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1 = 71) of the 76 episodes of candidiasis were mucocutaneous.
2 failure syndrome characterized by a triad of mucocutaneous abnormalities and a predisposition to canc
3 failure syndrome characterized by a triad of mucocutaneous abnormalities and an increased predisposit
4 congenita, a rare condition characterized by mucocutaneous abnormalities and bone marrow failure, is
5 characterized by multiple features including mucocutaneous abnormalities, bone marrow failure and an
6 lopecia in addition to the dramatic skin and mucocutaneous acantholysis observed in pemphigus patient
7 tivity, and oral ulcers, and 3 (23%) met the mucocutaneous ACR criteria plus positive antinuclear and
8 uring our study did so mostly by meeting the mucocutaneous ACR criteria, and the majority developed n
9  and pathologic description of the lichenoid mucocutaneous adverse effects seen in patients receiving
10    Of the 13 patients, 1 (8%) solely met the mucocutaneous American College of Rheumatology (ACR) cri
11 13-cRA reports and included mild to moderate mucocutaneous and flu-like symptoms; occasional signific
12 on Willebrand disease (VWD) with significant mucocutaneous and joint bleeding.
13 ient showed a significant improvement in the mucocutaneous and nail dyspigmentation.
14 s a dimorphic fungus responsible for chronic mucocutaneous and systemic infections.
15 s: (1) Langerhans-related, (2) cutaneous and mucocutaneous, and (3) malignant histiocytoses as well a
16 bone marrow failure syndrome associated with mucocutaneous anomalies, pulmonary fibrosis, and cirrhos
17 ders suggest that autoantibodies to specific mucocutaneous antigens are involved.
18 l-mediated, cytotoxic reaction involving the mucocutaneous areas.
19 ly exclusive pathways underlying immunity to mucocutaneous as opposed to invasive fungal infections.
20 molysis bullosa acquisita (EBA) is a chronic mucocutaneous autoimmune skin blistering disease.
21 ly tested, however, acute major bleeding and mucocutaneous bleeding during chronic administration wer
22            We investigated the cause of mild mucocutaneous bleeding in a 14-year-old male patient (P1
23 udied a 16-year-old white male with lifelong mucocutaneous bleeding manifestations and abnormal plate
24  is characterized by low platelet counts and mucocutaneous bleeding.
25 ers of platelet function cause petechiae and mucocutaneous bleeding.
26 ofiban for 30 days reported episodes of mild mucocutaneous bleeding.
27 molysis bullosa is an incurable, often fatal mucocutaneous blistering disease caused by mutations in
28 ne pemphigoid or cicatricial pemphigoid is a mucocutaneous blistering disease characterized by autoan
29 phigus vulgaris (PV) is a potentially lethal mucocutaneous blistering disease characterized by cell-c
30 s vulgaris is a potentially fatal autoimmune mucocutaneous blistering disease.
31 garis (PV) is a potentially fatal autoimmune mucocutaneous blistering disease.
32 nt of CVA6 as the causative agent for severe mucocutaneous blistering reactions mimicking SCAR.
33 s study, we present a patient with extensive mucocutaneous blisters, epidermolytic palmoplantar kerat
34  autoantibodies to type VII collagen causing mucocutaneous blisters.
35 alpha/beta that causes platelet dysfunction, mucocutaneous blood loss and suppression of erythropoies
36 ty to take clopidogrel 75 mg daily without a mucocutaneous, bronchial, or anaphylactic response.
37  cells are also critical in host immunity to mucocutaneous candida infections and Staphylococcus aure
38                        Patients with chronic mucocutaneous candidiasis (CMC) are selectively unable t
39                                      Chronic mucocutaneous candidiasis (CMC) is characterized by recu
40 have recently been shown to underlie chronic mucocutaneous candidiasis (CMC), while inborn errors of
41 such as disseminated candidiasis and chronic mucocutaneous candidiasis (CMC).
42 ukin-17F (IL-17F) or IL-17RA display chronic mucocutaneous candidiasis (CMC).
43 matophyte infections and suffer with chronic mucocutaneous candidiasis (CMC).
44 ial disease (hypomorphic alleles) to chronic mucocutaneous candidiasis (CMC; hypermorphic alleles).
45 rge family in which a combination of chronic mucocutaneous candidiasis (fungal infections of the skin
46                                              Mucocutaneous candidiasis and dermatophyte infections oc
47 ator of transcription 1 (STAT1) with chronic mucocutaneous candidiasis and PML was reported previousl
48  linkage region on chromosome 2p for chronic mucocutaneous candidiasis and thyroid disease, previousl
49 cells; meanwhile, some patients with chronic mucocutaneous candidiasis disease might also have viral
50 tor of transcription 1 (STAT1) cause chronic mucocutaneous candidiasis disease.
51 nti-IL-17F, or anti-IL-22 autoantibodies and mucocutaneous candidiasis in the setting of either APECE
52 ciency (AI), hypoparathyroidism, and chronic mucocutaneous candidiasis plus autoantibodies neutralizi
53 ients with unusual susceptibility to chronic mucocutaneous candidiasis resulting from T(H)17 deficien
54         Data on patients affected by chronic mucocutaneous candidiasis underscore the preponderant ro
55  yeast infections and development of chronic mucocutaneous candidiasis were extensively studied.
56 d clinical manifestations, including chronic mucocutaneous candidiasis, AI, and asplenia, respectivel
57 matoceles, eczema, staphylococcal abscesses, mucocutaneous candidiasis, and abnormalities of bone and
58 ponses, improved TH17 differentiation, cured mucocutaneous candidiasis, and maintained remission of i
59 rized by multiple endocrine failure, chronic mucocutaneous candidiasis, and various ectodermal defect
60  in IL17F and IL17R in patients with chronic mucocutaneous candidiasis, as well as neutralizing autoa
61  mutations have been associated with chronic mucocutaneous candidiasis, but the role of CARD9 in inte
62 eficiency in mice or humans leads to chronic mucocutaneous candidiasis, but the specific downstream m
63 rent bacterial infections, viral infections, mucocutaneous candidiasis, cutaneous warts, and skin abs
64                     In patients with chronic mucocutaneous candidiasis, disease-associated polymorphi
65                     In patients with chronic mucocutaneous candidiasis, gain-of-function STAT1 mutati
66 autoimmune disorder characterized by chronic mucocutaneous candidiasis, hypoparathyroidism, and adren
67 pecies infection, Norwegian scabies, chronic mucocutaneous candidiasis, hypothyroidism, and esophagea
68           About 25% of patients also display mucocutaneous candidiasis, probably owing to impaired in
69 nt, both subjects with mosaicism had chronic mucocutaneous candidiasis, suggesting that candidiasis i
70 risingly, it is also associated with chronic mucocutaneous candidiasis, through as yet undetermined m
71 -17A and interleukin-17F (IL-17A/F) underlie mucocutaneous candidiasis, whereas inborn errors of inte
72 utations, including recurrent infections and mucocutaneous candidiasis, which are suggestive of TH17
73 iseases, including invasive tuberculosis and mucocutaneous candidiasis.
74 t linkage assignment of a dominant locus for mucocutaneous candidiasis.
75 dism, autoimmune adrenocortical failure, and mucocutaneous candidiasis.
76 hreatening autoimmune cytopenias and chronic mucocutaneous candidiasis.
77 entiation (STAT3, STAT1, CARD9) are prone to mucocutaneous candidiasis.
78 owever, they still had infections, including mucocutaneous candidiasis.
79  1 (STAT1) have been associated with chronic mucocutaneous candidiasis.
80                  Four patients had recurrent mucocutaneous candidiasis.
81 ive stomatitis (CUS) is a recently described mucocutaneous condition in which patients experience chr
82                                              Mucocutaneous discoloration induced by antiepileptic dru
83 e added to the list of drugs that can induce mucocutaneous discoloration.
84 ratin 14 (K14) promoter, developed GVHD-like mucocutaneous disease and weight loss following transfer
85                  KS develops as a multifocal mucocutaneous disease with subsequent spread to visceral
86 nts with advanced disease such as widespread mucocutaneous disease, lymphedema, and visceral disease
87 disease, such as in patients with widespread mucocutaneous disease, lymphedema, and visceral disease,
88 g mule deer (Odocoileus hemionus) exhibiting mucocutaneous disease.
89 ug for treatment against CD8 T-cell-mediated mucocutaneous diseases in patients with GVHD.
90                                      Certain mucocutaneous diseases present with painful, ulcerative,
91 crolysis (TEN) are rare but life-threatening mucocutaneous diseases.
92 significantly less frequent nonopportunistic mucocutaneous disorders and respiratory infections (P<.0
93 Cicatricial pemphigoid is one of a number of mucocutaneous disorders that can present in the oral cav
94 frequency of minor opportunistic infections, mucocutaneous disorders, and respiratory infections and
95 mon human colonizers with a species-specific mucocutaneous distribution.
96 luded generally mild to moderate fatigue and mucocutaneous dryness, moderate to severe neutropenia (3
97 that preferentially infect the cutaneous and mucocutaneous epithelia of vertebrates.
98                  HPV infects the squamous or mucocutaneous epithelium; hematogenic spread into other
99                              We describe the mucocutaneous features and histologic correlation in a p
100 ratosis congenita, typically with associated mucocutaneous features, and others (TERC and TERT) for m
101 one marrow failure syndrome characterized by mucocutaneous features.
102                      A detailed awareness of mucocutaneous findings associated with Zika virus infect
103 d with severe disseminated mycobacterial and mucocutaneous fungal infections and was ultimately cured
104 ly from that of Crohn disease (CD); however, mucocutaneous granulomatous lesions have not been consid
105 ted in two distinct clinical patterns; minor mucocutaneous hemorrhage and major hemoptysis.
106 hrombasthenia is clinically characterized by mucocutaneous hemorrhage with episodes of intracranial a
107 ms involved in host clearance of symptomatic mucocutaneous herpes simplex virus (HSV) infection are u
108 ils and macrophages, respectively, in native mucocutaneous host defenses to S. aureus.
109  famciclovir, and valacyclovir, treatment of mucocutaneous HSV is a practice of everyday medical care
110  through the posthealing phases of recurrent mucocutaneous HSV-2 infection.
111 srupt various cytokine pathways that control mucocutaneous immunity against Candida species, especial
112 indicate that human IL-17RC is essential for mucocutaneous immunity to C. albicans but is otherwise l
113                                              Mucocutaneous immunity to C. albicans requires T helper
114 tations in either STAT1 or STAT3 that affect mucocutaneous immunity to Candida and Staphylococcus spe
115                              In humans, both mucocutaneous immunity to Candida and systemic immunity
116  of IL-17 receptor A (IL-17RA) in preserving mucocutaneous immunity.
117  IL-17F depend on ACT1 to mediate protective mucocutaneous immunity.
118  a range of diseases from mild uncomplicated mucocutaneous infection to those that are life threateni
119 from an immunocompromised woman with chronic mucocutaneous infection with ACV-resistant HSV-1.
120 es a wide spectrum of diseases, ranging from mucocutaneous infections like oral thrush to disseminate
121 d fertile and only rarely develop the severe mucocutaneous infections or pulmonary inflammation chara
122 ssing all three selectins (ELP(-/-)) develop mucocutaneous infections that eventually lead to death.
123 amily with 2 siblings who have had recurrent mucocutaneous infections with Candida albicans and Staph
124 ukocyte adhesion deficiency characterized by mucocutaneous infections, plasma cell proliferation, hyp
125 sufficiency, hypoparathyroidism, and chronic mucocutaneous infections.
126 hway, conferring susceptibility to recurrent mucocutaneous infections.
127 fense mechanisms for resolution of S. aureus mucocutaneous infections.
128         KS causes significant morbidity from mucocutaneous involvement and mortality from complicatio
129 to 20.8%) had pulmonary KS in the absence of mucocutaneous involvement.
130 re was a focus of PCNA-positive cells in the mucocutaneous junction and a few scattered PCNA-positive
131  gland volume and a forward migration of the mucocutaneous junction anterior to the gland orifice; si
132 tival cells remained within 1 to 2 mm of the mucocutaneous junction at all postinjection intervals.
133  at progressively greater distances from the mucocutaneous junction in the animals killed at 1, 3, an
134          Long-term retention of label at the mucocutaneous junction indicates that slow-cycling stem
135                                          The mucocutaneous junction may provide a therapeutically sig
136                                          The mucocutaneous junction of the conjunctival epithelium is
137 counted in a series of 0.4-mm zones from the mucocutaneous junction of the eyelid, through the fornix
138 l epithelial stem cells are located near the mucocutaneous junction.
139 es, BrdU-labeled nuclei were retained at the mucocutaneous junction.
140 tibody-mediated blistering disease targeting mucocutaneous keratinocytes (KCs).
141                                Patients with mucocutaneous KS and tuberculosis-IRIS experienced great
142 ithout IRIS (+158 vs +53 cells/muL, P = .04, mucocutaneous KS; +261 vs +113, P = .04, tuberculosis).
143 ght a distinct biosignature in patients with mucocutaneous leishmaniasis (MCL) or localized cutaneous
144  localized cutaneous leishmaniasis (LCL) and mucocutaneous leishmaniasis (MCL).
145 nnia) braziliensis is the causative agent of mucocutaneous leishmaniasis (ML) in South America, and M
146 species responsible for the vast majority of mucocutaneous leishmaniasis cases.
147 tive vaccine candidate against VL as well as mucocutaneous leishmaniasis causing parasites.
148  sera from human patients with cutaneous and mucocutaneous leishmaniasis indicated that these individ
149           Appropriate regimens for New World mucocutaneous leishmaniasis need to be established, alth
150 t infection with L. braziliensis that causes mucocutaneous leishmaniasis.
151 virus (VZV) on 695 consecutive cutaneous and mucocutaneous lesion specimens.
152 characterized by the development of multiple mucocutaneous lesions and benign tumors, and enhanced ca
153 ons in the genital tract are responsible for mucocutaneous lesions and transmission and manifest as d
154  Laboratory diagnosis of HSV in cutaneous or mucocutaneous lesions has historically been performed wi
155                                   Therefore, mucocutaneous lesions in PV patients could be caused by
156                                              Mucocutaneous lesions of patients with ACV resistance co
157 ge of diseases in humans, from uncomplicated mucocutaneous lesions to life-threatening infections.
158                           Protection against mucocutaneous lesions was observed, but the dosage was p
159   Twenty-one patients (47%) had more than 50 mucocutaneous lesions, 14 (32%) had lymphedema, and none
160 ), promotes the rapid regression of advanced mucocutaneous lesions.
161  respiratory symptoms even in the absence of mucocutaneous lesions.
162 D-like disease manifested by weight loss and mucocutaneous lesions.
163 ually associated with a slightly more severe mucocutaneous lipoid proteinosis phenotype, but neurolog
164 and marrow transplantation can attenuate the mucocutaneous manifestations of the disease and improve
165 cterized by intestinal hamartomatous polyps, mucocutaneous melanin deposition, and increased risk of
166 by gastrointestinal hamartomatous polyps and mucocutaneous melanin pigmentation.
167 he alimentary tract and also is found on the mucocutaneous membranes of the healthy host.
168 the normal flora of the alimentary tract and mucocutaneous membranes, is the leading cause of invasiv
169 tment, remission was induced, notably in the mucocutaneous, musculoskeletal, cardiovascular/respirato
170   Protocol-defined "minor" bleeding, usually mucocutaneous, occurred in 0% to 32% of patients in the
171 f the patients developed fever, respiratory, mucocutaneous, or central nervous system manifestations.
172 cal disease that can present with cutaneous, mucocutaneous, or visceral manifestation and affects mil
173 fragments (scFvs) from a patient with active mucocutaneous pemphigus vulgaris.
174 drome associated with benign tumours, spotty mucocutaneous pigmentation, and endocrine overactivity (
175 hers syndrome (PJS), which includes aberrant mucocutaneous pigmentation, and somatic LKB1 mutations o
176 eutz-Jeghers syndrome (PJS) characterized by mucocutaneous pigmentation, predisposition to benign ham
177 pemphigus vulgaris (PV)-mucosal PV (mPV) and mucocutaneous PV (mcPV).
178                    One patient experienced a mucocutaneous reaction described as a Stevens-Johnson sy
179 patients who developed widespread blistering mucocutaneous reactions without any suspected drug causa
180                       Other features include mucocutaneous scarring and progressive poikiloderma.
181 tency within long-lived neurons and frequent mucocutaneous shedding.
182            HSV was detected in 29% and 4% of mucocutaneous specimens obtained during placebo and vala
183 (HSV-1) and HSV-2 DNA in 1,351 cutaneous and mucocutaneous specimens.
184 f the epithelial lineage, causing lesions on mucocutaneous surfaces, HSVs also establish latent infec
185 with biallelic RASGRP2 variants had abnormal mucocutaneous, surgical, and dental bleeding from childh
186 ntiation of HSV-1 and HSV-2 in cutaneous and mucocutaneous swab specimens.
187 ity of clinical features, ranging from small mucocutaneous telangiectases to life-threatening viscera
188 ascular disorder characterized by epistaxis, mucocutaneous telangiectases, and arteriovenous malforma
189 ch is characterized by recurrent nosebleeds, mucocutaneous telangiectases, and visceral AVMs and caus
190 , numerous secondary lesions on the skin and mucocutaneous tissues, severe respiratory disease, death
191    Both regimens were quite toxic, with more mucocutaneous toxicity in the FAP arm and more myelosupp
192 ut an increase in cardiac toxicity, although mucocutaneous toxicity was more common.
193 Dyskeratosis congenita is characterized by a mucocutaneous triad, bone marrow failure (BMF), and pres
194 (n=13) and FS (n=15) patients, and in 79% of mucocutaneous-type PV patients (n=33), but in none of th
195 hic extranodal LPD were classified as EBV(+) mucocutaneous ulcer.
196 pectively, and 100% for patients with EBV(+) mucocutaneous ulcer.
197 stigated the etiology of autosomal-dominant, mucocutaneous ulceration in a family whose proband was d
198                     The treatment of chronic mucocutaneous ulceration is challenging, and only some p
199 pes simplex virus 1 (HSV-1) causes recurrent mucocutaneous ulcers and is the leading cause of infecti
200 g specific types of fungal infections (e.g., mucocutaneous versus systemic).
201 in IL-12Rbeta1 may have candidiasis, usually mucocutaneous, which is frequently recurrent or persiste

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