, may be observed. Telomeres are shortened compared to controls (Kelich et al., 2022). For a discussion of genetic heterogeneity of telomere-related pulmonary fibrosis and/or bone marrow failure, see PFBMFT1 (614742).
Pulmonary fibrosis and/or bone marrow failure syndrome, telomere-related, 9
MedGen UID:
1841196
Concept ID:
C5830560
Disease or Syndrome
Telomere-related pulmonary fibrosis and/or bone marrow failure syndrome-9 (PFBMFT9) is an autosomal dominant short telomere syndrome characterized by the development of pulmonary fibrosis or hematologic abnormalities, including leukopenia and leukemia, in adulthood. Liver disease may also be present. There is incomplete penetrance and evidence of genetic anticipation. Affected individuals have shortened telomeres, but do not show mucocutaneous manifestations (Kannengiesser et al., 2020). For a discussion of genetic heterogeneity of telomere-related pulmonary fibrosis and/or bone marrow failure, see PFBMFT1 (614742).

Professional guidelines

PubMed

Yoshida N, Kojima S
Curr Oncol Rep 2018 Jun 30;20(9):67. doi: 10.1007/s11912-018-0716-8. PMID: 29961134

Recent clinical studies

Etiology

Bussa RM, Mora-Plazas M, Marín C, Villamor E
Eur J Clin Nutr 2023 Feb;77(2):295-297. Epub 2022 Nov 8 doi: 10.1038/s41430-022-01236-w. PMID: 36347948
Wang XF, Xu WJ, Wang FF, Leng R, Yang XK, Ling HZ, Fan YG, Tao JH, Shuai ZW, Zhang L, Ye DQ, Leng RX
Arthritis Rheumatol 2022 Dec;74(12):1984-1990. Epub 2022 Nov 4 doi: 10.1002/art.42304. PMID: 35830513
Palmos AB, Duarte RRR, Smeeth DM, Hedges EC, Nixon DF, Thuret S, Powell TR
Neuropsychopharmacology 2020 Dec;45(13):2239-2247. Epub 2020 Sep 13 doi: 10.1038/s41386-020-00863-w. PMID: 32920596Free PMC Article
Aviv A
FASEB J 2020 Jun;34(6):7247-7252. Epub 2020 May 19 doi: 10.1096/fj.202001025. PMID: 32427393Free PMC Article
Jin X, Pan B, Dang X, Wu H, Xu D
Medicine (Baltimore) 2018 Sep;97(39):e12489. doi: 10.1097/MD.0000000000012489. PMID: 30278538Free PMC Article

Diagnosis

Wang XF, Xu WJ, Wang FF, Leng R, Yang XK, Ling HZ, Fan YG, Tao JH, Shuai ZW, Zhang L, Ye DQ, Leng RX
Arthritis Rheumatol 2022 Dec;74(12):1984-1990. Epub 2022 Nov 4 doi: 10.1002/art.42304. PMID: 35830513
Alder JK, Armanios M
Physiol Rev 2022 Oct 1;102(4):1703-1720. Epub 2022 May 9 doi: 10.1152/physrev.00046.2021. PMID: 35532056Free PMC Article
Pusceddu I, Kleber M, Delgado G, Herrmann W, März W, Herrmann M
PLoS One 2018;13(6):e0198373. Epub 2018 Jun 19 doi: 10.1371/journal.pone.0198373. PMID: 29920523Free PMC Article
Hwang SM, Kim SY, Kim JA, Park HS, Park SN, Im K, Kim K, Kim SM, Lee DS
J Hematol Oncol 2016 Jul 28;9(1):62. doi: 10.1186/s13045-016-0287-9. PMID: 27465399Free PMC Article
Weischer M, Nordestgaard BG, Cawthon RM, Freiberg JJ, Tybjærg-Hansen A, Bojesen SE
J Natl Cancer Inst 2013 Apr 3;105(7):459-68. Epub 2013 Mar 6 doi: 10.1093/jnci/djt016. PMID: 23468462

Therapy

Wang XF, Xu WJ, Wang FF, Leng R, Yang XK, Ling HZ, Fan YG, Tao JH, Shuai ZW, Zhang L, Ye DQ, Leng RX
Arthritis Rheumatol 2022 Dec;74(12):1984-1990. Epub 2022 Nov 4 doi: 10.1002/art.42304. PMID: 35830513
Song S, Lee E, Kim H
Medicina (Kaunas) 2022 Feb 5;58(2) doi: 10.3390/medicina58020242. PMID: 35208566Free PMC Article
Myllymäki M, Redd R, Reilly CR, Saber W, Spellman SR, Gibson CJ, Hu ZH, Wang T, Orr EH, Grenier JG, Chen MM, Steensma DP, Cutler C, De Vivo I, Antin JH, Neuberg D, Agarwal S, Lindsley RC
Blood 2020 Dec 24;136(26):3070-3081. doi: 10.1182/blood.2020005397. PMID: 33367544Free PMC Article
Doherty JA, Grieshober L, Houck JR, Barnett MJ, Tapsoba JD, Thornquist M, Wang CY, Goodman GE, Chen C
Cancer Epidemiol Biomarkers Prev 2018 Jul;27(7):829-837. Epub 2018 May 9 doi: 10.1158/1055-9965.EPI-17-1183. PMID: 29743162Free PMC Article
Benetos A, Toupance S, Gautier S, Labat C, Kimura M, Rossi PM, Settembre N, Hubert J, Frimat L, Bertrand B, Boufi M, Flecher X, Sadoul N, Eschwege P, Kessler M, Tzanetakou IP, Doulamis IP, Konstantopoulos P, Tzani A, Korou M, Gkogkos A, Perreas K, Menenakos E, Samanidis G, Vasiloglou-Gkanis M, Kark JD, Malikov S, Verhulst S, Aviv A
Circ Res 2018 Feb 16;122(4):616-623. Epub 2017 Dec 14 doi: 10.1161/CIRCRESAHA.117.311751. PMID: 29242238Free PMC Article

Prognosis

Wang XF, Xu WJ, Wang FF, Leng R, Yang XK, Ling HZ, Fan YG, Tao JH, Shuai ZW, Zhang L, Ye DQ, Leng RX
Arthritis Rheumatol 2022 Dec;74(12):1984-1990. Epub 2022 Nov 4 doi: 10.1002/art.42304. PMID: 35830513
Alder JK, Armanios M
Physiol Rev 2022 Oct 1;102(4):1703-1720. Epub 2022 May 9 doi: 10.1152/physrev.00046.2021. PMID: 35532056Free PMC Article
Aviv A
FASEB J 2020 Jun;34(6):7247-7252. Epub 2020 May 19 doi: 10.1096/fj.202001025. PMID: 32427393Free PMC Article
Pusceddu I, Kleber M, Delgado G, Herrmann W, März W, Herrmann M
PLoS One 2018;13(6):e0198373. Epub 2018 Jun 19 doi: 10.1371/journal.pone.0198373. PMID: 29920523Free PMC Article
Hwang SM, Kim SY, Kim JA, Park HS, Park SN, Im K, Kim K, Kim SM, Lee DS
J Hematol Oncol 2016 Jul 28;9(1):62. doi: 10.1186/s13045-016-0287-9. PMID: 27465399Free PMC Article

Clinical prediction guides

Bussa RM, Mora-Plazas M, Marín C, Villamor E
Eur J Clin Nutr 2023 Feb;77(2):295-297. Epub 2022 Nov 8 doi: 10.1038/s41430-022-01236-w. PMID: 36347948
Wang XF, Xu WJ, Wang FF, Leng R, Yang XK, Ling HZ, Fan YG, Tao JH, Shuai ZW, Zhang L, Ye DQ, Leng RX
Arthritis Rheumatol 2022 Dec;74(12):1984-1990. Epub 2022 Nov 4 doi: 10.1002/art.42304. PMID: 35830513
Myllymäki M, Redd R, Reilly CR, Saber W, Spellman SR, Gibson CJ, Hu ZH, Wang T, Orr EH, Grenier JG, Chen MM, Steensma DP, Cutler C, De Vivo I, Antin JH, Neuberg D, Agarwal S, Lindsley RC
Blood 2020 Dec 24;136(26):3070-3081. doi: 10.1182/blood.2020005397. PMID: 33367544Free PMC Article
Torrance JB, Goldband S
Int J Mol Sci 2020 Oct 27;21(21) doi: 10.3390/ijms21217959. PMID: 33120877Free PMC Article
Toupance S, Labat C, Temmar M, Rossignol P, Kimura M, Aviv A, Benetos A
Hypertension 2017 Aug;70(2):420-425. Epub 2017 Jun 19 doi: 10.1161/HYPERTENSIONAHA.117.09354. PMID: 28630210Free PMC Article

Recent systematic reviews

Song S, Lee E, Kim H
Medicina (Kaunas) 2022 Feb 5;58(2) doi: 10.3390/medicina58020242. PMID: 35208566Free PMC Article
Butt HZ, Atturu G, London NJ, Sayers RD, Bown MJ
Eur J Vasc Endovasc Surg 2010 Jul;40(1):17-26. Epub 2010 May 23 doi: 10.1016/j.ejvs.2010.04.012. PMID: 20547081

Supplemental Content

Table of contents

    Clinical resources

    Practice guidelines

    • PubMed
      See practice and clinical guidelines in PubMed. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.
    • Bookshelf
      See practice and clinical guidelines in NCBI Bookshelf. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.

    Consumer resources

    Recent activity

    Your browsing activity is empty.

    Activity recording is turned off.

    Turn recording back on

    See more...