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1  can be utilized for effective management of lymphedema.
2 ecessary axillary lymph node dissections and lymphedema.
3 stases, but is associated with a 14% risk of lymphedema.
4 ene cause Hennekam syndrome, a primary human lymphedema.
5 n promising results in preclinical models of lymphedema.
6 ting their possible involvement in secondary lymphedema.
7 of VEGFR3 has been reported to cause primary lymphedema.
8 ique provided a fresh hope for patients with lymphedema.
9 s immediately applicable to reduce secondary lymphedema.
10 oma formation was increased in patients with lymphedema.
11 with a frameshift mutation also have primary lymphedema.
12 atic vessel function in 5 of 6 patients with lymphedema.
13 ed lymphatic maps in patients with secondary lymphedema.
14 th symptomatic pathologic conditions such as lymphedema.
15  and normal limbs of patients with secondary lymphedema.
16  lymphatic function that result in inherited lymphedema.
17 l that manifested lymphatic hyperplasia with lymphedema.
18 ng lymphatic development result in inherited lymphedema.
19 gents as potential therapy for some forms of lymphedema.
20 ise did not result in increased incidence of lymphedema.
21 ngs, such as radiation or associated chronic lymphedema.
22 as used to ascertain factors associated with lymphedema.
23 ics within the axilla and its use may reduce lymphedema.
24  patients had claims indicating treatment of lymphedema.
25 d symptoms can be early signs of progressing lymphedema.
26 e presence of measured and patient-perceived lymphedema.
27  there remains a clinically relevant risk of lymphedema.
28 recautions if they had measured or perceived lymphedema.
29 phedema development and treating established lymphedema.
30  and 2% reported chronically moderate/severe lymphedema.
31 ients reporting no arm swelling had measured lymphedema.
32  are significant risk factors for developing lymphedema.
33  are significant risk factors for perceiving lymphedema.
34 oderate/severe lymphedema than women with no lymphedema.
35 esia, arm morbidity and range of motion, and lymphedema.
36 or those with arm symptoms without diagnosed lymphedema.
37             She did not develop postsurgical lymphedema.
38 with 5% and 16%, respectively, with measured lymphedema.
39 -gestation after development of interstitial lymphedema.
40 s with a FOXC2 mutation, including 3 without lymphedema.
41 e B4 (LTB4) in the molecular pathogenesis of lymphedema.
42 lay a key role in mediating the pathology of lymphedema.
43 yed hypoplastic facial lymphatics and severe lymphedema.
44  institution were screened prospectively for lymphedema.
45 reatment risk, prevention, and management of lymphedema.
46 al manifestation of lymphatic malfunction is lymphedema.
47 breast reconstruction impacts development of lymphedema.
48 phangiogenesis in clinical settings, such as lymphedema.
49 tic endothelial cells at the early stages of lymphedema.
50 9-cis RA significantly prevents postsurgical lymphedema.
51 s treated for breast cancer and screened for lymphedema.
52 ent to limit the development of postsurgical lymphedema.
53 ing lymph nodes for the purpose of relieving lymphedema.
54 atalogue of human GATA2 mutations results in lymphedema.
55 es of bilateral lower extremity inflammatory lymphedema.
56 se of bilateral lower extremity inflammatory lymphedema.
57 h both cancer-related and non-cancer-related lymphedema.
58 that VLNT may help alleviate the severity of lymphedema.
59 , vascular/lymphatic (venous thrombosis 25%, lymphedema 11%), sensorineural hearing loss 76%, miscarr
60  for 3 years, 23% reported no more than mild lymphedema, 12% reported moderate/severe lymphedema, and
61 one results in a significantly lower rate of lymphedema 5 years postoperatively.
62 cute pneumonitis (1.2% vs. 0.2%, P=0.01) and lymphedema (8.4% vs. 4.5%, P=0.001).
63                                    Secondary lymphedema, a life-long complication of cancer treatment
64       In breast cancer survivors at risk for lymphedema, a program of slowly progressive weight lifti
65 ctive formation of lymphatic valves leads to lymphedema, a progressive and debilitating condition for
66 idelines for breast cancer survivors without lymphedema advise against upper body exercise, preventin
67                                              Lymphedema affects up to 1 in 6 patients who undergo tre
68                                              Lymphedema after breast cancer is common but mostly mild
69                                Postoperative lymphedema after breast cancer surgery is a challenging
70  2.5-fold greater fluid retention and severe lymphedema after inflammation.
71 es may represent a novel means of preventing lymphedema after lymph node resection.
72 an ideal option for patients who suffer from lymphedema after mastectomy and axillary dissection.
73 was to determine the long-term prevalence of lymphedema after SLN biopsy (SLNB) alone and after SLNB
74 uman lymphatic system and reduce the risk of lymphedema after surgery for melanoma and other cancers.
75      Thirty-seven percent of women with mild lymphedema and 68% with moderate/severe lymphedema recei
76 ional analyses to describe the prevalence of lymphedema and arm symptoms and multivariate-adjusted ge
77                            Patient-perceived lymphedema and avoidant behaviors were assessed through
78 or lymphatic related diseases, which include lymphedema and cancer.
79  was lower for BrCa survivors with diagnosed lymphedema and for those with arm symptoms without diagn
80              Two larger families cosegregate lymphedema and GJC2 mutation (LOD score = 6.5).
81 ped a highly reproducible model of secondary lymphedema and have demonstrated that 9-cis RA significa
82  to determine what interventions can improve lymphedema and impact HRQOL for BrCa survivors.
83 ng tissue fibrosis, we used a mouse model of lymphedema and inhibited TGF-beta function either system
84  consecutive patients with uni- or bilateral lymphedema and lymph vessel transplants of the lower ext
85 iated with several human diseases, including lymphedema and metastatic spread of cancer.
86                         Associations between lymphedema and potential risk factors were examined.
87 aploinsufficiency of GATA2 underlies primary lymphedema and predisposes to acute myeloid leukemia in
88 berger syndrome, a disorder characterized by lymphedema and predisposition to myelodysplastic syndrom
89 deficient in lymphovenous hemostasis exhibit lymphedema and sometimes chylothorax phenotypes indicati
90 tations to include predisposition to primary lymphedema and suggest that complete haploinsufficiency
91 tissue fibrosis and lymphatic dysfunction in lymphedema and that inhibition of Th2 differentiation ma
92 thogenesis of many human diseases, including lymphedema and tumor metastasis.
93 undertaken to examine patient perceptions of lymphedema and use of precautionary behaviors several ye
94 her 15 unrelated microcephalic probands with lymphedema and/or chorioretinopathy identified additiona
95 osomal-dominant microcephaly associated with lymphedema and/or chorioretinopathy.
96 s correlated positively with the severity of lymphedema (and presumed inflammation) in filarial-disea
97 ild lymphedema, 12% reported moderate/severe lymphedema, and 2% reported chronically moderate/severe
98 BrCa survivors, 8.1% self-reported diagnosed lymphedema, and 37.2% self-reported arm symptoms.
99 patients reporting arm swelling had measured lymphedema, and 5% of patients reporting no arm swelling
100 L) among working-age women, the incidence of lymphedema, and associated risk factors.
101 e recently identified to cause microcephaly, lymphedema, and chorioretinal dysplasia (MLCRD) as well
102 e formation in lymphatic collecting vessels, lymphedema, and chylothorax.
103 ts molecular regulation during inflammation, lymphedema, and lymphatic metastasis.
104 utation is associated with immunodeficiency, lymphedema, and myelodysplastic syndrome.
105 incidence of long-term side effects, notably lymphedema, and the procedure is of no therapeutic benef
106 ymphatic development, the pathophysiology of lymphedema, and the role of leukotrienes in lymphedema p
107 nt of various human diseases such as cancer, lymphedema, and tissue allograft rejection.
108 disease, obesity, cancer, and cancer-related lymphedema are highlighted.
109 ue node metastases, axillary recurrence, and lymphedema as measured by volume displacement.
110  surgery were prospectively screened for arm lymphedema as quantified by the weight-adjusted volume c
111                        Using mouse models of lymphedema, as well as clinical lymphedema specimens, we
112       The difference between the two groups' lymphedema, assessed by arm measurements at 30 days (P =
113 rger syndrome, an autosomal dominant primary lymphedema associated with a predisposition to acute mye
114           We sought to determine the risk of lymphedema associated with immediate breast reconstructi
115 pression of several molecules, including the lymphedema-associated transcription factor FOXC2.
116                   There was no difference in lymphedema at any time point.
117                 Thirteen women had prevalent lymphedema at baseline.
118 005 and 2013 were prospectively screened for lymphedema at our institution, with 22.2 months' median
119 ated in a number of chronic diseases such as lymphedema, atherosclerosis, and cancer.
120  into therapies for conditions as diverse as lymphedema, autoimmunity, and cancer.
121 the economic burden of breast cancer-related lymphedema (BCRL) among working-age women, the incidence
122 and risk of developing breast cancer-related lymphedema (BCRL) in patients who underwent axillary lym
123 nd rate of infections likely associated with lymphedema between a woman with BCRL and a matched contr
124 postoperative recovery between the 2 groups (lymphedema breast reconstruction and breast reconstructi
125 verage operation time was 426 minutes in the lymphedema breast reconstruction group and 391 minutes i
126 ckade prevents initiation and progression of lymphedema by decreasing tissue fibrosis and significant
127 cacy in ameliorating experimental mouse tail lymphedema by enhancing lymphatic vessel regeneration.
128  T cells play a key role in the pathology of lymphedema by promoting tissue fibrosis and inhibiting l
129 iopsy use and 5-year cumulative incidence of lymphedema by race.
130 y account for about one third of all primary lymphedema cases, underscoring the existence of addition
131 implicate it as a candidate gene for primary lymphedema caused by valve defects.
132 dred inheriting a unique autosomal-recessive lymphedema-choanal atresia syndrome.
133 clerosing cholangitis and was diagnosed with lymphedema cholestasis syndrome (LCS).
134 rocephaly and lymphedema from a microcephaly-lymphedema-chorioretinal-dysplasia cohort.
135 ilial forms of primary lymphedema, secondary lymphedema, chylothorax and chylous ascites, lymphatic m
136 resided in the West were more likely to have lymphedema claims than those in the Northeast (OR = 2.05
137 ted as cancer-related and non-cancer-related lymphedema cohorts.
138 reconstruction does not increase the risk of lymphedema compared to mastectomy alone.
139 ociated with a significantly reduced risk of lymphedema compared to no reconstruction.
140 ostsurgical edema and significantly less paw lymphedema compared with vehicle-treated animals at all
141                Of the 654 arms, 83 developed lymphedema, defined as a WAC >/= 10% relative to baselin
142 sive drug, is highly effective in preventing lymphedema development and treating established lymphede
143 e that debilitating and persistent preputial lymphedema develops after a prepuce-sparing penile deglo
144 he prepuce can at times be preserved even if lymphedema develops.
145 s, or lymphatic vessel obstruction can cause lymphedema, disfiguring tissue swelling often associated
146                                      Because lymphedema distichiasis is believed to be caused by lymp
147            Mutations in the FOXC2 gene cause lymphedema distichiasis, an inherited primary lymphedema
148 genital fibrosis of the extraocular muscles, lymphedema-distichiasis syndrome, neurofibromatosis type
149                       As FOXC2 is mutated in lymphedema-distichiasis syndrome, our data also undersco
150 econd row of eyelashes is a feature of human lymphedema-distichiasis syndrome, which is associated wi
151 ranscription factor that is mutated in human lymphedema-distichiasis syndrome.
152  causes congenital lymphatic dysfunction and lymphedema due to defective lymphatic vessel patterning
153 ssociated with a higher probability of later lymphedema (eg, hazard ratio for jewelry too tight = 7.3
154 en genes have already been linked to primary lymphedema, either isolated, or as part of a syndrome.
155 undation for clinical investigations whereby lymphedema etiogenesis and therapies may be interrogated
156 me are strongly linked to a history of fetal lymphedema, evidenced by the presence of neck webbing an
157 r both comparisons) and a lower incidence of lymphedema exacerbations as assessed by a certified lymp
158 ility in the study of diseases as diverse as lymphedema, filariasis, transplant rejection, obesity, a
159                Among the 238 affected women, lymphedema first occurred within 2 years of diagnosis in
160 duals with a combination of microcephaly and lymphedema from a microcephaly-lymphedema-chorioretinal-
161 lymphedema or arm symptoms without diagnosed lymphedema had lower physical and mental HRQOL compared
162 esults with the use of VLNT for treatment of lymphedema have been largely positive, further explorati
163                     Patients who suffer from lymphedema have impaired immunity and, as a result, are
164 echanisms by which GATA2 mutations result in lymphedema have not been characterized.
165 C2 are dominantly associated with late-onset lymphedema; however, the precise role of FOXC2 and a clo
166    Arm circumference measurements documented lymphedema in 5% of SLNB alone patients, compared with 1
167  the lifestyle and clinical risk factors for lymphedema in a cohort of patients who underwent bilater
168 roach to the management of treatment-induced lymphedema in cancer survivors.
169 sed as a preventative agent for postsurgical lymphedema in humans.
170 egulation of GATA2, which has been linked to lymphedema in patients with Emberger syndrome.
171 ymphedema distichiasis, an inherited primary lymphedema in which a significant number of patients hav
172  assumption that it would reduce the risk of lymphedema in women with breast cancer.
173  assumption that it would reduce the risk of lymphedema in women with breast cancer.
174 quivalence margin was defined as doubling of lymphedema incidence.
175 s expressed in tissue components affected by lymphedema, including epidermis, lymphatics, and blood v
176 is necessary for the pathological changes of lymphedema, including fibrosis, adipose deposition, and
177  system in edema, genetic aspects of primary lymphedema, infection (cellulitis/erysipelas), Crohn's d
178 olved in many pathological processes such as lymphedema, inflammatory diseases, and tumor metastasis.
179 s that although cellulitis increases risk of lymphedema, ipsilateral blood draws, injections, blood p
180                                              Lymphedema is a common complication that occurs after br
181                                              Lymphedema is a complication of cancer treatment occurri
182                                              Lymphedema is a debilitating condition that often result
183                                    Secondary lymphedema is a debilitating condition, and genetic fact
184                                              Lymphedema is a dreaded complication of cancer treatment
185                                      Primary lymphedema is due to developmental and/or functional def
186        The prevalence and clinical burden of lymphedema is known to be increasing.
187                                              Lymphedema is the clinical manifestation of defects in l
188 uman analog is mutated in some families with lymphedema, is also highly enriched in a subset of endot
189 to determine whether improvement of filarial lymphedema (LE) by doxycycline is restricted to patients
190                       PURPOSE Cancer-related lymphedema (LE) is an incurable condition associated wit
191 uineous family with two children affected by lymphedema, lymphangiectasia and distinct facial feature
192 of pathological tissue changes that occur in lymphedema may be a viable treatment strategy for this d
193 the time of surgery, or have upper extremity lymphedema may be less likely to undergo repeated mammog
194 phatic drainage after injection of MSCs in a lymphedema model indicates that MSCs play a role in lymp
195          We used an experimental murine tail lymphedema model where sustained fluid stasis was genera
196                                  In a murine lymphedema model, galectin-1(-/-) animals had increased
197 es lymphatic regeneration in an experimental lymphedema model, presenting it as a promising novel the
198  GATA2 mutation is associated with deafness, lymphedema, mononuclear cytopenias, infection, myelodysp
199 e than a quarter of the incidence of primary lymphedema, mostly of inherited forms.
200 ma was low among survivors without diagnosed lymphedema (n = 1,183).
201  following three survivor groups: women with lymphedema (n = 104), women with arm symptoms without di
202 ), women with arm symptoms without diagnosed lymphedema (n = 475), and women without lymphedema or ar
203 we assigned a score indicating the degree of lymphedema (none, mild, or moderate/severe) to each mont
204 s included the incidence of exacerbations of lymphedema, number and severity of lymphedema symptoms,
205 %) of bilateral lower extremity inflammatory lymphedema occurred during the first 120 hours of traini
206                                      Primary lymphedema occurs as a result of aberrations in the deve
207 ving 141 breast-cancer survivors with stable lymphedema of the arm.
208 ould like to know what she can do to prevent lymphedema on her upcoming flight to Vienna.
209                                              Lymphedema onset was associated with pronounced infiltra
210 utations, is the key predisposing factor for lymphedema onset.
211 osed lymphedema (n = 475), and women without lymphedema or arm symptoms (n = 708).
212 ultivariate adjustment, women with diagnosed lymphedema or arm symptoms without diagnosed lymphedema
213 and mental HRQOL compared with women without lymphedema or arm symptoms.
214 e impaired immune responses in patients with lymphedema or following lymphatic injury remain unknown.
215 ically tractable system for the treatment of lymphedema or inhibition of tumor metastasis.
216 s that involve the lymphatic system, such as lymphedema or lymphatic metastasis.
217                                The impact of lymphedema or related arm symptoms on health-related qua
218  by mycobacterial infection, myelodysplasia, lymphedema, or aplastic anemia that progress to myeloid
219 quent long-term effects (eg, second cancers, lymphedema, osteoporosis).
220 nd, potentially, tumor lymphangiogenesis and lymphedema (pages 993-994).
221 r endogenous AM as a key factor in secondary lymphedema pathogenesis and provided experimental in viv
222  lymphedema, and the role of leukotrienes in lymphedema pathogenesis.
223 ermine the role of inflammatory responses in lymphedema pathology.
224                                              Lymphedema patients have decreased quality of life and r
225 ovides a basis for future clinical trials in lymphedema patients.
226 ising novel therapeutic agent to treat human lymphedema patients.
227 we have provided a molecular explanation for lymphedema predisposition in a subset of patients with g
228 scribed for women with breast-cancer-related lymphedema, preventing them from obtaining the well-esta
229 e lymphatic vasculature during the course of lymphedema progression.
230         A 52-year old patient presented with lymphedema, protein loosing enteropathy, and sclerosing
231 tion of GJC2 mutations as a cause of primary lymphedema raises the possibility of novel gap-junction-
232 ression analyses were performed to determine lymphedema rates and risk factors.
233                                              Lymphedema rates are dramatically reduced using ARM when
234                                    Objective lymphedema rates for SLNB and ALND were 0.8% and 6.5% re
235           We hypothesized that disconcerting lymphedema rates in both sentinel lymph node biopsy (SLN
236 mild lymphedema and 68% with moderate/severe lymphedema received treatment.
237 in a decreased incidence of exacerbations of lymphedema, reduced symptoms, and increased strength.
238               Among the cancer cohort, total lymphedema-related costs per patient, excluding medical
239                                              Lymphedema-related direct costs were measured for home h
240 in the noncancer cohort; P < .001 for both), lymphedema-related manual therapy (from 35.6% to 24.9%in
241                  Rates of cellulitis, use of lymphedema-related manual therapy, outpatient hospital v
242 Because of its morbidity and chronicity, arm lymphedema remains a concerning complication of breast c
243 is limited by the fact that the pathology of lymphedema remains unknown.
244 oportions of women with increasing degree of lymphedema reported symptoms (eg, jewelry too tight, tir
245                   Podoconiosis is a tropical lymphedema resulting from long-term barefoot exposure to
246 ompletely characterized, and their effect on lymphedema risk is not known.
247 gs may help to guide patient education about lymphedema risk reduction strategies for those who under
248 ratified by type of axillary surgery, 5-year lymphedema risk was 6.8% in whites undergoing SLNB (HR,
249               Overall, the 5-year cumulative lymphedema risk was 8.2% in whites and 12.3% in blacks (
250 LNB use contributed to racial disparities in lymphedema risk.
251  (P = 0.0324) were associated with increased lymphedema risk.
252 sels: sporadic and familial forms of primary lymphedema, secondary lymphedema, chylothorax and chylou
253              In breast-cancer survivors with lymphedema, slowly progressive weight lifting had no sig
254 ema exacerbations as assessed by a certified lymphedema specialist (14% vs. 29%, P=0.04).
255 se models of lymphedema, as well as clinical lymphedema specimens, we show that lymphatic stasis resu
256 tions in patients with chorioretinopathy and lymphedema suggests that EG5 is involved in the developm
257 ean (+/- SE) time between BrCa diagnosis and lymphedema survey was 8.1 +/- 0.2 years.
258                        For all patients with lymphedema symptoms (n = 9), we used a modified lower ab
259 er improvements in self-reported severity of lymphedema symptoms (P=0.03) and upper- and lower-body s
260 ations of lymphedema, number and severity of lymphedema symptoms, and muscle strength.
261                    Hennekam lymphangiectasia-lymphedema syndrome (Online Mendelian Inheritance in Man
262 ons that cause the Hennekam lymphangiectasia-lymphedema syndrome syndrome type1.
263 othelial markers and the study of congenital lymphedema syndromes.
264 of lymphatic vessels and valves causes human lymphedema syndromes.
265 times more likely to develop moderate/severe lymphedema than women with no lymphedema.
266 loped bilateral lower extremity inflammatory lymphedema that occurred during the 8(1/2)-week basic tr
267                                              Lymphedema, the most common lymphatic anomaly, involves
268 sed comparative effectiveness data regarding lymphedema therapeutic interventions have been poor.
269 lity was evaluated in patients with stage II lymphedema (three women; age range, 43-64 years) and in
270 These results have profound implications for lymphedema treatment as topical tacrolimus is FDA-approv
271 led equivalence trial (Physical Activity and Lymphedema trial) in the Philadelphia metropolitan area
272 lysis of data from the Physical Activity and Lymphedema Trial, we examined incident deterioration of
273            Five-year cumulative incidence of lymphedema was 42 (42%) per 100 women.
274         The two-year cumulative incidence of lymphedema was as follows: 4.08% [95% confidence interva
275              At median follow-up of 5 years, lymphedema was assessed in 936 women with clinically nod
276 resthesia, brachial plexus injury (BPI), and lymphedema was available for 821 patients.
277                                              Lymphedema was defined as 10% or more arm volume increas
278                                              Lymphedema was induced in the right hind limb after a si
279                                 Knowledge of lymphedema was low among survivors without diagnosed lym
280                                              Lymphedema was monitored at baseline and 6 months by mea
281                                              Lymphedema was more common after SLND + ALND but was sig
282 g our combined injury protocol, postsurgical lymphedema was observed 89% of the time.
283                                              Lymphedema was observed in 24.1% of the patients in the
284                                    Secondary lymphedema was prevented when circulating AM levels in A
285                                   At 1 year, lymphedema was reported subjectively by 13% (37 of 288)
286  group of families with dominantly inherited lymphedema, we identified six probands with unique misse
287 ether AM deficiency predisposes to secondary lymphedema, we used heterozygous adult mice with Adm gen
288 ptoms present before the first occurrence of lymphedema were associated with a higher probability of
289 me since surgery, and having upper extremity lymphedema were associated with lower mammography adhere
290 en previously treated for breast cancer with lymphedema were enrolled from six institutions.
291        Risk factors associated with measured lymphedema were greater body weight (P < .0001), higher
292                         Viral infections and lymphedema were more common in individuals with null mut
293                              Women with mild lymphedema were more than three times more likely to dev
294                     Toxic effects, including lymphedema, were increased in the cohorts receiving comp
295 e characteristic swelling of tissues, called lymphedema, which arises as a consequence of insufficien
296                                Patients with lymphedema who received an APCD who were commercially in
297  to demonstrate a significant improvement in lymphedema with decongestive therapy compared with a mor
298 ukemia (AML); and Emberger syndrome (primary lymphedema with MDS).
299 data may underestimate the true incidence of lymphedema, women with BCRL had a greater risk of infect
300 function of lymphatic valves underlies human lymphedema, yet the process of valve morphogenesis is po

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