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Drug-Induced Pemphigus

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1. Drug-Induced Pemphigus

Drug-Induced Pemphigus Drug-Induced Pemphigus Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Drug-Induced Pemphigus Drug-Induced (...) Pemphigus Aka: Drug-Induced Pemphigus , Drug-Triggered Pemphigus From Related Chapters II. Mechanism of Drug-Induced Pemphigus Sulfhydryl groups lyse disulfide bonds Results in formation III. Causes of Drug-Induced Pemphigus (5% with ) IV. Signs of Drug-Induced Pemphigus follows medication use of >2 month duration Similar to ( ) Most cases are mild V. Differential Diagnosis of Drug-Induced Pemphigus Drug-Triggered Pemphigus (unmasks ) Gold Piroxicam Phenobarbital VI. Course Drug-Induced Pemphigus Remits

2018 FP Notebook

2. A new ex vivo human oral mucosa model reveals that p38MAPK inhibition is not effective to prevent autoantibody-induced mucosal blistering in pemphigus. (PubMed)

A new ex vivo human oral mucosa model reveals that p38MAPK inhibition is not effective to prevent autoantibody-induced mucosal blistering in pemphigus. Pemphigus vulgaris (PV) is an autoimmune disease characterised by blister formation in the epidermis and oral mucosa due to loss of keratinocyte cohesion. Autoantibodies present in PV patients (PV-IgG) are known to primarily target desmoglein (Dsg) 1 and Dsg3 in desmosomes. The mucosal-dominant (mdPV) subtype of PV is caused by PV-IgG (...) autoantibodies against the cadherin-type adhesion molecule Dsg3. p38 mitogen-activated protein kinase (p38MAPK) signaling has been characterised as an important pathway downstream of PV-IgG binding and its inhibition is protective in ex vivo human skin. However, the role of p38MAPK in mdPV is unknown since no experimental model was available.Establish a human ex vivo oral mucosa culture and evaluate the p38MAPK dependency of blister formation and of ultrastructural alterations of desmosomes induced by mdPV

2019 British Journal of Dermatology

3. Rituximab (MabThera) Treatment of patients with moderate to severe pemphigus vulgaris.

Rituximab (MabThera) Treatment of patients with moderate to severe pemphigus vulgaris. Published 13 May 2019 Statement of advice SMC2193 rituximab 100mg Concentrate for Solution for Infusion (MabThera®) Roche Products Ltd 5 April 2019 ADVICE: in the absence of a submission from the holder of the marketing authorisation rituximab (MabThera®) is not recommended for use within NHSScotland. Indication under review: treatment of patients with moderate to severe pemphigus vulgaris. The holder (...) of the marketing authorisation has not made a submission to SMC regarding this product in this setting. As a result we cannot recommend its use within NHSScotland. Advice context: No part of this advice may be used without the whole of the advice being quoted in full. This advice represents the view of the Scottish Medicines Consortium and was arrived at after careful consideration and evaluation of the available evidence. It is provided to inform the considerations of Area Drug & Therapeutics Committees

2019 Scottish Medicines Consortium

4. Keratin Retraction and Desmoglein3 Internalization Independently Contribute to Autoantibody-Induced Cell Dissociation in Pemphigus Vulgaris (PubMed)

Keratin Retraction and Desmoglein3 Internalization Independently Contribute to Autoantibody-Induced Cell Dissociation in Pemphigus Vulgaris Pemphigus vulgaris (PV) is a potentially lethal autoimmune disease characterized by blister formation of the skin and mucous membranes and is caused by autoantibodies against desmoglein (Dsg) 1 and Dsg3. Dsg1 and Dsg3 are linked to keratin filaments in desmosomes, adhering junctions abundant in tissues exposed to high levels of mechanical stress (...) dissociation assays and were followed by a condensation of keratin filaments into thick bundles after several hours. Dsg3 internalization started at 90 min of PV-IgG treatment, thus following the early keratin changes. By inhibiting casein kinase 1 (CK-1), we provoked keratin alterations resembling the effects of PV-IgG. Although CK-1-induced loss of peripheral keratin network correlated with loss of cell cohesion and Dsg3 clustering in the membrane, it was not sufficient to trigger the internalization

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2018 Frontiers in immunology

5. Immunoadsorption of Desmoglein-3-Specific IgG Abolishes the Blister-Inducing Capacity of Pemphigus Vulgaris IgG in Neonatal Mice (PubMed)

Immunoadsorption of Desmoglein-3-Specific IgG Abolishes the Blister-Inducing Capacity of Pemphigus Vulgaris IgG in Neonatal Mice Pemphigus vulgaris (PV) is a potentially life-threatening autoimmune blistering disease which is associated with autoantibodies directed against two desmosomal proteins, desmoglein (Dsg) 3 and 1. Treatment of PV is rather challenging and relies on the long-term use of systemic corticosteroids and additional immunosuppressants. More recently, autoantibody-depleting (...) in a complete loss of pathogenicity when injected into neonatal mice. In contrast, injection of anti-Dsg3-specific IgG, eluted from the column, induced gross blistering in the mice. Our data clearly show that anti-Dsg3-specific IgG alone is pathogenic in vitro and in vivo, whereas Dsg3/1-depletion results in a complete loss of pathogenicity. Furthermore, our data suggest that Dsg-specific adsorption may be a suitable therapeutic modality to efficiently reduce pathogenic autoantibodies in patients

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2018 Frontiers in immunology

6. Immunological markers as predictors of developing steroid-induced diabetes mellitus in pemphigus vulgaris patients: An observational study. (PubMed)

Immunological markers as predictors of developing steroid-induced diabetes mellitus in pemphigus vulgaris patients: An observational study. The aim of this study was to evaluate the clinical importance of autoantibodies in pemphigus vulgaris patients who developed steroid-induced diabetes mellitus (SID) because of the glucocorticoid therapy of pemphigus.A total of 137 patients with pemphigus vulgaris were studied. Patients with SID and pemphigus were compared with those that had only pemphigus (...) . The variables recorded were: age at diagnosis, sex, body mass index, presence of diabetes mellitus (DM), cumulative cortisone dose, treatment duration, value of anti-desmoglein 1 and 3, and anti-glutamic acid decarboxylase autoantibodies.A total of 31 patients (22.62%) that developed steroid-induced DM were identified. Anti-glutamic acid decarboxylase autoantibodies were positive in 20.75% of patients with pemphigus vulgaris and in 25.75% of patients with pemphigus vulgaris and SID.The overall anti-glutamic

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2018 Medicine

7. British Association of Dermatologists guidelines for the management of pemphigus vulgaris

are con?ned to case reports and small case series in which cases of PV of vari- able severity may be included, often with other subtypes of pemphigus. Follow-up periods are often short, even in the lar- ger trials, and dosing schedules vary widely. Trial design is © 2017 British Association of Dermatologists British Journal of Dermatology (2017) 177, pp1170–1201 1172 Guidelines for the management of pemphigus vulgaris 2017, K.E. Harman et al.often poor, with different drug combinations used (...) bene?t is relatively limited because of their slower onset. They are rarely used alone to induce remission in PV. After disease control is achieved there follows a consolida- tion phase during which the drug doses used to induce dis- ease control are continued. The end of this consolidation phase is de?ned arbitrarily as being reached when 80% of lesions have healed, both mucosal and skin, and there have been no new lesions for at least 2 weeks. 47 This phase may be relatively short, but could

2017 British Association of Dermatologists

8. Inhibition of p38MAPK signaling prevents epidermal blistering and alterations of desmosome structure induced by pemphigus autoantibodies in human epidermis. (PubMed)

Inhibition of p38MAPK signaling prevents epidermal blistering and alterations of desmosome structure induced by pemphigus autoantibodies in human epidermis. Pemphigus vulgaris (PV) is a skin blistering disease caused by autoantibodies targeting the desmosomal adhesion proteins desmoglein (Dsg) 3 and 1. The mechanisms underlying pemphigus skin blistering are not fully elucidated but p38 mitogen-activated protein kinase (p38MAPK) activation is one of the signalling events necessary for full loss (...) of cell cohesion. However, it is unclear whether ultrastructural hallmarks of desmosome morphology as observed in patients' lesions are mediated by p38MAPK signalling.In this study, we tested the relevance of p38MAPK for blister formation and the ultrastructural changes induced by PV autoantibodies in human skin.Human skin samples were injected with IgG fractions of one patient suffering from mucocutaneous PV (mcPV-IgG), one from mucosal-dominant PV (mdPV-IgG) or AK23, a pathogenic monoclonal Dsg3

2017 British Journal of Dermatology

9. NUDT15 polymorphism and severe azathioprine-induced myelosuppression in a Chinese man with pemphigus vulgaris. (PubMed)

NUDT15 polymorphism and severe azathioprine-induced myelosuppression in a Chinese man with pemphigus vulgaris. 28733976 2018 12 20 1365-2133 178 1 2018 01 The British journal of dermatology Br. J. Dermatol. NUDT15 polymorphism and severe azathioprine-induced myelosuppression in a Chinese man with pemphigus vulgaris. e40-e41 10.1111/bjd.15840 Yan W W 0000-0002-6735-6066 Department of Dermatology and Venereology, West China Hospital, Sichuan University, Chengdu, Sichuan, China. Zhou Y H YH

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2017 British Journal of Dermatology

10. Pemphigus. (PubMed)

Pemphigus. Pemphigus consists of a group of rare and severe autoimmune blistering diseases mediated by pathogenic autoantibodies mainly directed against two desmosomal adhesion proteins, desmoglein (Dsg)1 and Dsg3 (also known as DG1 and DG3), which are present in the skin and surface-close mucosae. The binding of autoantibodies to Dsg proteins induces a separation of neighbouring keratinocytes, in a process known as acantholysis. The two main pemphigus variants are pemphigus vulgaris, which (...) often originates with painful oral erosions, and pemphigus foliaceus, which is characterised by exclusive skin lesions. Pemphigus is diagnosed on the basis of either IgG or complement component 3 deposits (or both) at the keratinocyte cell membrane, detected by direct immunofluorescence microscopy of a perilesional biopsy, with serum anti-Dsg1 or anti-Dsg3 antibodies (or both) detected by ELISA. Corticosteroids are the therapeutic mainstay, which have recently been complemented by the anti-CD20

2019 Lancet

11. Reviewing putative industrial triggering in pemphigus: cluster of pemphigus in the area near the wastewater treatment plant (PubMed)

Reviewing putative industrial triggering in pemphigus: cluster of pemphigus in the area near the wastewater treatment plant A range of pemphigus is relatively rare potentially fatal group of autoimmune blistering dermatoses. Usually, there is no apparent triggering, while in some predisposed patients there are alleged environmental/industrial inducing factors. In a short time period (4 years), we diagnosed 3 novel cases of pemphigus (1 pemphigus vulgaris, 1 pemphigus foliaceus and 1 shift from (...) pemphigus foliaceus into pemphigus vulgaris) at a clinical and laboratory level (ELISA, immunofluorescence studies). We discuss a possible common inducing mechanism as these patients inhabit one estate of the Poznan suburbia (Kozieglowy, population < 12,000), Greater Poland district, Poland, and review literature data on alleged pemphigus triggers. To the best of our knowledge, this is the first report exploring the putative association between pemphigus diseases and wastewater treatment plant

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2017 Advances in Dermatology and Allergology/Postȩpy Dermatologii i Alergologii

12. Pemphigus Autoantibodies Induce Blistering in Human Conjunctiva. (PubMed)

Pemphigus Autoantibodies Induce Blistering in Human Conjunctiva. The autoimmune blistering skin disease pemphigus vulgaris (PV) is caused by autoantibodies against desmosomal adhesion molecules. Patients may suffer conjunctival involvement, yet the underlying mechanisms are largely unclear. We characterized human and murine conjunctiva with respect to the PV autoantigens, and evaluated the effects and mechanisms of PV autoantibodies applied to human conjunctiva ex vivo.We obtained human (...) conjunctiva specimens from surgical explants and established a short-term culture model to study the alterations induced by antibody fractions of PV patients (PV-IgG). Furthermore, we applied a mouse model depleted of the desmosomal cadherin desmoglein 3 (Dsg3), the primary autoantigen in PV. Murine and human conjunctiva also was used to analyze the expression pattern of desmosomal proteins by immunostaining and Western blotting.Human and murine conjunctiva samples expressed the majority of desmosomal

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2016 Investigative Ophthalmology & Visual Science

13. Sarcoidosis following successful treatment of pemphigus vulgaris with rituximab: a rituximab-induced reaction further supporting B-cell contribution to sarcoidosis pathogenesis? (PubMed)

Sarcoidosis following successful treatment of pemphigus vulgaris with rituximab: a rituximab-induced reaction further supporting B-cell contribution to sarcoidosis pathogenesis? The anti-CD20 peripheral B-cell depleting monoclonal antibody, rituximab, has been shown to be a safe and effective treatment for refractory pemphigus vulgaris (PV), a potentially fatal autoimmune blistering disease. We report a patient who developed skin nodules and arthralgias following successful treatment (...) -rituximab period and the immunological environment described in patients with idiopathic sarcoidosis, strongly implicates exposure to rituximab as the trigger for sarcoidosis development in our patient. We propose that rituximab-induced sarcoidal granulomas may be a rare adverse effect of treatment with this medication, providing further support for an important role of B cells in the pathogenesis of sarcoidosis. With better understanding of the circumstances surrounding sarcoidosis development

2016 Clinical & Experimental Dermatology

14. Abnormal uterine bleeding induced by glucocorticoid treatment for pemphigus: Case series and proposed treatment algorithm (PubMed)

Abnormal uterine bleeding induced by glucocorticoid treatment for pemphigus: Case series and proposed treatment algorithm Glucocorticoids are the first-line treatment option for pemphigus. Moreover, abnormal uterine bleeding (AUB) is a rarely reported side effect of glucocorticoid treatment that usually manifests as abnormal and excessive endometrial bleeding; in fact, AUB can be induced by the systemic or topical application of glucocorticoids. In the present report, we describe the cases of 3 (...) patients with pemphigus who developed AUB following glucocorticoid administration. It is important to note that the administration mode of glucocorticoids, and the onset time and duration of AUB differed among these patients. Thus, we propose the following treatment algorithm for AUB following glucocorticoid administration: 1. perform a gynecological and physical examination to exclude organic diseases. 2. continue glucocorticoid treatment. 3. if AUB persists, change the mode of administration

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2016 Saudi medical journal

15. The use of biological agents in the treatment of oral lesions due to pemphigus, mucous membrane pemphigoid (MMP), oral lichen planus (OLP), recurrent aphthous ulcers and Beh‡et's disease: a systematic review

The use of biological agents in the treatment of oral lesions due to pemphigus, mucous membrane pemphigoid (MMP), oral lichen planus (OLP), recurrent aphthous ulcers and Beh‡et's disease: a systematic review Print | PDF PROSPERO This information has been provided by the named contact for this review. CRD has accepted this information in good faith and registered the review in PROSPERO. The registrant confirms that the information supplied for this submission is accurate and complete. CRD bears (...) are used to explore between-study heterogeneity and can provide insight into the relationship between study characteristics (e.g. species, sex or drug class or dose) and effect size. They should be considered hypothesis-generating. Ideally, a threshold describing the number of studies per subgroup required for analysis should be specified. For further guidance please refer to the and to pre-clinical meta-analysis. Example: The following study characteristics will be examined as potential source

2019 PROSPERO

16. Clinical and immunological profiles in 17 Japanese patients with drug-induced pemphigus studied at Kurume University. (PubMed)

Clinical and immunological profiles in 17 Japanese patients with drug-induced pemphigus studied at Kurume University. Drug-induced pemphigus (DIP) shows clinical, histopathological and immunological features of pemphigus. However, little is known about immunological profiles in DIP.To characterize clinical and immunological profiles in patients with DIP.We studied 17 Japanese patients with DIP who were treated at Kurume University Hospital or who consulted from other hospitals between 1997 (...) and 2012. Complicated diseases, clinical and histopathological manifestations, responsible drugs and findings in immunofluorescence, enzyme-linked immunosorbent assays (ELISAs), immunoblotting (IB) and prognosis were analysed.Eight of the 17 patients with DIP showed pemphigus foliaceus-like appearance, three showed pemphigus herpetiformis-like appearance, and six showed atypical bullous lesions. Responsible drugs were thiol-containing drugs in 16 patients (bucillamine in nine cases, d-penicillamine

2014 British Journal of Dermatology

17. Pemphigus and mucous membrane pemphigoid: An update from diagnosis to therapy. (PubMed)

Pemphigus and mucous membrane pemphigoid: An update from diagnosis to therapy. Pemphigus diseases (PDs) and mucous membrane pemphigoid (MMP) are a group of immune-mediated mucocutaneous disorders clinically characterized by the formation of blisters, erosions and ulcers. The skin and mucous membranes are predominantly affected, with the oropharyngeal mucosa as the initially involved site. Ocular involvement is also a frequent feature of these diseases. Because of the considerable overlap (...) in their clinical presentations, the diagnosis of PDs vs. MMP can be challenging. A recognition of their specific immunological and histopathologic features is crucial in the differential diagnosis. Treatment modalities include systemically administered corticosteroids, steroid-sparing immunosuppressive agents, and biologic therapies (rituximab, intravenous immunoglobulins, and anti-tumor necrosis factor agents). Topical, oral, conjunctival, or intralesional corticosteroids as well as anti-inflammatory drugs

2019 Autoimmunity reviews

18. The involvement of ADAM10 in mucocutaneous pemphigus vulgaris acantholysis depends on the autoantibody profile in each patient. (PubMed)

The involvement of ADAM10 in mucocutaneous pemphigus vulgaris acantholysis depends on the autoantibody profile in each patient. Acantholysis in pemphigus vulgaris (PV) may be triggered by desmoglein (Dsg) and non-Dsg autoantibodies. The autoantibody profile of each patient results in distinct intracellular signaling patterns.Based on our previous findings, we aimed to elucidate whether PV acantholysis in a mouse model may be mediated by a disintegrin and metalloproteinase 10 (ADAM10 (...) ) activation.We used three PV-IgG fractions from different patients containing high or low levels of anti-Dsg1 and 3 antibodies, and the presence or not of anti-desmocollin (Dsc) antibodies, using a passive transfer mouse model of PV.Although all the PV-IgG fractions produced suprabasal acantholysis, only those containing anti-Dsg1/3, but not anti-Dsc2/3 antibodies, induced ADAM10 activation in a Src-dependent way, and an increase in the epidermal growth factor receptor (EGFR) ligands EGF and betacellulin

2019 British Journal of Dermatology

19. The clinical, immunological and pathological features for relapse of pemphigus herpetiformis: a univariate analysis of 26 cases. (PubMed)

The clinical, immunological and pathological features for relapse of pemphigus herpetiformis: a univariate analysis of 26 cases. Pemphigus herpetiformis (PH) is a rare autoimmune blistering disease that accounts for only about 7% of all pemphigus patients1 . Various factors may contribute to PH relapse that requires hospitalization and reintroduction of a high-dose of the first-line drugs such as glucocorticoids, potentially leading to severe complications and high medical cost. Our study

2019 British Journal of Dermatology

20. Pemphigus, Drug-Induced (Overview)

Pemphigus, Drug-Induced (Overview) Drug-Induced Pemphigus: Background, Pathophysiology, Epidemiology Edition: No Results No Results Please confirm that you would like to log out of Medscape. If you log out, you will be required to enter your username and password the next time you visit. https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTA2MzY4NC1vdmVydmlldw== processing > Drug-Induced Pemphigus (...) Updated: Jun 28, 2017 Author: Chris G Adigun, MD, FAAD; Chief Editor: Dirk M Elston, MD Share Email Print Feedback Close Sections Sections Drug-Induced Pemphigus Overview Background Pemphigus is an autoimmune bullous disease characterized by blisters and erosions of the skin and mucous membranes. Several variants of the disease exist, including pemphigus vulgaris, pemphigus foliaceous, and drug-induced pemphigus. Patients with drug-induced pemphigus have autoantibodies that are either circulating

2014 eMedicine.com

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