ライフサイエンスコーパス: SJS

1 SJS is an autosomal recessive skeletal dysplasia charact

2 SJS, SJS/TEN, and TEN pose a substantial health care bur

3 SJS/TEN mostly manifest as a reaction to new drug use, b

4 SJS/TEN was associated with nonwhite race, particularly

5 emic Symptoms (DRESS) were suspected, with 2 SJS and 3 DRESS cases considered likely.

6 A total of 20 SJS and 12 TEN cases were included.

7 The studies included 227 SJS or TEN cases, 602 matched control subjects, and 2949

8 ity (15 drug-induced liver injury [DILI], 33 SJS/TEN, 20 hypersensitivity syndrome, and 46 nevirapine

9 nts, we calculated an incidence rate of 5.76 SJS/TEN cases per million person-years between 1995 and

10 re (SJS: 9.8 +/- 0.3 days, $21,437 +/- $807; SJS/TEN: 16.5 +/- 1.0 days, $58,954 +/- $5,238; TEN: 16.

11 Early AMT is an effective treatment of acute SJS.

12 in the phenotypic severity between DDSH and SJS.

13 apine-induced rash plus 3 with both DILI and SJS phenotype) and 155 age-, sex- and ethnicity-matched

14 Causality assessment for DILI and SJS/TEN was carried out with the Roussel Uclaf Causality

15 The basis of the association between SJS and ECT is considered, as well as the role of plausi

16 atistically significant associations between SJS/TEN and pre-existing depression, lupus erythematosus

17 pare the acute ocular manifestations between SJS and TEN.

18 on was common during the acute phase in both SJS and TEN.

19 to identify patients with diagnoses of both SJS and ECT.

20 ients were identified with diagnoses of both SJS and ECT.

21 ased cytotoxicity in in vitro models of both SJS/TEN (elicited by drug-specific antigen) and GVHD (el

22 ged length of stay and higher costs of care (SJS: 9.8 +/- 0.3 days, $21,437 +/- $807; SJS/TEN: 16.5 +

23 9 patients with ocular symptoms from chronic SJS who were referred for PROSE fitting evaluation.

24 g ophthalmic records of patients with either SJS (<30% body surface area involvement) or TEN (> = 30%

25 justed mortality was 4.8% for SJS, 19.4% for SJS/TEN, and 14.8% for TEN.

26 Mean adjusted mortality was 4.8% for SJS, 19.4% for SJS/TEN, and 14.8% for TEN.

27 modulating therapies or supportive care) for SJS/TEN were selected.

28 CARs were penicillins and cephalosporins for SJS/TEN and AGEP; glycopeptides for DRESS.

29 The most common reported etiologies for SJS/TENS were antibiotics (n = 25), ibuprofen (n = 15),

30 nternational experts, a case report form for SJS/TEN has been created to help standardize the collect

31 tion may represent the disease mechanism for SJS.

32 anguages looking for treatment proposals for SJS/TEN.

33 ents with epilepsy and gout, odds ratios for SJS/TEN were significantly increased only in the presenc

34 was found to markedly increase the risk for SJS (odds ratio [OR] = 17.52; 95% confidence interval, 3

35 sing systemic immunomodulating therapies for SJS/TEN.

36 on possible immunomodulating treatments for SJS/TEN and estimate their effects on mortality compared

37 sed systemic immunomodulating treatments for SJS/TEN, which is of great relevance for treating physic

38 those who have already suffered damage from SJS, but emphasis on the prevention of damage in the acu

39 ion, Clinical Modification codes to identify SJS, SJS/TEN, and TEN (n = 2,591, n = 502, and n = 564,

40 14 +/- 0.22 logMAR post-PROSE (P = .0007) in SJS patients.

41 0.05) comparing between the moderate (15% in SJS, 0% in TEN) and severe groups (20% in SJS, 33% in TE

42 in SJS, 0% in TEN) and severe groups (20% in SJS, 33% in TEN).

43 number of cases with mild involvement (5% in SJS, 42% in TEN, p = 0.01), while no statistically signi

44 rce of elevated enzymes, including MMP-9, in SJS and OCP tears.

45 The TIMP-1 levels were decreased in SJS and OCP patients when compared with those in control

46 9-to-TIMP-1 ratios were markedly elevated in SJS and OCP tears (SJS>OCP) when compared with those of

47 for improving visual acuity and function in SJS patients who failed conventional treatment.

48 The MMP activity was highest in SJS patients, whereas OCP patients and controls showed l

49 Ocular involvement in SJS, TEN, and Overlap syndrome is common and the ocular

50 wann cell physiology and suggest that PNH in SJS originates distally from synergistic actions of peri

51 th MPO, but it did not reach significance in SJS patients.

52 nd MPO levels were elevated significantly in SJS and OCP tears (SJS>OCP) when compared with controls.

53 were 69 cases of PPI-related DHR, including SJS/TEN (n=27) and DRESS (n=10).

54 between HLA-B*1502 and carbamazepine-induced SJS and TEN and that reported sufficient data for calcul

55 HLA-B*1502 allele and carbamazepine-induced SJS and TEN in Han-Chinese, Thai, and Malaysian populati

56 between HLA-B*1502 and carbamazepine-induced SJS and TEN was 79.84 (95% CI, 28.45-224.06).

57 he primary outcome was carbamazepine-induced SJS and TEN.

58 ocytes (CTLs) from patients with CBZ-induced SJS/TEN and analyzed the interaction between HLA-B and C

59 al correlations for CBZ-related drug-induced SJS/TEN.

60 iage as a risk factor for nevirapine-induced SJS/TEN in a Malawian HIV cohort.

61 son syndrome and toxic epidermal necrolysis (SJS/TEN) are rare but severe adverse reactions with high

62 son syndrome and toxic epidermal necrolysis (SJS/TEN), although a detailed description is lacking in

63 ty-five patients (50 eyes) with acute ocular SJS who presented within 4 weeks of onset of symptoms we

64 able ocular surface in cases of acute ocular SJS.

65 Overall, 40% of SJS and 75% of TEN patients had acute ocular surface inf

66 opriate and useful" for documenting cases of SJS/TEN, making it more reliable and valuable for future

67 skeletal disease phenotype characteristic of SJS patients.

68 he medical record revealed that diagnosis of SJS preceded that of ECT.

69 l observational study on the epidemiology of SJS/TEN contributes to the understanding of this still u

70 e observational study on the epidemiology of SJS/TEN using data from the UK-based Clinical Practice R

71 32Y mutation as the sole causative factor of SJS in the human family harboring this alteration and im

72 h 2015, 36 (4.8%) had associated features of SJS/TEN.

73 -expected rate in patients with a history of SJS.

74 luded 86 patients (167 eyes) with history of SJS/TEN who underwent PROSE treatment from January 1, 20

75 ed 35 males and 51 females with a history of SJS/TENS; median age was 36 years.

76 The mean estimated incidences of SJS, SJS/TEN, and TEN were 9.2, 1.6, and 1.9 per million

77 gement of the acute ocular manifestations of SJS and TEN.

78 We therefore studied a mouse model of SJS to determine whether a role for perlecan in these fu

79 gth of stay, comorbidities, and mortality of SJS and TEN in US adults.

80 a quality based on an international panel of SJS/TEN experts who performed a Delphi consensus-buildin

81 n suggestive of resorption among patients of SJS was 36.7 months and among patients of chemical injur

82 o the eyes and eyelids in the acute phase of SJS can prevent the devastating scarring and visual prob

83 the chondrodystrophic myotonia phenotype of SJS is unknown.

84 ging, the severe, chronic ocular problems of SJS can be at least partially alleviated with autologous

85 ality findings to improve prognostication of SJS/TEN.

86 After remission of SJS/TEN, a complete ENT mucosal healing occurred in 36 p

87 The OR for absolute risk of SJS/TEN associated with carriage of HLA-C*04:01 was 5.17

88 and Asian patients were at a 2-fold risk of SJS/TEN when compared with white patients.

89 or dyspnea is observed at the acute stage of SJS/TEN.

90 ong signal for an increased risk of DRESS or SJS requires particular vigilance in telaprevir-treated

91 toprosthesis surgery in dry keratinized post-SJS eyes.

92 SJS, SJS/TEN, and TEN pose a substantial health care burden.

93 Clinical Modification codes to identify SJS, SJS/TEN, and TEN (n = 2,591, n = 502, and n = 564, respe

94 The mean estimated incidences of SJS, SJS/TEN, and TEN were 9.2, 1.6, and 1.9 per million adul

95 he relatively mild Schwartz-Jampel syndrome (SJS) and severe neonatal lethal dyssegmental dysplasia,

96 Schwartz-Jampel syndrome (SJS) is a form of PNH that is due to hypomorphic mutatio

97 developed to model Schwartz-Jampel syndrome (SJS), a skeletal disease resulting from decreased perlec

98 een HLA-B*1502 and Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) among carbamaz

99 Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threa

100 Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but l

101 Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but l

102 stering conditions Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN).

103 crolysis (TEN) and Stevens-Johnson Syndrome (SJS) are rare, acute, life-threatening dermatologic diso

104 eatments for acute Stevens-Johnson syndrome (SJS) as well as the emerging treatment options for patie

105 12 laminae) to the Stevens-Johnson syndrome (SJS) group.

106 By comparison, Stevens-Johnson syndrome (SJS) is a life-threatening severe cutaneous adverse reac

107 injury (DILI) and Stevens-Johnson syndrome (SJS) or toxic epidermal necrosis (TEN) is even rarer and

108 Three cases of Stevens-Johnson Syndrome (SJS), and 11 cases of Drug Reaction with Eosinophilia an

109 Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), and graft-versus

110 f SCARs, including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), drug rash with e

111 ed by PPI, such as Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), or drug rash wit

112 pine (CBZ)-induced Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) as a model to stud

113 elevated significantly in SJS and OCP tears (SJS>OCP) when compared with controls.

114 were markedly elevated in SJS and OCP tears (SJS>OCP) when compared with those of controls.

115 Unlike DDSH, the SJS mutations result in different forms of perlecan in r

116 ury group and 8 out of the 12 laminae in the SJS group.

117 Fatality was more frequent in the SJS/TEN group.

118 es of highly cited manuscripts pertaining to SJS/TEN.

119 th chronic ocular surface disease related to SJS/TEN, PROSE treatment offers sustained and significan

120 Among 551 validated SJS/TEN patients, we calculated an incidence rate of 5.7

121 for Sick Children between 2001 and 2011 with SJS, TEN, and Overlap syndrome were reviewed.

122 harboring only the mutation associated with SJS, displayed a mild phenotype, inconsistent with SJS.

123 DILI associated with SJS/TEN is rare and associated with a high death rate, p

124 ients who developed DILI in association with SJS/TEN from a registry of DILI patients from a single c

125 rience of DILI occurring in association with SJS/TEN including the etiologic agents, clinical and bio

126 h mild ocular involvement when compared with SJS, but no significant difference between the number of

127 sharing the histopathological features with SJS.

128 isplayed a mild phenotype, inconsistent with SJS.

129 Thus, it is crucial that all patients with SJS be evaluated by an ophthalmologist familiar with the

130 Heterozygous mutations in two patients with SJS either produced truncated perlecan that lacked domai

131 or Japanese race/ethnicity, no patients with SJS or TEN were carriers of the HLA-B*1502 allele.

132 onia and chondrodysplasia, and patients with SJS survive.

133 s study included 30 eyes of 30 patients with SJS-induced dry keratinized ocular surfaces; the patient

134 of perlecan in three unrelated patients with SJS.

135 l was noted to be higher among patients with SJS.

136 Retrospective study of 49 patients with SJS/TEN hospitalized in a referral care center from 2005

137 NA chimera on CTL responses in patients with SJS/TEN or GVHD.

138 systemic inflammation seen in patients with SJS/TEN or GVHD.

139 sitivity, such as that seen in patients with SJS/TEN, as well as the alloreactivity seen in patients

140 In patients with SJS/TEN, higher mortality was associated with old age an