U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination

Petechiae

MedGen UID:
10680
Concept ID:
C0031256
Disease or Syndrome
Synonyms: Petechia; Petechial hemorrhage
SNOMED CT: Petechiae (271813007); Petechia (50091001); Petechial hemorrhage (50091001); Petechiae (50091001)
 
HPO: HP:0000967

Definition

Petechiae are pinpoint-sized reddish/purple spots, resembling a rash, that appear just under the skin or a mucous membrane when capillaries have ruptured and some superficial bleeding into the skin has happened. This term refers to an abnormally increased susceptibility to developing petechiae. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVPetechiae

Conditions with this feature

Fucosidosis
MedGen UID:
5288
Concept ID:
C0016788
Disease or Syndrome
Fucosidosis is an autosomal recessive lysosomal storage disease caused by defective alpha-L-fucosidase with accumulation of fucose in the tissues. Clinical features include angiokeratoma, progressive psychomotor retardation, neurologic signs, coarse facial features, and dysostosis multiplex. Fucosidosis has been classified into 2 major types. Type 1 is characterized by rapid psychomotor regression and severe neurologic deterioration beginning at about 6 months of age, elevated sweat sodium chloride, and death within the first decade of life. Type 2 is characterized by milder psychomotor retardation and neurologic signs, the development of angiokeratoma corporis diffusum, normal sweat salinity, and longer survival (Kousseff et al., 1976).
Wiskott-Aldrich syndrome
MedGen UID:
21921
Concept ID:
C0043194
Disease or Syndrome
The WAS-related disorders, which include Wiskott-Aldrich syndrome, X-linked thrombocytopenia (XLT), and X-linked congenital neutropenia (XLN), are a spectrum of disorders of hematopoietic cells, with predominant defects of platelets and lymphocytes caused by pathogenic variants in WAS. WAS-related disorders usually present in infancy. Affected males have thrombocytopenia with intermittent mucosal bleeding, bloody diarrhea, and intermittent or chronic petechiae and purpura; eczema; and recurrent bacterial and viral infections, particularly of the ear. At least 40% of those who survive the early complications develop one or more autoimmune conditions including hemolytic anemia, immune thrombocytopenic purpura, immune-mediated neutropenia, rheumatoid arthritis, vasculitis, and immune-mediated damage to the kidneys and liver. Individuals with a WAS-related disorder, particularly those who have been exposed to Epstein-Barr virus (EBV), are at increased risk of developing lymphomas, which often occur in unusual, extranodal locations including the brain, lung, or gastrointestinal tract. Males with XLT have thrombocytopenia with small platelets; other complications of Wiskott-Aldrich syndrome, including eczema and immune dysfunction, are usually mild or absent. Males with XLN have congenital neutropenia, myeloid dysplasia, and lymphoid cell abnormalities.
Prolidase deficiency
MedGen UID:
120647
Concept ID:
C0268532
Disease or Syndrome
Prolidase deficiency is characterized by skin lesions (typically severe, chronic, recalcitrant, and painful skin ulcers of the lower extremities and telangiectasias of the face and hands), recurrent infections (particularly of the skin and respiratory tract), dysmorphic facial features, variable intellectual disability, and organomegaly (typically splenomegaly but occasionally associated with hepatomegaly) with elevated liver enzymes. Skeletal anomalies, chronic pulmonary disease, anemia, thrombocytopenia, hypergammaglobulinemia, and hypocomplementemia are observed in a minority of affected individuals. An association between prolidase deficiency and autoimmune conditions – particularly systemic lupus erythematosus (SLE) – has been described.
Aicardi-Goutieres syndrome 1
MedGen UID:
162912
Concept ID:
C0796126
Disease or Syndrome
Most characteristically, Aicardi-Goutières syndrome (AGS) manifests as an early-onset encephalopathy that usually, but not always, results in severe intellectual and physical disability. A subgroup of infants with AGS present at birth with abnormal neurologic findings, hepatosplenomegaly, elevated liver enzymes, and thrombocytopenia, a picture highly suggestive of congenital infection. Otherwise, most affected infants present at variable times after the first few weeks of life, frequently after a period of apparently normal development. Typically, they demonstrate the subacute onset of a severe encephalopathy characterized by extreme irritability, intermittent sterile pyrexias, loss of skills, and slowing of head growth. Over time, as many as 40% develop chilblain skin lesions on the fingers, toes, and ears. It is becoming apparent that atypical, sometimes milder, cases of AGS exist, and thus the true extent of the phenotype associated with pathogenic variants in the AGS-related genes is not yet known.
Alpha-N-acetylgalactosaminidase deficiency type 2
MedGen UID:
324539
Concept ID:
C1836522
Disease or Syndrome
Alpha-N-acetylgalactosaminidase (NAGA) deficiency is a very rare lysosomal storage disorder with atypical features. It is clinically heterogeneous with 3 main phenotypes: type I is an infantile-onset neuroaxonal dystrophy (609241); type II, also known as Kanzaki disease, is an adult-onset disorder characterized by angiokeratoma corporis diffusum and mild intellectual impairment; and type III is an intermediate disorder (see 609241) with mild to moderate neurologic manifestations (Desnick and Schindler, 2001).
Beta-thalassemia-X-linked thrombocytopenia syndrome
MedGen UID:
326415
Concept ID:
C1839161
Disease or Syndrome
GATA1-related cytopenia is characterized by thrombocytopenia and/or anemia ranging from mild to severe. One or more of the following may also be present: platelet dysfunction, mild ß-thalassemia, neutropenia, and congenital erythropoietic porphyria (CEP) in males. Thrombocytopenia typically presents in infancy as a bleeding disorder with easy bruising and mucosal bleeding (e.g., epistaxis). Anemia ranges from minimal (mild dyserythropoiesis) to severe (hydrops fetalis requiring in utero transfusion). At the extreme end of the clinical spectrum, severe hemorrhage and/or erythrocyte transfusion dependence are life long; at the milder end, anemia and the risk for bleeding may decrease spontaneously with age. Heterozygous females may have mild-to-moderate symptoms such as menorrhagia.
Thrombocytopenia 1
MedGen UID:
326416
Concept ID:
C1839163
Disease or Syndrome
The WAS-related disorders, which include Wiskott-Aldrich syndrome, X-linked thrombocytopenia (XLT), and X-linked congenital neutropenia (XLN), are a spectrum of disorders of hematopoietic cells, with predominant defects of platelets and lymphocytes caused by pathogenic variants in WAS. WAS-related disorders usually present in infancy. Affected males have thrombocytopenia with intermittent mucosal bleeding, bloody diarrhea, and intermittent or chronic petechiae and purpura; eczema; and recurrent bacterial and viral infections, particularly of the ear. At least 40% of those who survive the early complications develop one or more autoimmune conditions including hemolytic anemia, immune thrombocytopenic purpura, immune-mediated neutropenia, rheumatoid arthritis, vasculitis, and immune-mediated damage to the kidneys and liver. Individuals with a WAS-related disorder, particularly those who have been exposed to Epstein-Barr virus (EBV), are at increased risk of developing lymphomas, which often occur in unusual, extranodal locations including the brain, lung, or gastrointestinal tract. Males with XLT have thrombocytopenia with small platelets; other complications of Wiskott-Aldrich syndrome, including eczema and immune dysfunction, are usually mild or absent. Males with XLN have congenital neutropenia, myeloid dysplasia, and lymphoid cell abnormalities.
Gaucher disease perinatal lethal
MedGen UID:
374996
Concept ID:
C1842704
Disease or Syndrome
Gaucher disease (GD) encompasses a continuum of clinical findings from a perinatal lethal disorder to an asymptomatic type. The identification of three major clinical types (1, 2, and 3) and two other subtypes (perinatal-lethal and cardiovascular) is useful in determining prognosis and management. GD type 1 is characterized by the presence of clinical or radiographic evidence of bone disease (osteopenia, focal lytic or sclerotic lesions, and osteonecrosis), hepatosplenomegaly, anemia and thrombocytopenia, lung disease, and the absence of primary central nervous system disease. GD types 2 and 3 are characterized by the presence of primary neurologic disease; in the past, they were distinguished by age of onset and rate of disease progression, but these distinctions are not absolute. Disease with onset before age two years, limited psychomotor development, and a rapidly progressive course with death by age two to four years is classified as GD type 2. Individuals with GD type 3 may have onset before age two years, but often have a more slowly progressive course, with survival into the third or fourth decade. The perinatal-lethal form is associated with ichthyosiform or collodion skin abnormalities or with nonimmune hydrops fetalis. The cardiovascular form is characterized by calcification of the aortic and mitral valves, mild splenomegaly, corneal opacities, and supranuclear ophthalmoplegia. Cardiopulmonary complications have been described with all the clinical subtypes, although varying in frequency and severity.
Ehlers-Danlos syndrome, fibronectinemic type
MedGen UID:
346497
Concept ID:
C1857038
Disease or Syndrome
Ehlers-Danlos syndromes (EDS) form a heterogeneous group of inherited connective tissue disorders characterized by variable joint hypermobility and cutaneous hyperextensibility. Type X is distinguished by platelet dysfunction associated with a fibronectin abnormality. Type X EDS has been described in only one family so far. Age of onset is about 13-25 years. Transmission is autosomal recessive.
Autoimmune lymphoproliferative syndrome type 2A
MedGen UID:
349065
Concept ID:
C1858968
Disease or Syndrome
Autoimmune lymphoproliferative syndrome (ALPS), caused by defective lymphocyte homeostasis, is characterized by the following: Non-malignant lymphoproliferation (lymphadenopathy, hepatosplenomegaly with or without hypersplenism) that often improves with age. Autoimmune disease, mostly directed toward blood cells. Lifelong increased risk for both Hodgkin and non-Hodgkin lymphoma. In ALPS-FAS (the most common and best-characterized type of ALPS, associated with heterozygous germline pathogenic variants in FAS), non-malignant lymphoproliferation typically manifests in the first years of life, inexplicably waxes and wanes, and then often decreases without treatment in the second decade of life; in many affected individuals, however, neither splenomegaly nor the overall expansion of lymphocyte subsets in peripheral blood decreases. Although autoimmunity is often not present at the time of diagnosis or at the time of the most extensive lymphoproliferation, autoantibodies can be detected before autoimmune disease manifests clinically. In ALPS-FAS caused by homozygous or compound heterozygous (biallelic) pathogenic variants in FAS, severe lymphoproliferation occurs before, at, or shortly after birth, and usually results in death at an early age. ALPS-sFAS, resulting from somatic FAS pathogenic variants in selected cell populations, notably the alpha/beta double-negative T cells (a/ß-DNT cells), appears to be similar to ALPS-FAS resulting from heterozygous germline pathogenic variants in FAS, although lower incidence of splenectomy and lower lymphocyte counts have been reported in ALPS-sFAS and no cases of lymphoma have yet been published.
Platelet-type bleeding disorder 17
MedGen UID:
396078
Concept ID:
C1861194
Disease or Syndrome
Platelet-type bleeding disorder-17 is an autosomal dominant disorder characterized by increased bleeding tendency due to abnormal platelet function. It is a type of 'gray platelet syndrome' because the platelets appear abnormal on light microscopy. Electron microscopy shows decreased or absent alpha-granules within platelets, and bone marrow biopsy shows increased numbers of abnormal megakaryocytes, suggesting a defect in megakaryopoiesis and platelet production. The bleeding severity is variable (summary by Monteferrario et al., 2014).
Ethylmalonic encephalopathy
MedGen UID:
355966
Concept ID:
C1865349
Disease or Syndrome
Ethylmalonic encephalopathy (EE) is a severe, early-onset, progressive disorder characterized by developmental delay / mild-to-severe intellectual disability; generalized infantile hypotonia that evolves into hypertonia, spasticity, and (in some instances) dystonia; generalized tonic-clonic seizures; and generalized microvascular damage (diffuse and spontaneous relapsing petechial purpura, hemorrhagic suffusions of mucosal surfaces, and chronic hemorrhagic diarrhea). Infants sometimes have frequent vomiting and loss of social interaction. Speech is delayed and in some instances absent. Swallowing difficulties and failure to thrive are common. Children may be unable to walk without support and may be wheelchair bound. Neurologic deterioration accelerates following intercurrent infectious illness, and the majority of children die in the first decade.
Autosomal recessive osteopetrosis 4
MedGen UID:
370598
Concept ID:
C1969106
Disease or Syndrome
The spectrum of CLCN7-related osteopetrosis includes infantile malignant CLCN7-related autosomal recessive osteopetrosis (ARO), intermediate autosomal osteopetrosis (IAO), and autosomal dominant osteopetrosis type II (ADOII; Albers-Schönberg disease). ARO. Onset is at birth. Findings may include: fractures; reduced growth; sclerosis of the skull base (with or without choanal stenosis or hydrocephalus) resulting in optic nerve compression, facial palsy, and hearing loss; absence of the bone marrow cavity resulting in severe anemia and thrombocytopenia; dental abnormalities, odontomas, and risk for mandibular osteomyelitis; and hypocalcemia with tetanic seizures and secondary hyperparathyroidism. Without treatment maximal life span in ARO is ten years. IAO. Onset is in childhood. Findings may include: fractures after minor trauma, characteristic skeletal radiographic changes found incidentally, mild anemia, and occasional visual impairment secondary to optic nerve compression. Life expectancy in IAO is usually normal. ADOII. Onset is usually late childhood or adolescence. Findings may include: fractures (in any long bone and/or the posterior arch of a vertebra), scoliosis, hip osteoarthritis, and osteomyelitis of the mandible or septic osteitis or osteoarthritis elsewhere. Cranial nerve compression is rare.
Thrombocytopenia 3
MedGen UID:
437174
Concept ID:
C2678311
Disease or Syndrome
Thrombocytopenia-3 (THC3) is an autosomal recessive hematologic disorder characterized by onset of small-platelet thrombocytopenia in infancy. Patients may show variable bleeding tendency, manifest as petechiae, epistaxis, or heavy menstrual bleeding (summary by Levin et al., 2015). For a general phenotypic description and a discussion of genetic heterogeneity of thrombocytopenia, see 313900.
Leukocyte adhesion deficiency 3
MedGen UID:
411605
Concept ID:
C2748536
Disease or Syndrome
Leukocyte adhesion deficiency-3 (LAD3), also known as LAD1 variant (LAD1V), is an autosomal recessive disorder characterized by LAD1 (116920)-like immune deficiency and Glanzmann thrombasthenia (GT; 273800)-like bleeding problems. LAD3 results from mutations in FERMT3, or KINDLIN3, which encodes an intracellular protein that interacts with beta-integrins in hematopoietic cells. In LAD3, the adhesive functions of integrins on both leukocytes and platelets are disrupted, most likely due to defects in activation-dependent alterations of surface integrins that enable high-avidity binding to ligands on target cells, a process termed 'inside-out signaling' (Svensson et al., 2009; Zimmerman, 2009). For a discussion of genetic heterogeneity of leukocyte adhesion deficiency, see 116920.
Bernard-Soulier syndrome, type A2, autosomal dominant
MedGen UID:
478706
Concept ID:
C3277076
Disease or Syndrome
Autosomal dominant Bernard-Soulier syndrome type A2 (BSSA2) is characterized by chronic macrothrombocytopenia with mild or no clinical symptoms, normal platelet function, and normal megakaryocyte count. When present, clinical findings include excessive ecchymoses, frequent epistaxis, gingival bleeding, prolonged menstrual periods, or prolonged bleeding after tooth extraction (Savoia et al., 2001). Genetic Heterogeneity of Bernard-Soulier Syndrome Homozygous or compound heterozygous mutations in the GP1BA gene cause classic autosomal recessive Bernard-Soulier syndrome (BSSA1; 231200).
Thrombocytopenia, X-linked, with or without dyserythropoietic anemia
MedGen UID:
763703
Concept ID:
C3550789
Disease or Syndrome
GATA1-related cytopenia is characterized by thrombocytopenia and/or anemia ranging from mild to severe. One or more of the following may also be present: platelet dysfunction, mild ß-thalassemia, neutropenia, and congenital erythropoietic porphyria (CEP) in males. Thrombocytopenia typically presents in infancy as a bleeding disorder with easy bruising and mucosal bleeding (e.g., epistaxis). Anemia ranges from minimal (mild dyserythropoiesis) to severe (hydrops fetalis requiring in utero transfusion). At the extreme end of the clinical spectrum, severe hemorrhage and/or erythrocyte transfusion dependence are life long; at the milder end, anemia and the risk for bleeding may decrease spontaneously with age. Heterozygous females may have mild-to-moderate symptoms such as menorrhagia.
Thrombocytopenia 5
MedGen UID:
863974
Concept ID:
C4015537
Disease or Syndrome
Individuals with ETV6 thrombocytopenia and predisposition to leukemia most often present with a lifelong history of thrombocytopenia, which is usually in the mild to moderate range. No syndromic features or associations are consistently shared across pedigrees. Affected individuals also have a moderate risk of developing a hematologic malignancy (with B-cell acute lymphoblastic leukemia [B-ALL] being the most common) and possibly other malignant solid tumors, particularly colorectal cancer.
MIRAGE syndrome
MedGen UID:
924576
Concept ID:
C4284088
Disease or Syndrome
MIRAGE syndrome is an acronym for the major findings of myelodysplasia, infection, restriction of growth, adrenal hypoplasia, genital phenotypes, and enteropathy. Cytopenias are typically seen soon after birth; thrombocytopenia is the most common followed by anemia and pancytopenia. Recurrent infections from early infancy include pneumonia, urinary tract infection, gastroenteritis, meningitis, otitis media, dermatitis, subcutaneous abscess, and sepsis. Reported genital phenotypes in those with 46,XY karyotype included hypospadias, microphallus, bifid shawl scrotum, ambiguous genitalia, or complete female genitalia. Hypoplastic or dysgenetic ovaries have been reported in females. Gastrointestinal complications include chronic diarrhea and esophageal dysfunction. Moderate-to-severe developmental delay is reported in most affected individuals. Autonomic dysfunction and renal dysfunction are also reported.
Pseudo-TORCH syndrome 2
MedGen UID:
1373355
Concept ID:
C4479376
Disease or Syndrome
Pseudo-TORCH syndrome-2 (PTORCH2) is an autosomal recessive multisystem disorder characterized by antenatal onset of intracranial hemorrhage, calcification, brain malformations, liver dysfunction, and often thrombocytopenia. Affected individuals tend to have respiratory insufficiency and seizures, and die in infancy. The phenotype resembles the sequelae of intrauterine infection, but there is no evidence of an infectious agent. The disorder results from inappropriate activation of the interferon (IFN) immunologic pathway (summary by Meuwissen et al., 2016). For a discussion of genetic heterogeneity of PTORCH, see PTORCH1 (251290).
Radioulnar synostosis with amegakaryocytic thrombocytopenia 1
MedGen UID:
1637913
Concept ID:
C4551975
Disease or Syndrome
Radioulnar synostosis with amegakaryocytic thrombocytopenia (RUSAT) is characterized by thrombocytopenia that progresses to pancytopenia, in association with congenital proximal fusion of the radius and ulna that results in extremely limited pronation and supination of the forearm (summary by Niihori et al., 2015). Genetic Heterogeneity of Radioulnar Synostosis with Amegakaryocytic Thrombocytopenia Radioulnar synostosis with amegakaryocytic thrombocytopenia-2 (RUSAT2; 616738) is caused by heterozygous mutation in the MECOM gene (165215) on chromosome 3q26.
Pseudo-TORCH syndrome 1
MedGen UID:
1639355
Concept ID:
C4552078
Disease or Syndrome
Platelet-type bleeding disorder 16
MedGen UID:
1781222
Concept ID:
C5442010
Disease or Syndrome
Platelet-type bleeding disorder-16 (BDPLT16) is an autosomal dominant form of congenital macrothrombocytopenia associated with platelet anisocytosis. It is a disorder of platelet production. Affected individuals may have no or only mildly increased bleeding tendency. In vitro studies show mild platelet functional abnormalities (summary by Kunishima et al., 2011 and Nurden et al., 2011). Genetic Heterogeneity of Glanzmann Thrombasthenia-like with Macrothromocytopenia See BDPLT24 (619271), caused by mutation in the ITGB3 gene (173470) on chromosome 17q21.32. Together the ITGB2B and ITBG3 genes form an integrin, known as platelet glycoprotein GPIIb/III, that is expressed on platelets.
Immunodeficiency 81
MedGen UID:
1788669
Concept ID:
C5543540
Disease or Syndrome
Immunodeficiency-81 (IMD81) is an autosomal recessive complex disorder with onset of recurrent infections, including fungal infections, in early infancy, associated with T-cell, neutrophil, and NK dysfunction. B cells may also show maturation abnormalities. Other features include autoimmune hemolytic anemia and abnormal platelet aggregation, indicating a complex disorder with a wide range of hematopoietic disturbances. The disorder is caused by a defect in intracellular signaling pathways (summary by Lev et al., 2021).
Portal hypertension, noncirrhotic, 2
MedGen UID:
1794158
Concept ID:
C5561948
Disease or Syndrome
Noncirrhotic portal hypertension-2 (NCPH2) is an autosomal recessive disorder characterized by signs of liver dysfunction that become apparent in the first decades of life. Affected individuals have jaundice, hyperbilirubinemia, pancytopenia, including neutropenia, lymphopenia, and thrombocytopenia, hepatosplenomegaly, and esophageal varices. Some patients may have recurrent infections or features suggestive of an immunodeficiency. Liver biopsy is notable for the absence of cirrhosis and the presence of nodular regeneration. Liver sinusoidal endothelial cells (LSECs) have abnormal expression of CD34 (142230) (summary by Drzewiecki et al., 2021). For a discussion of genetic heterogeneity of NCPH, see 617068.
Dyskeratosis congenita, autosomal recessive 8
MedGen UID:
1824030
Concept ID:
C5774257
Disease or Syndrome
Autosomal recessive dyskeratosis congenita-8 (DKCB8) is characterized by progressive bone marrow failure affecting all lineages apparent from infancy or early childhood. More variable features may include poor growth, mild developmental delay, immunodeficiency, and gastrointestinal manifestations, such as esophageal stricture or inflammatory bowel disease. Some patients may have mucocutaneous features, including oral leukoplakia, nail dystrophy, or pigmentary skin abnormalities, although these features may be absent. Unlike patients with other forms of DKC, those with DKCB8 do not have shortened telomeres, although there is evidence of telomere instability. Hematopoietic stem cell transplant may be curative (Kermasson et al., 2022). For a discussion of genetic heterogeneity of dyskeratosis congenita, see DKCA1 (127550).
Autoinflammation with pulmonary and cutaneous vasculitis
MedGen UID:
1841007
Concept ID:
C5830371
Disease or Syndrome
Autoinflammation with pulmonary and cutaneous vasculitis (AIPCV) is a disorder of immune dysregulation manifest as skin lesions (petechiae and purpura) appearing soon after birth followed by progressive pulmonary involvement causing restrictive lung disease and respiratory insufficiency. Other features may include hepatosplenomegaly and anemia (Kanderova et al., 2022).
Hatipoglu immunodeficiency syndrome
MedGen UID:
1841075
Concept ID:
C5830439
Disease or Syndrome
Hatipoglu immunodeficiency syndrome (HATIS) is an autosomal recessive immunologic disorder characterized by childhood onset of failure to thrive, skin manifestations, pancytopenia, and susceptibility to recurrent infections (Harapas et al., 2022).

Professional guidelines

PubMed

Gauer RL, Whitaker DJ
Am Fam Physician 2022 Sep;106(3):288-298. PMID: 36126009
Johnstone C, Rich SE
Ann Palliat Med 2018 Apr;7(2):265-273. Epub 2017 Dec 18 doi: 10.21037/apm.2017.11.01. PMID: 29307210
Ozen S, Pistorio A, Iusan SM, Bakkaloglu A, Herlin T, Brik R, Buoncompagni A, Lazar C, Bilge I, Uziel Y, Rigante D, Cantarini L, Hilario MO, Silva CA, Alegria M, Norambuena X, Belot A, Berkun Y, Estrella AI, Olivieri AN, Alpigiani MG, Rumba I, Sztajnbok F, Tambic-Bukovac L, Breda L, Al-Mayouf S, Mihaylova D, Chasnyk V, Sengler C, Klein-Gitelman M, Djeddi D, Nuno L, Pruunsild C, Brunner J, Kondi A, Pagava K, Pederzoli S, Martini A, Ruperto N; Paediatric Rheumatology International Trials Organisation (PRINTO)
Ann Rheum Dis 2010 May;69(5):798-806. doi: 10.1136/ard.2009.116657. PMID: 20413568

Recent clinical studies

Etiology

Gauer RL, Whitaker DJ
Am Fam Physician 2022 Sep;106(3):288-298. PMID: 36126009
Bilotta C, Perrone G, Adelfio V, Spatola GF, Uzzo ML, Argo A, Zerbo S
Front Immunol 2021;12:729251. Epub 2021 Nov 29 doi: 10.3389/fimmu.2021.729251. PMID: 34912330Free PMC Article
Kohli R, Chaturvedi S
Hamostaseologie 2019 Aug;39(3):238-249. Epub 2019 Mar 13 doi: 10.1055/s-0039-1683416. PMID: 30868551
Clarke RT, Van den Bruel A, Bankhead C, Mitchell CD, Phillips B, Thompson MJ
Arch Dis Child 2016 Oct;101(10):894-901. doi: 10.1136/archdischild-2016-311251. PMID: 27647842
Womack J, Jimenez M
Am Fam Physician 2015 Mar 15;91(6):372-6. PMID: 25822555

Diagnosis

Iranmanesh B, Khalili M, Amiri R, Zartab H, Aflatoonian M
Dermatol Ther 2021 Jan;34(1):e14578. Epub 2020 Dec 13 doi: 10.1111/dth.14578. PMID: 33236823Free PMC Article
Haley KM
Pediatr Rev 2020 May;41(5):224-235. doi: 10.1542/pir.2018-0359. PMID: 32358028
Maher GM
S D Med 2014 Oct;67(10):415-7. PMID: 25423768
Adeyemo TA, Adeyemo WL, Adediran A, Akinbami AJ, Akanmu AS
Indian J Dent Res 2011 May-Jun;22(3):454-61. doi: 10.4103/0970-9290.87070. PMID: 22048588
Chi AC, Neville BW, Krayer JW, Gonsalves WC
Am Fam Physician 2010 Dec 1;82(11):1381-8. PMID: 21121523

Therapy

Broome CM, McDonald V, Miyakawa Y, Carpenedo M, Kuter DJ, Al-Samkari H, Bussel JB, Godar M, Ayguasanosa J, De Beuf K, Rodeghiero F, Michel M, Newland A; ADVANCE Investigator Study Group
Lancet 2023 Nov 4;402(10413):1648-1659. Epub 2023 Sep 28 doi: 10.1016/S0140-6736(23)01460-5. PMID: 37778358
Gauer RL, Whitaker DJ
Am Fam Physician 2022 Sep;106(3):288-298. PMID: 36126009
Jayanth SH, Hugar BS, Praveen S, Girish Chandra YP
Med Leg J 2017 Mar;85(1):38-42. Epub 2016 Sep 30 doi: 10.1177/0025817216671106. PMID: 27694447
Reichman O, Sobel J
Best Pract Res Clin Obstet Gynaecol 2014 Oct;28(7):1042-50. Epub 2014 Jul 17 doi: 10.1016/j.bpobgyn.2014.07.003. PMID: 25132275
Ebell MH
Am Fam Physician 2004 Oct 1;70(7):1279-87. PMID: 15508538

Prognosis

Sibaud V, Beylot-Barry M, Protin C, Vigarios E, Recher C, Ysebaert L
Am J Clin Dermatol 2020 Dec;21(6):799-812. doi: 10.1007/s40257-020-00535-x. PMID: 32613545
Ramos W, Luna M, Alarcón T, Jiménez G, Díaz J, Calderón M, Gutierrez EL
J Cutan Med Surg 2020 Jan/Feb;24(1):33-40. Epub 2019 Sep 26 doi: 10.1177/1203475419878160. PMID: 31556723
Kohli R, Chaturvedi S
Hamostaseologie 2019 Aug;39(3):238-249. Epub 2019 Mar 13 doi: 10.1055/s-0039-1683416. PMID: 30868551
Ebell MH
Am Fam Physician 2004 Oct 1;70(7):1279-87. PMID: 15508538
DiMaio VJ
Am J Forensic Med Pathol 2000 Mar;21(1):1-4. doi: 10.1097/00000433-200003000-00001. PMID: 10739219

Clinical prediction guides

Tully KM, Tendler S, Carter LM, Sharma SK, Samuels ZV, Mandleywala K, Korsen JA, Delos Reyes AM, Piersigilli A, Travis WD, Sen T, Pillarsetty N, Poirier JT, Rudin CM, Lewis JS
Clin Cancer Res 2022 Apr 1;28(7):1391-1401. doi: 10.1158/1078-0432.CCR-21-1533. PMID: 35046060Free PMC Article
Buscatti IM, Simon JR, Viana VSL, Arabi TMA, Trindade VC, Maia ACC, Melo LRC, Ihara BP, Aikawa NE, Silva CA
Rev Paul Pediatr 2021;40:e2020202. Epub 2021 Sep 1 doi: 10.1590/1984-0462/2022/40/2020202. PMID: 34495272Free PMC Article
Ramos W, Luna M, Alarcón T, Jiménez G, Díaz J, Calderón M, Gutierrez EL
J Cutan Med Surg 2020 Jan/Feb;24(1):33-40. Epub 2019 Sep 26 doi: 10.1177/1203475419878160. PMID: 31556723
Yinon Y, Farine D, Yudin MH
J Obstet Gynaecol Can 2018 Feb;40(2):e134-e141. doi: 10.1016/j.jogc.2017.11.018. PMID: 29447718
Dioguardi M, Caloro GA, Troiano G, Giannatempo G, Laino L, Petruzzi M, Lo Muzio L
Ren Fail 2016;38(1):1-6. Epub 2015 Oct 29 doi: 10.3109/0886022X.2015.1103639. PMID: 26513593

Recent systematic reviews

Bilotta C, Perrone G, Adelfio V, Spatola GF, Uzzo ML, Argo A, Zerbo S
Front Immunol 2021;12:729251. Epub 2021 Nov 29 doi: 10.3389/fimmu.2021.729251. PMID: 34912330Free PMC Article
Paolino G, Di Nicola MR, Pontara A, Didona D, Moliterni E, Mercuri SR, Grano M, Borgianni N, Kumar R, Pampena R
J Eur Acad Dermatol Venereol 2020 Oct;34(10):2247-2260. Epub 2020 Jul 20 doi: 10.1111/jdv.16722. PMID: 32530549
Roerdink RL, Dietvorst M, van der Zwaard B, van der Worp H, Zwerver J
Int J Surg 2017 Oct;46:133-145. Epub 2017 Sep 7 doi: 10.1016/j.ijsu.2017.08.587. PMID: 28890412
Clarke RT, Van den Bruel A, Bankhead C, Mitchell CD, Phillips B, Thompson MJ
Arch Dis Child 2016 Oct;101(10):894-901. doi: 10.1136/archdischild-2016-311251. PMID: 27647842
Potts JA, Rothman AL
Trop Med Int Health 2008 Nov;13(11):1328-40. Epub 2008 Sep 16 doi: 10.1111/j.1365-3156.2008.02151.x. PMID: 18803612Free PMC Article

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...