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Lymphoedema

MedGen UID:
6155
Concept ID:
C0024236
Disease or Syndrome
Synonyms: Lymphedema; Lymphedemas
SNOMED CT: Lymphatic edema (234097001); Lymphedema (234097001); Lymphatic edema (30213001); Acquired lymphedema (30213001); Lymphedema (30213001)
 
HPO: HP:0001004
Orphanet: ORPHA79383

Definition

Edema due to obstruction of lymph vessels or disorders of the lymph nodes. [from MeSH]

Conditions with this feature

Fabry disease
MedGen UID:
8083
Concept ID:
C0002986
Disease or Syndrome
Fabry disease results from deficient activity of the enzyme alpha-galactosidase A (a-Gal A) and progressive lysosomal deposition of globotriaosylceramide (GL-3) in cells throughout the body. The classic form, occurring in males with less than 1% a-Gal A enzyme activity, usually has its onset in childhood or adolescence with periodic crises of severe pain in the extremities (acroparesthesia), the appearance of vascular cutaneous lesions (angiokeratomas), sweating abnormalities (anhidrosis, hypohidrosis, and rarely hyperhidrosis), characteristic corneal and lenticular opacities, and proteinuria. Gradual deterioration of renal function to end-stage renal disease (ESRD) usually occurs in men in the third to fifth decade. In middle age, most males successfully treated for ESRD develop cardiac and/or cerebrovascular disease, a major cause of morbidity and mortality. Heterozygous females typically have milder symptoms at a later age of onset than males. Rarely, they may be relatively asymptomatic throughout a normal life span or may have symptoms as severe as those observed in males with the classic phenotype. In contrast, males with greater than 1% a-Gal A activity may have: (1) a cardiac variant phenotype that usually presents in the sixth to eighth decade with left ventricular hypertrophy, cardiomyopathy and arrhythmia, and proteinuria, but without ESRD; or (2) a renal variant phenotype, associated with ESRD but without the skin lesions or pain; or (3) cerebrovascular disease presenting as stroke or transient ischemic attack.
Klippel Trenaunay syndrome
MedGen UID:
9646
Concept ID:
C0022739
Congenital Abnormality
Klippel-Trenaunay syndrome is a condition that affects the development of blood vessels, soft tissues (such as skin and muscles), and bones. The disorder has three characteristic features: a red birthmark called a port-wine stain, abnormal overgrowth of soft tissues and bones, and vein malformations.Most people with Klippel-Trenaunay syndrome are born with a port-wine stain. This type of birthmark is caused by swelling of small blood vessels near the surface of the skin. Port-wine stains are typically flat and can vary from pale pink to deep maroon in color. In people with Klippel-Trenaunay syndrome, the port-wine stain usually covers part of one limb. The affected area may become lighter or darker with age. Occasionally, port-wine stains develop small red blisters that break open and bleed easily.Klippel-Trenaunay syndrome is also associated with overgrowth of bones and soft tissues beginning in infancy. Usually this abnormal growth is limited to one limb, most often one leg. However, overgrowth can also affect the arms or, rarely, the torso. The abnormal growth can cause pain, a feeling of heaviness, and reduced movement in the affected area. If the overgrowth causes one leg to be longer than the other, it can also lead to problems with walking.Malformations of veins are the third major feature of Klippel-Trenaunay syndrome. These abnormalities include varicose veins, which are swollen and twisted veins near the surface of the skin that often cause pain. Varicose veins usually occur on the sides of the upper legs and calves. Veins deep in the limbs can also be abnormal in people with Klippel-Trenaunay syndrome. Malformations of deep veins increase the risk of a type of blood clot called a deep vein thrombosis (DVT). If a DVT travels through the bloodstream and lodges in the lungs, it can cause a life-threatening blood clot known as a pulmonary embolism (PE).Other complications of Klippel-Trenaunay syndrome can include a type of skin infection called cellulitis, swelling caused by a buildup of fluid (lymphedema), and internal bleeding from abnormal blood vessels. Less commonly, this condition is also associated with fusion of certain fingers or toes (syndactyly) or the presence of extra digits (polydactyly).
Noonan syndrome 1
MedGen UID:
22527
Concept ID:
C0041409
Disease or Syndrome
Noonan syndrome (NS) is characterized by characteristic facies, short stature, congenital heart defect, and developmental delay of variable degree. Other findings can include broad or webbed neck, unusual chest shape with superior pectus carinatum and inferior pectus excavatum, cryptorchidism, varied coagulation defects, lymphatic dysplasias, and ocular abnormalities. Although birth length is usually normal, final adult height approaches the lower limit of normal. Congenital heart disease occurs in 50%-80% of individuals. Pulmonary valve stenosis, often with dysplasia, is the most common heart defect and is found in 20%-50% of individuals. Hypertrophic cardiomyopathy, found in 20%-30% of individuals, may be present at birth or develop in infancy or childhood. Other structural defects include atrial and ventricular septal defects, branch pulmonary artery stenosis, and tetralogy of Fallot. Up to one fourth of affected individuals have mild intellectual disability, and language impairments in general are more common in NS than in the general population.
Yellow nail syndrome
MedGen UID:
113164
Concept ID:
C0221348
Disease or Syndrome
Yellow nail syndrome (YNS) is classically considered to comprise a clinical triad of yellow nails, lymphedema, and respiratory tract involvement. Two of these symptoms are required for the diagnosis, since the complete triad is only observed in about one-third of patients. Onset is usually after puberty (Hoque et al., 2007).
Distichiasis-lymphedema syndrome
MedGen UID:
75566
Concept ID:
C0265345
Disease or Syndrome
Lymphedema-distichiasis syndrome is characterized by lower-limb lymphedema and distichiasis (aberrant eyelashes ranging from a full set of extra eyelashes to a single hair). Lymphedema typically appears in late childhood or puberty, is confined to the lower limbs, and is often asymmetric; severity varies within families. Males develop edema at an earlier age and have more problems with cellulitis than females. Distichiasis, which may be present at birth, is observed in 94% of affected individuals. About 75% of affected individuals have ocular findings including corneal irritation, recurrent conjunctivitis, and photophobia; other common findings include varicose veins, congenital heart disease, and ptosis. About 25% of individuals are asymptomatic.
Fetal trimethadione syndrome
MedGen UID:
120538
Concept ID:
C0265373
Disease or Syndrome
A pattern of abnormalities in infants born to epileptic mothers who were treated during their pregnancies with trimethadione anticonvulsant drugs. The abnormalities include developmental delay, craniofacial dysmorphism (midfacial flattening, V-shaped eyebrows, short nose, synophrys, malformed ears, and strabismus), cardiovascular abnormalities, absent kidney and ureter, omphalocele, meningocele, and other defects.
Cholestasis-edema syndrome, Norwegian type
MedGen UID:
78658
Concept ID:
C0268314
Disease or Syndrome
A rare genetic syndrome which occurs primarily among individuals of Norwegian descent with an autosomal recessive pattern of inheritance. It is caused, in some cases, by the inheritance of a mutation of the LSC1 gene on chromosome 15. Clinical signs include lymphedema of the lower extremities and cholestasis. The clinical course includes giant-cell hepatitis and progression to cirrhosis.
Hennekam lymphangiectasia-lymphedema syndrome
MedGen UID:
137946
Concept ID:
C0340834
Disease or Syndrome
Hennekam lymphangiectasia-lymphedema syndrome is an autosomal recessive disorder characterized by generalized lymphatic dysplasia affecting various organs, including the intestinal tract, pericardium, and limbs. Additional features of the disorder include facial dysmorphism and cognitive impairment (summary by Alders et al., 2014). Genetic Heterogeneity of Hennekam Lymphangiectasia-Lymphedema Syndrome See also HKLLS2 (616006), caused by mutation in the FAT4 gene (612411) on chromosome 4q28.
Hypertrichotic osteochondrodysplasia
MedGen UID:
208647
Concept ID:
C0795905
Disease or Syndrome
Cantú syndrome and the related disorders acromegaloid facial appearance (AFA) and hypertrichosis and acromegaloid facial features (HAFF) are characterized by congenital hypertrichosis; distinctive coarse facial features (including broad nasal bridge, wide mouth with full lips and macroglossia); enlarged heart (increased ventricular mass, enlarged chambers, and normal cardiac function); and skeletal abnormalities (thickening of the calvaria, broad ribs, scoliosis, and flaring of the metaphyses). Other cardiovascular abnormalities may include patent ductus arteriosus (PDA) (in 50%), pericardial effusion (20%), and increased vascular tortuosity. Intellect is typically normal; behavioral problems can include anxiety, mood swings, obsessive-compulsive disorder, and tics.
Microcephaly with or without chorioretinopathy, lymphedema, or mental retardation
MedGen UID:
320559
Concept ID:
C1835265
Disease or Syndrome
Microcephaly with or without chorioretinopathy, lymphedema, or mental retardation is an autosomal dominant disorder that involves an overlapping but variable spectrum of central nervous system and ocular developmental anomalies. Microcephaly ranges from mild to severe and is often associated with mild to moderate developmental delay and a characteristic facial phenotype with upslanting palpebral fissures, broad nose with rounded tip, long philtrum with thin upper lip, prominent chin, and prominent ears. Chorioretinopathy is the most common eye abnormality, but retinal folds, microphthalmia, and myopic and hypermetropic astigmatism have also been reported, and some individuals have no overt ocular phenotype. Congenital lymphedema, when present, is typically confined to the dorsa of the feet, and lymphoscintigraphy reveals the absence of radioactive isotope uptake from the webspaces between the toes (summary by Ostergaard et al., 2012). Robitaille et al. (2014) found that MCLMR includes a broader spectrum of ocular disease, including retinal detachment with avascularity of the peripheral retina, and noted phenotypic overlap with familial exudative vitreoretinopathy (FEVR; see EVR1, 133780). An autosomal recessive form of microcephaly with chorioretinopathy (251270) is caused by mutation in the TUBGCP6 gene (610053) on chromosome 22q. See also Mirhosseini-Holmes-Walton syndrome (autosomal recessive microcephaly with pigmentary retinopathy and mental retardation; 268050), which has been mapped to chromosome 8q21.3-q22.1. A patient with microcephaly, congenital retinal fold, mental retardation, and lymphedema who had a pericentric inversion of chromosome 6 resulting in haploinsufficiency of the CDK19 gene (614720) has been reported.
Lymphedema and cerebral arteriovenous anomaly
MedGen UID:
322617
Concept ID:
C1835272
Disease or Syndrome
Kanzaki disease
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).
Oculoectodermal syndrome
MedGen UID:
333068
Concept ID:
C1838329
Disease or Syndrome
Glomerulonephritis with sparse hair and telangiectases
MedGen UID:
374835
Concept ID:
C1841989
Disease or Syndrome
Hypotrichosis-lymphedema-telangiectasia-renal defect syndrome is an autosomal dominant disorder characterized by these 4 features, which begin in early childhood and are progressive (summary by Moalem et al., 2015).
Ectodermal dysplasia, anhidrotic, with immunodeficiency, osteopetrosis, and lymphedema
MedGen UID:
337348
Concept ID:
C1845919
Disease or Syndrome
Osteopetrosis is a bone disease that makes bones abnormally dense and prone to breakage (fracture). Researchers have described several major types of osteopetrosis, which are usually distinguished by their pattern of inheritance: autosomal dominant, autosomal recessive, or X-linked. The different types of the disorder can also be distinguished by the severity of their signs and symptoms.Autosomal dominant osteopetrosis (ADO), which is also called Albers-Schönberg disease, is typically the mildest type of the disorder. Some affected individuals have no symptoms. In these people, the unusually dense bones may be discovered by accident when an x-ray is done for another reason. In affected individuals who develop signs and symptoms, the major features of the condition include multiple bone fractures, abnormal side-to-side curvature of the spine (scoliosis) or other spinal abnormalities, arthritis in the hips, and a bone infection called osteomyelitis. These problems usually become apparent in late childhood or adolescence.Autosomal recessive osteopetrosis (ARO) is a more severe form of the disorder that becomes apparent in early infancy. Affected individuals have a high risk of bone fracture resulting from seemingly minor bumps and falls. Their abnormally dense skull bones pinch nerves in the head and face (cranial nerves), often resulting in vision loss, hearing loss, and paralysis of facial muscles. Dense bones can also impair the function of bone marrow, preventing it from producing new blood cells and immune system cells. As a result, people with severe osteopetrosis are at risk of abnormal bleeding, a shortage of red blood cells (anemia), and recurrent infections. In the most severe cases, these bone marrow abnormalities can be life-threatening in infancy or early childhood.Other features of autosomal recessive osteopetrosis can include slow growth and short stature, dental abnormalities, and an enlarged liver and spleen (hepatosplenomegaly). Depending on the genetic changes involved, people with severe osteopetrosis can also have brain abnormalities, intellectual disability, or recurrent seizures (epilepsy).A few individuals have been diagnosed with intermediate autosomal osteopetrosis (IAO), a form of the disorder that can have either an autosomal dominant or an autosomal recessive pattern of inheritance. The signs and symptoms of this condition become noticeable in childhood and include an increased risk of bone fracture and anemia. People with this form of the disorder typically do not have life-threatening bone marrow abnormalities. However, some affected individuals have had abnormal calcium deposits (calcifications) in the brain, intellectual disability, and a form of kidney disease called renal tubular acidosis.Rarely, osteopetrosis can have an X-linked pattern of inheritance. In addition to abnormally dense bones, the X-linked form of the disorder is characterized by abnormal swelling caused by a buildup of fluid (lymphedema) and a condition called anhydrotic ectodermal dysplasia that affects the skin, hair, teeth, and sweat glands. Affected individuals also have a malfunctioning immune system (immunodeficiency), which allows severe, recurrent infections to develop. Researchers often refer to this condition as OL-EDA-ID, an acronym derived from each of the major features of the disorder.
Macrocephaly with multiple epiphyseal dysplasia and distinctive facies
MedGen UID:
335505
Concept ID:
C1846722
Disease or Syndrome
22q13.3 deletion syndrome
MedGen UID:
339994
Concept ID:
C1853490
Disease or Syndrome
Phelan-McDermid syndrome (22q13.3 deletion syndrome) is characterized by neonatal hypotonia, global developmental delay, absent to severely delayed speech, and normal to accelerated growth. Most individuals have moderate to profound intellectual disability. Other features include large fleshy hands, dysplastic toenails, and decreased perspiration that results in a tendency to overheat. Behavior characteristics include mouthing or chewing non-food items, decreased perception of pain, and autistic-like affect.
Dahlberg Borer Newcomer syndrome
MedGen UID:
383693
Concept ID:
C1855477
Disease or Syndrome
A very rare ectodermal dysplasia syndrome, described in 2 adult brothers, characterised by the association of hypoparathyroidism, nephropathy, congenital lymphoedema, mitral valve prolapse and brachytelephalangy. Additional features include mild facial dysmorphism, hypertrichosis and nail abnormalities.
Urioste Martinez-Frias syndrome
MedGen UID:
343489
Concept ID:
C1856159
Disease or Syndrome
Campomelia Cumming type
MedGen UID:
347864
Concept ID:
C1859371
Disease or Syndrome
The association of limb defects and multivisceral anomalies. The syndrome has been reported in eight infants from four different families. Skeletal features include tetramelic campomelia and short long bones. Extraskeletal manifestations may include cervical lymphocele, generalised hydrops, polycystic kidneys, pancreas and liver, fibrotic liver or pancreas, polysplenia, heterotaxia, hypoplastic lung, short bowel. All newborns reported so far were either stillborn or died shortly after birth.
Lymphedema, cardiac septal defects, and characteristic facies
MedGen UID:
383042
Concept ID:
C2677167
Disease or Syndrome
This syndrome is characterised by congenital lymphoedema of the lower limbs, atrial septal defect and a characteristic facies (a round face with a prominent forehead, a flat nasal bridge with a broad nasal tip, epicanthal folds, a thin upper lip and a cleft chin). It has been described in two brothers and a sister. Transmission appears to be autosomal recessive.
Lymphedema, hereditary, IB
MedGen UID:
437039
Concept ID:
C2677787
Disease or Syndrome
Hereditary primary lymphedema is caused by anatomic or functional defects in the lymphatic system, resulting in chronic swelling of body parts. There may be accompanying nail and skin changes, such as nail dysplasia or papillomatosis. Onset is usually at birth or in early childhood but can occur later, and the severity is variable (summary by Gordon et al., 2013 and Balboa-Beltran et al., 2014).
Aarskog syndrome, autosomal dominant
MedGen UID:
460570
Concept ID:
C3149220
Disease or Syndrome
Aarskog syndrome is characterized by short stature and facial, limb, and genital anomalies. One form of the disorder is X-linked (see 305400), but there is also evidence for autosomal dominant and autosomal recessive (227330) inheritance (summary by Grier et al., 1983).
Lymphedema, hereditary, IC
MedGen UID:
462082
Concept ID:
C3150732
Disease or Syndrome
Hereditary primary lymphedema is caused by anatomic or functional defects in the lymphatic system, resulting in chronic swelling of body parts. There may be accompanying nail and skin changes, such as nail dysplasia or papillomatosis. Onset is usually at birth or in early childhood but can occur later, and the severity is variable (summary by Gordon et al., 2013 and Balboa-Beltran et al., 2014). For a discussion of genetic heterogeneity of hereditary lymphedema, see LMPH1A (153100).
Noonan syndrome-like disorder with or without juvenile myelomonocytic leukemia
MedGen UID:
462153
Concept ID:
C3150803
Disease or Syndrome
Noonan syndrome-like disorder is a developmental disorder resembling Noonan syndrome (NS1; 163950) and characterized by facial dysmorphism, a wide spectrum of cardiac disease, reduced growth, variable cognitive deficits, and ectodermal and musculoskeletal anomalies. There is extensive phenotypic heterogeneity and variable expressivity (summary by Martinelli et al., 2010). Patients with heterozygous germline CBL mutations have an increased risk for certain malignancies, particularly juvenile myelomonocytic leukemia (JMML; 607785), as also seen in patients with Noonan syndrome (summary by Niemeyer et al., 2010).
Choanal atresia and lymphedema
MedGen UID:
462225
Concept ID:
C3150875
Disease or Syndrome
Agenesis of the corpus callosum and congenital lymphedema
MedGen UID:
462237
Concept ID:
C3150887
Disease or Syndrome
Lymphedema, primary, with myelodysplasia
MedGen UID:
481294
Concept ID:
C3279664
Disease or Syndrome
Lymphedema, hereditary, ID
MedGen UID:
863065
Concept ID:
C4014628
Disease or Syndrome
Hennekam lymphangiectasia-lymphedema syndrome 2
MedGen UID:
863376
Concept ID:
C4014939
Disease or Syndrome
Hennekam lymphangiectasia-lymphedema syndrome is an autosomal recessive disorder characterized by generalized lymphatic dysplasia affecting various organs, including the intestinal tract, pericardium, and limbs. Additional features of the disorder include facial dysmorphism and cognitive impairment (summary by Alders et al., 2014). For a discussion of genetic heterogeneity of Hennekam lymphangiectasia-lymphedema syndrome, see HKLLS1 (235510).
Lissencephaly 7 with cerebellar hypoplasia
MedGen UID:
895680
Concept ID:
C4225359
Disease or Syndrome
Lissencephaly-7 with cerebellar hypoplasia is a severe neurodevelopmental disorder characterized by lack of psychomotor development, facial dysmorphism, arthrogryposis, and early-onset intractable seizures resulting in death in infancy (summary by Magen et al., 2015). For a general description and a discussion of genetic heterogeneity of lissencephaly, see LIS1 (607432).

Recent clinical studies

Etiology

Gjorup CA, Groenvold M, Hendel HW, Dahlstroem K, Drzewiecki KT, Klausen TW, Hölmich LR
Eur J Cancer 2017 Nov;85:122-132. Epub 2017 Sep 15 doi: 10.1016/j.ejca.2017.07.052. PMID: 28918186
Watt H, Singh-Grewal D, Wargon O, Adams S
J Paediatr Child Health 2017 Jan;53(1):38-42. Epub 2016 Oct 4 doi: 10.1111/jpc.13305. PMID: 27701785
Wang W, Keast DH
J Wound Care 2016 Apr;25(4):S11-2, S14-5. doi: 10.12968/jowc.2016.25.Sup4.S11. PMID: 27068342
Alcorso J, Sherman KA
Psychooncology 2016 Jul;25(7):865-72. Epub 2015 Nov 3 doi: 10.1002/pon.4021. PMID: 26525309
Sackey H, Johansson H, Sandelin K, Liljegren G, MacLean G, Frisell J, Brandberg Y
Eur J Surg Oncol 2015 Apr;41(4):577-84. Epub 2015 Jan 13 doi: 10.1016/j.ejso.2014.12.006. PMID: 25659877

Diagnosis

Watt H, Singh-Grewal D, Wargon O, Adams S
J Paediatr Child Health 2017 Jan;53(1):38-42. Epub 2016 Oct 4 doi: 10.1111/jpc.13305. PMID: 27701785
Wang W, Keast DH
J Wound Care 2016 Apr;25(4):S11-2, S14-5. doi: 10.12968/jowc.2016.25.Sup4.S11. PMID: 27068342
Alcorso J, Sherman KA
Psychooncology 2016 Jul;25(7):865-72. Epub 2015 Nov 3 doi: 10.1002/pon.4021. PMID: 26525309
van de Pas CB, Biemans AA, Boonen RS, Viehoff PB, Neumann HA
Phlebology 2016 May;31(4):257-63. Epub 2015 May 8 doi: 10.1177/0268355515586312. PMID: 25956549
Sackey H, Johansson H, Sandelin K, Liljegren G, MacLean G, Frisell J, Brandberg Y
Eur J Surg Oncol 2015 Apr;41(4):577-84. Epub 2015 Jan 13 doi: 10.1016/j.ejso.2014.12.006. PMID: 25659877

Therapy

Gjorup CA, Groenvold M, Hendel HW, Dahlstroem K, Drzewiecki KT, Klausen TW, Hölmich LR
Eur J Cancer 2017 Nov;85:122-132. Epub 2017 Sep 15 doi: 10.1016/j.ejca.2017.07.052. PMID: 28918186
Stanton MC, Yamauchi M, Mkwanda SZ, Ndhlovu P, Matipula DE, Mackenzie C, Kelly-Hope LA
Infect Dis Poverty 2017 Apr 3;6(1):28. doi: 10.1186/s40249-017-0241-2. PMID: 28366168Free PMC Article
Pivetta E, Wassermann B, Del Bel Belluz L, Danussi C, Modica TM, Maiorani O, Bosisio G, Boccardo F, Canzonieri V, Colombatti A, Spessotto P
Clin Sci (Lond) 2016 Jul 1;130(14):1221-36. Epub 2016 Feb 26 doi: 10.1042/CS20160064. PMID: 26920215Free PMC Article
Jakes AD, Twelves C
Breast Cancer Res Treat 2015 Dec;154(3):455-61. Epub 2015 Nov 20 doi: 10.1007/s10549-015-3639-1. PMID: 26589315
Sackey H, Johansson H, Sandelin K, Liljegren G, MacLean G, Frisell J, Brandberg Y
Eur J Surg Oncol 2015 Apr;41(4):577-84. Epub 2015 Jan 13 doi: 10.1016/j.ejso.2014.12.006. PMID: 25659877

Prognosis

Lamprou DA, Voesten HG, Damstra RJ, Wikkeling OR
Br J Surg 2017 Jan;104(1):84-89. Epub 2016 Nov 3 doi: 10.1002/bjs.10325. PMID: 27809337
Teo I, Munnoch DA
J Plast Reconstr Aesthet Surg 2015 Oct;68(10):1395-401. Epub 2015 May 29 doi: 10.1016/j.bjps.2015.05.016. PMID: 26058726
Bundred NJ, Stockton C, Keeley V, Riches K, Ashcroft L, Evans A, Skene A, Purushotham A, Bramley M, Hodgkiss T; Investigators of BEA/PLACE studies.
Breast Cancer Res Treat 2015 May;151(1):121-9. Epub 2015 Apr 8 doi: 10.1007/s10549-015-3357-8. PMID: 25850535
Cromwell KD, Chiang YJ, Armer J, Heppner PP, Mungovan K, Ross MI, Gershenwald JE, Lee JE, Royal RE, Lucci A, Cormier JN
Eur J Cancer Care (Engl) 2015 Sep;24(5):724-33. Epub 2015 Mar 24 doi: 10.1111/ecc.12311. PMID: 25809989Free PMC Article
Akita S, Mitsukawa N, Kuriyama M, Hasegawa M, Kubota Y, Tokumoto H, Ishigaki T, Hanaoka H, Satoh K
J Plast Reconstr Aesthet Surg 2014 Apr;67(4):520-5. Epub 2014 Jan 8 doi: 10.1016/j.bjps.2013.12.056. PMID: 24480651

Clinical prediction guides

Gjorup CA, Groenvold M, Hendel HW, Dahlstroem K, Drzewiecki KT, Klausen TW, Hölmich LR
Eur J Cancer 2017 Nov;85:122-132. Epub 2017 Sep 15 doi: 10.1016/j.ejca.2017.07.052. PMID: 28918186
Stanton MC, Yamauchi M, Mkwanda SZ, Ndhlovu P, Matipula DE, Mackenzie C, Kelly-Hope LA
Infect Dis Poverty 2017 Apr 3;6(1):28. doi: 10.1186/s40249-017-0241-2. PMID: 28366168Free PMC Article
Alcorso J, Sherman KA
Psychooncology 2016 Jul;25(7):865-72. Epub 2015 Nov 3 doi: 10.1002/pon.4021. PMID: 26525309
van de Pas CB, Biemans AA, Boonen RS, Viehoff PB, Neumann HA
Phlebology 2016 May;31(4):257-63. Epub 2015 May 8 doi: 10.1177/0268355515586312. PMID: 25956549
Iuchi T, Dai M, Sanada H, Okuwa M, Nakatani T, Sugama J
Int J Nurs Stud 2015 May;52(5):913-9. Epub 2015 Feb 18 doi: 10.1016/j.ijnurstu.2015.01.011. PMID: 25769476

Recent systematic reviews

Jakes AD, Twelves C
Breast Cancer Res Treat 2015 Dec;154(3):455-61. Epub 2015 Nov 20 doi: 10.1007/s10549-015-3639-1. PMID: 26589315
Stuiver MM, ten Tusscher MR, Agasi-Idenburg CS, Lucas C, Aaronson NK, Bossuyt PM
Cochrane Database Syst Rev 2015 Feb 13;(2):CD009765. doi: 10.1002/14651858.CD009765.pub2. PMID: 25677413
Toyserkani NM, Christensen ML, Sheikh SP, Sørensen JA
J Plast Surg Hand Surg 2015 Apr;49(2):65-71. Epub 2014 Oct 1 doi: 10.3109/2000656X.2014.964726. PMID: 25272309
Phillips JJ, Gordon SJ
J Pediatr Rehabil Med 2014;7(4):361-72. doi: 10.3233/PRM-140306. PMID: 25547888
Paramanandam VS, Roberts D
J Physiother 2014 Sep;60(3):136-43. Epub 2014 Jul 30 doi: 10.1016/j.jphys.2014.07.001. PMID: 25086730

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