Database : MEDLINE
Search on : Vasculitis [Words]
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[PMID]: 25298695
[Au] Autor:Hakim K; Boussada R; Chaker L; Ouarda F
[Ad] Address:Department of Pediatric Cardiology, La Rabta Hospital, Tunia, Tunisia....
[Ti] Title:Giant aortic arch aneurysm complicating Kawasaki's disease.
[So] Source:Ann Pediatr Cardiol;7(3):201-3, 2014 Sep.
[Is] ISSN:0974-2069
[Cp] Country of publication:India
[La] Language:eng
[Ab] Abstract:Kawasaki disease (KD) is a common acute vasculitis in pediatric population that usually involves small- and middle-sized arteries, commonly coronary arteries. Although the incidence and natural course of coronary aneurysms after KD are well documented in studies, related reports on peripheral arterial and aortic aneurysms are scarce. We report the occurrence of a giant aortic aneurysm involving the horizontal part of aortic arch in a 28-month-old boy diagnosed with KD. This complication was managed by steroids therapy in the beginning. Because of mechanical complication and potential risk of rupture, surgery was undertaken.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Cu] Class update date: 141011
[Lr] Last revision date:141011
[Da] Date of entry for processing:141009
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.4103/0974-2069.140845

  2 / 32331 MEDLINE  
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[PMID]: 24552284
[Au] Autor:Zhou Q; Yang D; Ombrello AK; Zavialov AV; Toro C; Zavialov AV; Stone DL; Chae JJ; Rosenzweig SD; Bishop K; Barron KS; Kuehn HS; Hoffmann P; Negro A; Tsai WL; Cowen EW; Pei W; Milner JD; Silvin C; Heller T; Chin DT; Patronas NJ; Barber JS; Lee CC; Wood GM; Ling A; Kelly SJ; Kleiner DE; Mullikin JC; Ganson NJ; Kong HH; Hambleton S; Candotti F; Quezado MM; Calvo KR; Alao H; Barham BK; Jones A; Meschia JF; Worrall BB; Kasner SE; Rich SS; Goldbach-Mansky R; Abinun M; Chalom E; Gotte AC; Punaro M; Pascual V; Verbsky JW; Torgerson TR
[Ad] Address:The authors' affiliations are listed in the Appendix.
[Ti] Title:Early-onset stroke and vasculopathy associated with mutations in ADA2.
[So] Source:N Engl J Med;370(10):911-20, 2014 Mar 6.
[Is] ISSN:1533-4406
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: We observed a syndrome of intermittent fevers, early-onset lacunar strokes and other neurovascular manifestations, livedoid rash, hepatosplenomegaly, and systemic vasculopathy in three unrelated patients. We suspected a genetic cause because the disorder presented in early childhood. METHODS: We performed whole-exome sequencing in the initial three patients and their unaffected parents and candidate-gene sequencing in three patients with a similar phenotype, as well as two young siblings with polyarteritis nodosa and one patient with small-vessel vasculitis. Enzyme assays, immunoblotting, immunohistochemical testing, flow cytometry, and cytokine profiling were performed on samples from the patients. To study protein function, we used morpholino-mediated knockdowns in zebrafish and short hairpin RNA knockdowns in U937 cells cultured with human dermal endothelial cells. RESULTS: All nine patients carried recessively inherited mutations in CECR1 (cat eye syndrome chromosome region, candidate 1), encoding adenosine deaminase 2 (ADA2), that were predicted to be deleterious; these mutations were rare or absent in healthy controls. Six patients were compound heterozygous for eight CECR1 mutations, whereas the three patients with polyarteritis nodosa or small-vessel vasculitis were homozygous for the p.Gly47Arg mutation. Patients had a marked reduction in the levels of ADA2 and ADA2-specific enzyme activity in the blood. Skin, liver, and brain biopsies revealed vasculopathic changes characterized by compromised endothelial integrity, endothelial cellular activation, and inflammation. Knockdown of a zebrafish ADA2 homologue caused intracranial hemorrhages and neutropenia - phenotypes that were prevented by coinjection with nonmutated (but not with mutated) human CECR1. Monocytes from patients induced damage in cocultured endothelial-cell layers. CONCLUSIONS: Loss-of-function mutations in CECR1 were associated with a spectrum of vascular and inflammatory phenotypes, ranging from early-onset recurrent stroke to systemic vasculopathy or vasculitis. (Funded by the National Institutes of Health Intramural Research Programs and others.).
[Mh] MeSH terms primary: Adenosine Deaminase/deficiency
Adenosine Deaminase/genetics
Intercellular Signaling Peptides and Proteins/deficiency
Intercellular Signaling Peptides and Proteins/genetics
Mutation
Stroke/genetics
Vascular Diseases/genetics
[Mh] MeSH terms secundary: Age of Onset
Animals
Disease Models, Animal
Endothelium, Vascular/pathology
Female
Fever/genetics
Humans
Male
Pedigree
Polyarteritis Nodosa/genetics
Sequence Analysis, DNA
Skin/pathology
Vasculitis/genetics
Vasculitis/pathology
Zebrafish
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Intercellular Signaling Peptides and Proteins); EC 3.5.4.4 (Adenosine Deaminase); EC 3.5.4.4 (CECR1 protein, human)
[Em] Entry month:1403
[Cu] Class update date: 141011
[Lr] Last revision date:141011
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:140306
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMoa1307361

  3 / 32331 MEDLINE  
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[PMID]: 23911962
[Au] Autor:Uchida T; Nagai K; Sato T; Iizuka N; Arito M; Takakuwa Y; Nakano H; Ooka S; Kurokawa MS; Suematsu N; Okamoto K; Ozaki S; Kato T
[Ad] Address:Clinical Proteomics and Molecular Medicine, St. Marianna University Graduate School of Medicine, 2-16-1 Sugao, Miyamae-ku, Kawasaki-shi, Kanagawa-ken, Japan.
[Ti] Title:Comparative proteomic analysis of neutrophils from patients with microscopic polyangiitis and granulomatosis with polyangiitis.
[So] Source:J Proteomics;91:259-69, 2013 Oct 8.
[Is] ISSN:1876-7737
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:UNLABELLED: Both microscopic polyangiitis (MPA) and granulomatosis with polyangiitis (GPA) belong to ANCA-associated vasculitis (AAV), in which neutrophils play a key role in their pathology. In this study, in order to discriminate between MPA and GPA, protein profiles of peripheral blood polymorphonuclear cells (PMNs) of 11 MPA patients and 9 GPA patients and 10 healthy controls (HC) were analyzed by 2D-DIGE. In all the 864 spots detected, intensity of 55 spots was significantly different (p<0.05) among the three groups by ANOVA. 31 out of the 55 spots were identified by mass spectrometry. Orthogonal partial-least-squares-discriminate analysis revealed that the abundance profile of the protein spots discriminated the AAV group from the HC group, and the MPA group from the GPA group completely. 13 protein spots were considered as biomarker candidates to distinguish between MPA and GPA. In those, spots whose intensity was higher in MPA than in GPA included actin with various pI values, while a considerable part of spots whose intensity was higher in GPA were proteins related with the activity of neutrophils. Among the candidate proteins, ROC analysis showed that a combination of neutrophil gelatinase-associated lipocalin and a-kinase anchor protein 7 isoforms beta had a high diagnostic potential. BIOLOGICAL SIGNIFICANCE: In this study, protein profiles of polymorphonuclear cells (PMNs) of microscopic polyangiitis (MPA) and granulomatosis with polyangiitis (GPA) patients and healthy controls (HC) were investigated by 2D-DIGE, and MS analysis. As a result, we found that the protein profiles of PMNs were useful for distinguishing between patients (MPA and GPA) and HC, and between patients with MPA and patients with GPA. Especially, we found that the 13 protein spots that consisted of 10 proteins considerably contributed to the discrimination between MPA and GPA. This is the first to demonstrate that protein profiles of PMNs are different among MPA, GPA and healthy control. The 10 proteins we identified in this study would be new biomarkers for the diagnosis of the diseases, and may be reflect the pathology difference between MPA and GPA.
[Mh] MeSH terms primary: Gene Expression Profiling
Microscopic Polyangiitis/blood
Neutrophils/metabolism
Vasculitis, Central Nervous System/blood
[Mh] MeSH terms secundary: A Kinase Anchor Proteins/metabolism
Acute-Phase Proteins/metabolism
Aged
Biological Markers/metabolism
False Positive Reactions
Female
Humans
Inflammation
Leukocytes, Mononuclear/metabolism
Lipocalins/metabolism
Male
Membrane Proteins/metabolism
Microscopic Polyangiitis/classification
Middle Aged
Proteomics
Proto-Oncogene Proteins/metabolism
Vasculitis, Central Nervous System/classification
[Pt] Publication type:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Name of substance:0 (A Kinase Anchor Proteins); 0 (AKAP7 protein, human); 0 (Acute-Phase Proteins); 0 (Biological Markers); 0 (LCN2 protein, human); 0 (Lipocalins); 0 (Membrane Proteins); 0 (Proto-Oncogene Proteins)
[Em] Entry month:1410
[Js] Journal subset:IM
[Da] Date of entry for processing:131111
[St] Status:MEDLINE

  4 / 32331 MEDLINE  
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[PMID]: 24363101
[Au] Autor:Kawai H; Banno S; Kikuchi S; Nishimura N; Nobata H; Kimura Y; Takezawa Y; Ogawa M; Suzuki K; Kitagawa W; Miura N; Imai H
[Ad] Address:Division of Nephrology and Rheumatology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Aichi, 480-1195, Japan.
[Ti] Title:Retrospective analysis of factors predicting end-stage renal failure or death in patients with microscopic polyangiitis with mainly renal involvement.
[So] Source:Clin Exp Nephrol;18(5):795-802, 2014 Oct.
[Is] ISSN:1437-7799
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:BACKGROUND: The aim of this study was to identify risk factors for end-stage renal failure (ESRF) or death in Japanese patients with microscopic polyangiitis (MPA) with renal involvement. METHODS: From 54 consecutive patients with systemic vasculitis based on Watt's algorithm, we retrospectively analyzed 39 MPA patients with renal involvement, including 19 (48.7 %) with renal-limited vasculitis. RESULTS: Thirty-three of 39 patients (84.6 %) demonstrated rapidly progressive glomerulonephritis, and 13 (33.3 %) developed ESRF; 8 of 13 required dialysis within 1 week. Thirteen (33.3 %) died during follow-up of more than 12 months, and 7 died during the first 6 months, mainly because of opportunistic infections. Overall survival at 6 and 12 months was 79.5 and 71.1 %, respectively. Serum creatinine levels did not differ significantly between survivors and non-survivors (P = 0.092). The mean Birmingham Vasculitis Activity Score, version 3 (BVAS v.3), was 16.2 ± 6.5, with a renal subscore of over 12 points in 82.1 %, and BVAS v.3 was marginally higher in non-survivors than survivors (P = 0.045). An age- and sex-adjusted Cox proportional hazards analysis demonstrated that neither the serum creatinine level (P = 0.277) nor BVAS v.3 (P = 0.188) at initial diagnosis was a risk factor for overall survival. The baseline serum creatinine cutoff value for discriminating between ESRF and non-ESRF was 4.6 mg/dl, with a sensitivity and specificity of 92.3 and 84.6 %, respectively. CONCLUSIONS: Survival rates do not relate to ESRF in MPA patients with mainly renal involvement. Although patients with ESRF required regular hemodialysis, longer survival can be achieved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s10157-013-0926-1

  5 / 32331 MEDLINE  
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[PMID]: 25164257
[Au] Autor:Gasim A
[Ti] Title:Cathelicidin antimicrobial peptide as a serologic marker and potential pathogenic factor in antineutrophil cytoplasmic antibody-associated vasculitis.
[So] Source:Arthritis Res Ther;16(1):105, 2014.
[Is] ISSN:1478-6362
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Antineutrophil cytoplasmic antibodies are associated with pauci-immune small-vessel vasculitis and crescentic glomerulonephritis. Cathelicidin LL37 is the human member of a family of antimicrobial peptides that are released from activated neutrophils and monocytes at sites of acute inflammation. Zhang and colleagues evaluated serum levels of cathelicidin LL37 and interferon-alpha in patients with antineutrophil cytoplasmic antibody-associated vasculitis (AAV) and glomerulonephritis. Increased levels of cathelicidin LL37 and interferon-alpha were associated with AAV patients, particularly those with glomerular crescent formation. Cathelicidin LL37 may also be involved in the pathogenesis of AAV and thus could be a target for novel therapy. Cathelicidin LL37 is a promising new biomarker for active AAV, including aggressive crescentic glomerulonephritis, and may prove to be both a prognostic marker and a guide for treatment.
[Pt] Publication type:COMMENT; EDITORIAL
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Process

  6 / 32331 MEDLINE  
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[PMID]: 25295199
[Au] Autor:Sran S; Sran M; Patel N; Anand P
[Ad] Address:Department of Medicine, Nassau University Medical Center, 2201 Hempstead Turnpike, East Meadow, NY 11554, USA....
[Ti] Title:Lupus enteritis as an initial presentation of systemic lupus erythematosus.
[So] Source:Case Rep Gastrointest Med;2014:962735, 2014.
[Is] ISSN:2090-6528
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Systemic lupus erythematosus (SLE) is an autoimmune disorder which can affect multiple organs and clinical presentation is often a myriad of symptoms; therefore, the index of suspicion should rise when evaluating patients with multiorgan symptomatology. Lupus enteritis is a distinct subset of SLE, defined as either vasculitis or inflammation of the small bowel, with supportive image and/or biopsy findings. The clinical picture of lupus enteritis is often nonspecific, with mild to severe abdominal pain, diarrhea, and vomiting being the cardinal manifestations. Although considered a form of visceral or serosal vasculitis, lupus enteritis is seldom confirmed on histology, making computerized tomography (CT) the gold standard for diagnosis. Lupus enteritis is generally steroid-responsive, and the route of administration is based on clinical status and organ involvement, with preference for intravenous (IV) route in flares with significant tissue edema. The following case describes a young woman presenting with lupus enteritis and lupus panniculitis as an initial manifestation of SLE, the utilization of abdominal CT in diagnosis, and current treatment protocols used for lupus enteritis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Cu] Class update date: 141010
[Lr] Last revision date:141010
[Da] Date of entry for processing:141008
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1155/2014/962735

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[PMID]: 24113796
[Au] Autor:Araujo JA
[Ad] Address:UNIVERSITY OF CALIFORNIA, LOS ANGELES.
[Ti] Title:HO-1 and CO: fighters vs sickle cell disease?
[So] Source:Blood;122(15):2535-6, 2013 Oct 10.
[Is] ISSN:1528-0020
[Cp] Country of publication:United States
[La] Language:eng
[Mh] MeSH terms primary: Anemia, Sickle Cell/drug therapy
Carbon Monoxide/pharmacology
Heme Oxygenase-1/metabolism
Hemoglobins/pharmacology
Maleimides/pharmacology
Membrane Proteins/metabolism
Polyethylene Glycols/pharmacology
Vasculitis/drug therapy
[Mh] MeSH terms secundary: Animals
Female
Humans
Male
[Pt] Publication type:COMMENT; JOURNAL ARTICLE
[Nm] Name of substance:0 (Hemoglobins); 0 (Maleimides); 0 (Membrane Proteins); 0 (Polyethylene Glycols); 0 (maleimide-polyethylene glycol-modified hemoglobin, MP4); 7U1EE4V452 (Carbon Monoxide); EC 1.14.99.3 (Heme Oxygenase-1); EC 1.14.99.3 (Hmox1 protein, mouse)
[Em] Entry month:1312
[Cu] Class update date: 141010
[Lr] Last revision date:141010
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:131011
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2013-08-521922

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[PMID]: 23908468
[Au] Autor:Belcher JD; Young M; Chen C; Nguyen J; Burhop K; Tran P; Vercellotti GM
[Ad] Address:Hematology, Oncology, and Transplantation, University of Minnesota Medical School, Minneapolis, MN; and.
[Ti] Title:MP4CO, a pegylated hemoglobin saturated with carbon monoxide, is a modulator of HO-1, inflammation, and vaso-occlusion in transgenic sickle mice.
[So] Source:Blood;122(15):2757-64, 2013 Oct 10.
[Is] ISSN:1528-0020
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Transgenic sickle mice expressing ß(S) hemoglobin have activated vascular endothelium in multiple organs that exhibits enhanced expression of NF-ĸB and adhesion molecules and promotes microvascular stasis in sickle, but not normal, mice in response to hypoxia/reoxygenation (H/R), or heme. Induction of heme oxygenase-1 (HO-1) or administration of its products, carbon monoxide (CO) or biliverdin, inhibits microvascular stasis in sickle mice. Infusion of human hemoglobin conjugated with polyethylene glycol and saturated with CO (MP4CO) markedly induced hepatic HO-1 activity and inhibited NF-ĸB activation and H/R-induced microvascular stasis in sickle mice. These effects were mediated by CO; saline or MP4 saturated with O2 (MP4OX) had little to no effect on H/R-induced stasis, though unmodified oxyhemoglobin exacerbated stasis. The HO-1 inhibitor, tin protoporphyrin, blocked MP4CO protection, consistent with HO-1 involvement in the protection afforded by MP4CO. MP4CO also induced nuclear factor-erythroid 2 p45-related factor 2 (Nrf2), an important transcriptional regulator of HO-1 and other antioxidant genes. In a heterozygous (hemoglobin-AS) sickle mouse model, intravenous hemin induced cardiovascular collapse and mortality within 120 minutes, which was significantly reduced by MP4CO, but not MP4OX. These data demonstrate that MP4CO induces cytoprotective Nrf2 and HO-1 and decreases NF-ĸB activation, microvascular stasis, and mortality in transgenic sickle mouse models.
[Mh] MeSH terms primary: Anemia, Sickle Cell/drug therapy
Carbon Monoxide/pharmacology
Heme Oxygenase-1/metabolism
Hemoglobins/pharmacology
Maleimides/pharmacology
Membrane Proteins/metabolism
Polyethylene Glycols/pharmacology
Vasculitis/drug therapy
[Mh] MeSH terms secundary: Anemia, Sickle Cell/metabolism
Anemia, Sickle Cell/mortality
Animals
Carbon Monoxide/metabolism
Disease Models, Animal
Female
Hemin/metabolism
Hemin/pharmacology
Hemoglobins/metabolism
Humans
Inflammation/drug therapy
Inflammation/metabolism
Inflammation/mortality
Male
Maleimides/metabolism
Mice
Mice, Transgenic
Microcirculation/drug effects
Microcirculation/physiology
NF-E2-Related Factor 2/metabolism
NF-kappa B/metabolism
Polyethylene Glycols/metabolism
Vasculitis/metabolism
Vasculitis/mortality
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Hemoglobins); 0 (Maleimides); 0 (Membrane Proteins); 0 (NF-E2-Related Factor 2); 0 (NF-kappa B); 0 (Nfe2l2 protein, mouse); 0 (Polyethylene Glycols); 0 (maleimide-polyethylene glycol-modified hemoglobin, MP4); 743LRP9S7N (Hemin); 7U1EE4V452 (Carbon Monoxide); EC 1.14.99.3 (Heme Oxygenase-1); EC 1.14.99.3 (Hmox1 protein, mouse)
[Em] Entry month:1312
[Cu] Class update date: 141010
[Lr] Last revision date:141010
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:131011
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2013-02-486282

  9 / 32331 MEDLINE  
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[PMID]: 25182699
[Au] Autor:Needham E; Zandi MS
[Ad] Address:Department of Clinical Neurosciences, Addenbrooke's Hospital, University of Cambridge, Cambridge, CB2 0QQ, UK.
[Ti] Title:Recent advances in the neuroimmunology of cell-surface CNS autoantibody syndromes, Alzheimer's disease, traumatic brain injury and schizophrenia.
[So] Source:J Neurol;261(10):2037-42, 2014 Oct.
[Is] ISSN:1432-1459
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:In this update, we review recent advances in antibody-associated disorders of the central nervous system, and the immune mechanisms which may contribute to Alzheimer's disease, traumatic brain injury and schizophrenia. The field of neuroimmunology is rapidly developing and has concerned itself with an expanding portfolio of diseases. The core neuroimmunological diseases remain, multiple sclerosis, neuromyelitis optica, primary inflammatory and antibody-associated disorders of the central and peripheral nervous system (including Myasthenia Gravis and other disorders of neuromuscular junction and muscle, paraneoplastic syndromes, paraproteinaemic neuropathies), and the neurological involvement seen in systemic inflammatory diseases including lupus, sarcoidosis and vasculitis. But it is increasingly realised that immune mechanisms may contribute to the pathogenesis of degenerative diseases including Alzheimer's disease, traumatic brain disease and psychiatric diseases including schizophrenia and depression. These common and devastating disorders, often without effective disease-modifying therapies, are yet to be seen in a conventional neuroimmunology clinic, but the immune mechanisms identified have encouraged research into novel therapeutic approaches for them.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s00415-014-7473-x

  10 / 32331 MEDLINE  
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[PMID]: 25302231
[Au] Autor:Bondalapati S; V DR; Rampure D; S RR
[Ad] Address:Post Graduate, Department of General Medicine, Mamata Medical College , Khammam, Andhra Pradesh, India ....
[Ti] Title:Isoniazid Induced Cutaneous Leukocytoclastic Vasculitis in Extra Pulmonary Tuberculosis (Pott's Spine): A Case Report.
[So] Source:J Clin Diagn Res;8(8):MD03-5, 2014 Aug.
[Is] ISSN:2249-782X
[Cp] Country of publication:India
[La] Language:eng
[Ab] Abstract:Anti-tuberculosis drugs frequently result in cutaneous adverse reactions but Isoniazid is known to have least toxic potential for cutaneous reactions. We report a rare case of Isoniazid induced cutaneous leucocytoclastic vasculitis. A 64-year-old male was diagnosed to have Pott's spine with multiple vertebral body involvement (D8-12 vertebrae). Subsequently, he was treated with first line anti-TB drugs i.e., Isoniazid, Rifampicin, Pyrazinamide and Ethambutol. On the fourth day of treatment with Anti Tuberculosis Treatment (ATT), the patient developed an erythematosus rash over right upper limb not associated with itching or pain, non-blanchable macules and papules over bilateral shins on lower limbs, petechiae on both forearms and hyper pigmented, scaly rash over right axilla and buttocks. The skin biopsy report was consistent with cutaneous leukocytoclastic vasculitis. Although rare, Isoniazid among anti-tuberculosis drugs should be considered as potential cause of drug-induced cutaneous leukocytoclastic vasculitis in the differential diagnosis of erythematosus rash with petechiae.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Da] Date of entry for processing:141010
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.7860/JCDR/2014/9000.4688


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