Multiple other serious neurological and ocular disorders also result Selleckchem GSI-IX from VZV reactivation. This review summarizes the current state of knowledge of the clinical and pathological complications of neurological and ocular disease

produced by VZV reactivation, molecular aspects of VZV latency, VZV virology and VZV-specific immunity, the role of apoptosis in VZV-induced cell death and the development of an animal model provided by simian varicella virus infection of monkeys. “
“Papillary glioneuronal tumor (PGNT) is a rare type of primary brain tumor. Although PGNT has traditionally been defined as a clinically indolent neoplasm, several cases with high proliferative activity and tumor recurrence have recently been reported. We report a case of PGNT in a 12-year-old boy who presented with epilepsy and harbored a 64 mm cystic tumor with a high proliferative component in the right temporal lobe. 11C-methionine positron emission tomography (PET) showed high uptake in the solid mass. Gross total resection of

the tumor mass was achieved and the patient became seizure-free without any neurological deficits. Histologically, the tumor contained two distinct areas of a vasocentric papilliform structure and a desmoplastic component. Minigemistocytic cells and small necrotic regions were observed adjacent to the pseudopapillae. Immunohistochemical analyses revealed both glial and neuronal differentiation. The Ki-67 proliferation signaling pathway index was high (14%) in the area corresponding to the high uptake region in the 11C-methionine PET. No tumor recurrence was observed 20 months after surgery. High proliferative PGNTs selleck chemicals are rare and to our knowledge this is only the third pediatric case of PGNT with atypical features reported in the literature. Hence, we here review the reported cases of PGNT and discuss the clinical, radiological and histological features of this malignancy. “
“EphB2 is a member of receptor tyrosine kinases (RTKs) family that is essential for the cell adhesion, neural crest migration, axon guidance and synaptogenesis in the nervous system. Recent studies show that preservation of EphB2 in a transgenic mouse model of Alzheimer’s disease (AD)

rescues the cognitive deficit, suggesting a crucial role of EphB2 in AD. However, the expression and distribution profiles of EphB2 in the early stage of AD have not been reported. Immunohistochemistry, immunoblot and immunofluorescence were used to analyse the level of EphB2 in Tg2576 mice at different ages and in cultured neurones with Aβ treatment at different times. EphB2 was reduced in an age-dependent manner in the olfactory bulb and the hippocampus of Tg2576 mice. The decrease of EphB2 appeared earlier in the olfactory bulb than the hippocampus, and reduction of EphB2 appeared earlier than that of MAP2, a dendritic cytoskeleton marker. In the cortex, EphB2 displayed a significant translocation from the neuronal processes to the cell bodies with ageing.

The difference was not significant, as was the difference of the success rates in the composite primary endpoint (36% vs. 38%) made up of defervescence and absence of emergent fungal infection, discontinuation of study drug for toxicity or use of other systemic antifungals. At a first glance, these results may be interpreted as evidence that antifungal therapy is dispensable or ineffective in ICU patients with signs of systemic infection.

Yet, the efficacy of antifungals in documented candidaemia has been established in large prospective trials. We therefore Dabrafenib conclude that the criteria used for the identification of patients at high risk of IC in this study were not adequate and too broad to select for the relevant patient population. Recently updated guidelines from three international expert boards provide rather concise guidance on the choice of suitable antifungal agents for the initial therapy of invasive Candida infections. Treatment recommendations are mostly focussed on bloodstream infection, which is the most common manifestation of IC in intensive care patients. According to the 2009 guidelines of the Infectious Disease Society of America (IDSA),42 an echinocandin is the treatment of choice for candidaemia in moderately to severely ill patients with or without neutropenia and in all patients with previous exposure to azole antifungals. Fluconazole may be used

in less critically ill patients. To date, the term ‘moderately to severely ill’ has not been defined more precisely by the IDSA experts. In our view, intensive care patients generally must be allocated Selleckchem Olaparib to this high-risk category because of failure or major insufficiency of one or more organs and/or haemodynamic instability. The

European Conference on Infections in Leukemia (ECIL-3)43 confirms the notion of echinocandins being the first-choice option with grade A–I recommendations, particularly if therapy is initiated prior to species identification. Voriconazole is recommended with grade A–I in patients without previous azole prophylaxis. According to ECIL, liposomal amphotericin B is an equivalent alternative – which may appear less attractive because of a 30% rate of renal function deteriorations44 and excessive cost. Guanylate cyclase 2C The initial use of fluconazole is restricted to less severely ill patients without azole pre-exposure. Use of azoles is discouraged in C. glabrata infections. In the 2009 update of their guidelines on treatment of fungal infections in cancer patients, the German Society of Hematology and Oncology Infectious Diseases Working Group (DGHO-AGIHO)45 recommends the use of an echinocandin for the initial therapy of IC (grade A–I). Based on the randomised trial showing the inferiority of fluconazole in contrast to anidulafungin in non-neutropenic patients46 and the prevalence of Candida strains with reduced fluconazole susceptibility, the AGIHO explicitly recommends preference of an echinocandin as the primary treatment.

It has been demonstrated that ERK1/2 pathway plays a vital role in EMT. An ancient formula named QiFu Decoction (QFD) has been used to treat CON in China for many years. Nevertheless, the underlying mechanisms in vivo remain unknown. In this research, we investigated the effects of the combination of astragaloside and aconitine, two effective ingredients extracted from QFD in CON rats, and the related-mechanism of ameliorating RTIF by modulating ERK1/2 pathway. Methods: Sprague-Dawley

(SD) rats were given adenine (150 mg/kg/d) for 2 weeks and unilateral ureteral obstruction (UUO) operation at the end of week 2 to produce CON. Some MS-275 concentration CON rats were given the combination of astragaloside and aconitine (0.4 g/kg/d), while some others were given enalapril

(0.02 g/kg/d) for 3 weeks. Age and weight-matched rats were used as normal controls. Renal function, urinary beta2-MG and NAG, as well as tubulointerstitial histopathological changes were detected, respectively. The protein expressions of phenotype of EMT in renal tissue including E-cadherin and alpha-SMA, profibrotic cytokines containing TGF-beta1 and CTGF, as well as phosphorylated-ERK1/2 (p-ERK1/2), the key molecule in ERK 1/2 pathway, were observed by Western blots, respectively. Results: Adenine and UUO operation AZD2014 cost successfully induced CON models, which performed significant abnormal renal function, mass low-molecular www.selleck.co.jp/products/Decitabine.html weight proteinuria, and extracellular matrix deposition in tubulointerstitial district. After orally given the combination therapy for 3 weeks, low-molecular weight proteinuria and renal tubulointerstitial fibrosis were reduced. In addition, the E-cadherin protein

expression was up-regulated, while alpha-SMA, TGF-beta1, CTGF, and p-ERK1/2 protein expressions were down-regulated. However, the renal dysfunction cannot be improved by the combination therapy. Abnormalities in urinary parameters and renal tubulointerstitial fibrosis could also be attenuated by enalapril. Conclusion: RTIF can be ameliorated in CON rats by the combination of astragaloside and aconitine treatment via regulating E-cadherin, alpha-SMA, TGF-beta1, and CTGF protein expressions, as well as inhibiting ERK1/2 pathway. HAGIWARA MASAHIRO, HIWATASHI AKIRA, KAI HIRAYASU, USUI JOICHI, MORITO NAOKI, SAITO CHIE, YOH KEIGYO, YAMAGATA KUNIHIRO Department of Nephrology, Faculty of Medicine, University of Tsukuba Introduction: Podocalyxin (PCX), the major sialoprotein of glomerular epithelial cells (podocytes) is expressed on apical membrane, and helps maintain the architecture of the foot process and the patency of the filtration slits.

The phosphorylation of L-plastin relies on T-cell costimulation 8, 9, which R788 mouse means it is dependent on signals from the TCR/CD3 receptor complex as well as from signals that origin from accessory receptor. The inhibition of L-plastin phosphorylation by dexamethasone could be

reverted by the synthetic steroid mifepristone, which shows a glucocorticoid receptor dependency 36. Thus, effects of dexamethasone on L-plastin phosphorylation are most likely due to gene expression, suggesting an interference with the signaling pathway upstream of L-plastin phosphorylation. It is known that dexamethasone inhibits proximal signals induced by TCR triggering 37–40. In addition, dexamethasone could interfere with CD28-mediated signals. PI3K activity was shown to be involved in CD28-mediated costimulation 41–43 GSK-3 phosphorylation and its inhibition interferes with L-plastin phosphorylation in immune complex-stimulated

PMN 44. Dexamethasone inhibits PI3K in mast cells 45, which suggests PI3K and its inhibition might be involved in L-plastin phosphorylation upon T-cell costimulation. However, the relevance of dexamethasone for CD28-mediated PI3K activation in primary human T cells remains to be determined. One function of costimulation is the receptor movement to the immunological synapse 7, 12. Consequently, interference with L-plastin expression 5 or phosphorylation (this study) disturbed LFA-1 accumulation in the immune synapse. Interestingly, the effects on the accumulation of CD3 were much weaker and not significant in 5A-LPL-expressing T cells. It was therefore tempting to speculate that L-plastin phosphorylation Ureohydrolase plays a role in peripheral SMAC, but not in central SMAC formation. The fact that 5E-LPL expression rescued only the LFA-1, but not the CD3 enrichment in dexamethasone-treated T cells strengthened that assumption. Interestingly, migration

of the TCR/CD3 complex toward the central SMAC depends on the actin cytoskeleton, as shown by the application of mycotoxins (e.g. cytochalasin D) 2. However, although 5A-LPL expression led to a lower F-actin content in stimulated T cells, the CD3 accumulation was not significantly disturbed. This might be due to the mode of inhibition of the actin cytoskeleton. Thus, in contrast to 5A-LPL expression, the application of mycotoxins to inhibit the actin cytoskeleton does not take into account the complex and spatio-temporal regulation of the actin cytoskeleton. In contrast to 5A-LPL expression, dexamethasone inhibits both the enrichment of the central SMAC-marker CD3 and the peripheral SMAC-marker LFA-1 in the immune synapse significantly. The difference between 5A-LPL expression and dexamethasone treatment on the CD3 enrichment in the immune synapse could be due to additional effects of dexamethasone on the actin cytoskeleton or signaling cascades.

1 In primed T cells, topographical memory is endowed by the stable expression of homing and chemokine receptors that promote their interactions with ligands expressed

by the endothelium of specific organs, such as the skin and the gut.7 Memory T cells with tropism for the skin are characterized by the expression of the carbohydrate epitope cutaneous lymphocyte antigen (CLA),10 and the chemokine receptors CCR411 and/or CCR10.12 CLA mediates the tethering and rolling of T cells through interaction with its endothelial counter-receptor, E-selectin, which is constitutively expressed on skin post-capillary venules. The ligands for CCR4 and CCR10, which are, respectively, chemokine (C-C motif) ligand DAPT solubility dmso 17 (CCL17) thymus and activation-regulated chemokine (TARC) and CCL27 cutaneous T cell-attracting chemokine (CTACK), have been found on inflamed and non-inflamed skin endothelium.11,13 CCL17 (TARC) was shown to selectively induce Erastin datasheet integrin-dependent adhesion to intercellular adhesion molecule 1 (ICAM-1) of skin-derived memory T cells under static conditions and under physiological flow,11 while CCL27 (CTACK) was found to be preferentially produced by epidermal keratinocytes, and its chemotactic effect

on T cells was demonstrated in in vitro assays.13 Constitutive memory T-cell trafficking into the lamina propria of the small intestine requires the interaction of the integrin α4β7 and the chemokine receptor CCR9 on the lymphocyte surface14 with mucosal vascular addressin cell adhesion molecule 1 (MAdCAM-1) and CCL25 thymus-expressed chemokine (TECK) on endothelial cells of gut lamina propria venules, respectively.15 T cells lacking β7-integrin chain expression are severely impaired in their ability to localize to the intestinal mucosa16 and CCL25 blockade or genetic ablation of CCR9 significantly reduces antigen-specific Protein Tyrosine Kinase inhibitor CD8+ T-cell migration to the small

intestine.17 Additional adhesion molecules, such as vascular adhesion protein-1 (VAP-118) and CD44,19 may contribute to a significant diversity of potential address codes, but selectins, α4-integrins, β2-integrins, and chemokine receptors and their respective ligands appear to be the workhorses of the system with differential but broadly overlapping functions at the various destinations of lymphocyte trafficking. The paradigm of organ-specific homing is based on the assumption that T-cell priming within a specific tissue environment, such as cutaneous and mesenteric lymph nodes (MLNs), leads to an imprinting of the expression of specific homing receptors.17,20,21 Recent studies have shown that tissue-derived dendritic cells (DCs) are key mediators of the induction of T-cell tissue-specific homing potential.

We suggest that a perfusion augmented dorsal scapular artery perforator flap by harvesting multiple perforators could be a safe and useful alternative for reconstructive surgery of head and neck defects. © 2014 Wiley Periodicals, Inc. Microsurgery, 2014. “
“Radiation therapy is an essential treatment for head and neck cancer. However, the condition of the operative field is entirely altered after Acalabrutinib mw radiation therapy. This study aimed to examine the effects of preoperative radiation therapy on complications in patients who underwent

head and neck reconstruction with flaps. We retrospectively reviewed 252 instances of head and neck reconstruction with flaps in 240 patients between October 2000 and May 2011 at Okayama University Hospital. Of the participants, 51 had preoperative radiation exposure (21.3%) and 189 had no radiation exposure (78.7%). Postoperative complications were divided into three categories: minor complications that healed with conservative medical treatment within 4 weeks without a need for surgery; major complications requiring reoperation within 1 week after surgery (reoperation); and major complications needing additional operation later than 1 week after surgery (additional operation). Preoperative radiation therapy was only associated with major complications requiring reoperation later than 1 week after surgery (P < 0.001), open cervical wounds (P = 0.0030), and skin grafting

for cervical skin necrosis (P = 0.0031) when compared to no radiation exposure. The results of flap

failure were not significantly different between both groups (P = 0.3820). Minor complications and reoperation in the early postoperative GDC-0973 ic50 Amino acid period were not influenced by radiation exposure. The complications of radiation tend to be protracted and associated with additional operation later than 1 week after the initial surgery. It was thought that shortening of the duration of treatment was successful when we needed to perform early additional operations. © 2014 Wiley Periodicals, Inc. Microsurgery 34:516–521, 2014. “
“Distal radius fractures in the younger population are often comminuted and intra-articular, which can increase the complexity of their management. In addition, these patients tend to place high demands on their wrists, and the prevention of functional arthritis necessitates excellent anatomical reduction. Complicated cases such as these are often limited in their management options. We present a complex case of distal radius fracture and bone loss in which initial therapy with nonvascularized bone graft failed, and osteomyelitis was a further complicating factor. With the aid of preoperative planning with computed tomographic angiography (CTA), a deep circumflex iliac artery (DCIA) bone flap was able to be assessed as a reconstructive option. The use of preoperative CTA, the first description of such imaging in this role, was able to delineate the bone to be harvested, confirm its vascular supply, and plan flap harvest.

In line with this, we found that the combination of IL-12, IL-6 IGF-1R inhibitor and TGF-β is able to induce Th1, Th17 and IFN-γ/IL-17A double-positive cells. One might easily envisage that these distinct cytokines are expressed under inflammatory conditions and induce the typical picture of distinct T helper effector lineages in vivo. The data described here show that plasticity, at

least on a population level, is common to Th17 and Th1 cells. Whether this plasticity occurs during natural conditions such as infections or autoimmunity needs to be defined. The data by O’Connor et al. 15 suggested that Th17-transfer EAE can only be found under circumstances where a part of the transferred population shifts toward IFN-γ-producing cells. This was not the case for Th1-transfer EAE. Our finding that in some of the highly pure transferred Th1 cell population expression of IL-17A was induced indicates that also a Th1–Th17 shift may play a role in Th1-transfer EAE. Future experiments using either IL-17A/F knockout

Th1 GSI-IX manufacturer cells or IFN-γ or T-bet knockout Th17 cells for transfer EAE should clarify the role of the cytokine shift in EAE development. In a model for airway hyperresponsiveness, another group recently showed that a shift to IFN-γ expression is necessary to induce airway hyperresponsiveness, whereas IL-17A expression was necessary for neutrophil infiltration 39. In light of the beneficial effects of IFN-γ in EAE one might speculate whether the cytokine shift to IFN-γ expression may even have a certain protective role. Our finding that also highly pure Th1 cells are able to shift to cells that express both IFN-γ and IL-17A is new. We found these cells particularly in the mLN. Together with the finding that also Th17 cells recovered from the mLN contained

a large fraction of double-expressing cells, this indicates that the gut immune system creates Interleukin-3 receptor a specific local milieu, which favors this Th1/Th17 dichotomous response. Potential mechanisms for the bias to coexpress IL-17 might be the local presence of CD103+ and CD103− mLN DC, which may favor under certain conditions the development of Th17 cells 40, 41. In our transfer experiments, the driving force of trans-differentiation in the lymphopenic environment might be homeostatic proliferation of the transferred cells. Evidence against that is a recent report demonstrating that shifting of Th17 cells to IFN-γ expression was independent of IL-7 blockage 33, which largely inhibited proliferation of the injected cells. Whether, and which, other factors present in the lymphocyte-deficient lymphoid compartments trigger the reprogramming of Th17 cell populations needs to be determined. In transfers to RAG1−/−, and more strikingly in transfer experiments using WT mice, we found a strong downregulation of cytokine expression of the donor cells.

Multiple clinical parameters were obtained for the long-term stable patients within the GenHomme project, including donor and recipient demographic characteristics, clinical history of renal graft failure, transplantation

monitoring, full blood counts and medications biochemical screening. Non-transplanted patients with “non-immune” RFA (n=8) had a creatinemia 654±193 μmol/L and proteinuria >1 g 24 h−1. The causes of RFA were polycystic kidney (4/8 patients), renal dysplasia (2/8 patients), interstitial nephropathy (1/8 patients) and malformative uropathy (1/8 patients). Finally, healthy individuals (HEI, non-transplanted individuals, n=14) with normal renal function and no known infectious pathology for at least 6 months prior to the study were enrolled. selleck PBMC from HLA-A2 CMV+ patients were stained with PE-labeled anti-human CD8 mAb, Alexa700-labeled anti-human Opaganib price CD3 mAb, Alexa 647-labeled anti-human CD4 mAb and pp65-HLA-A2 APC-labeled multimer. DAPI was used to exclude dead cells. pp65-HLA-A2 APC-labeled multimer was prepared by incubating for 1h APC-streptavidin with biotinylated pp65-HLA-A2 monomer. All mAb were purchased from BD Biosciences and biotinylated pp65-HLA-A2 monomer was produced by INSERM core facility (Nantes, France). DAPI−CD3+CD4−CD8+, DAPI−CD3+CD4−CD8+pp65-HLA-A2 multimer− and DAPI−CD3+CD4−CD8+pp65-HLA-A2 multimer+

were separated from PBMC using a high-speed cell sorter (FACSAria, BD Biosciences). Purity was greater than 98%. Blood, collected in EDTA tubes, was obtained Dichloromethane dehalogenase from a peripheral vein or arteriovenous fistula. PBMC were separated

on an MSL layer (Eurobio) and frozen in TRIzol® reagent (Invitrogen) for RNA extraction. Total RNA was reverse-transcribed using a classical MMLV cDNA synthesis (Invitrogen). Complementary DNA was amplified by PCR using pairs of primers specific of each Vβ gene 10, elongated and electrophorezed using a gel sequencer (ABI Prism 377 DNA sequencer – Applied Biosystems) 35. The CDR3 profiles obtained were transformed into mathematical distributions and normalized so that the total area was equal to one. In parallel, the level of Vβ family transcripts was measured by real-time quantitative PCR and normalized by a housekeeping gene (HPRT). The CDR3-LD was then combined with each normalized Vβ transcript amounts to obtain the TcL data as described previously 15, 36, 37. Several parameters or metrics can be used to describe, and summarize with one value, the shape of the Vβ CDR3-LD. Indeed, the distribution of 13 lengths of Vβ CDR3 reflects different immunological situations which can be analyzed 12. Kurtosis, a mathematical index, has been chosen to quantify the CDR3-LD diversity 17. The Kurtosis reflects the degree of “peakedness” of a distribution 38 and is perfectly suitable for describing CDR3-LD with expansions.

Following stimulation, Smad6/7 could be detected in Foxp3− cells in the presence or absence of TGF-β, whereas Smad6/7 could not be detected in Foxp3+ cells cultured under any conditions. As the expression pattern of Smad6/7 in stimulated nTregs is similar to that seen in TGF-β/simvastatin-generated iTregs, it appears likely that one of the primary mechanisms responsible for the synergistic effects of simvastatin on TGF-β-mediated induction of Foxp3 is the inhibition or down-regulation of Smad6/7 expression. Statins are widely used drugs in the treatment of hypercholesterolaemia and have

proven to be extremely useful in the prevention of cardiovascular diseases. Studies since 2000 have also demonstrated that statins have pleiotropic effects on immune responses. They were initially shown to prevent and reverse relapsing and remitting experimental autoimmune encephalomyelitis in the mouse model by inducing a shift https://www.selleckchem.com/products/dorsomorphin-2hcl.html from a Th1 to a Th2 cytokine profile.7 Similarly, in acute graft-versus-host disease in the mouse, the effects of statins were mediated through induction Romidepsin cell line of Th2 cells with increased IL-4 production and reduced tumour necrosis factor-α and interferon-γ production.8 Subsequent studies have claimed that statins can act on many distinct cell types in

the immune system as well as vascular endothelial cells.17 Most recently, statins have been shown to modulate the production of IL-17 by inducing the expression of suppressors of cytokine signalling (SOCS) 3 and SOCS7 in monocytes resulting in inhibition of the transcription of IL-6 Protirelin and IL-23 and by inhibiting the transcription factor RORγT in CD4+ T cells.18 Very few studies have addressed the effects of statins on nTregs or on the developments of iTregs in peripheral sites. One study claimed that culture of human peripheral blood mononuclear cells in the presence of atorvastatin, but not mevastatin or pravastatin, increased the number of Foxp3+ T cells and claimed that the effects of atorvastatin were mediated by conversion of Foxp3− to Foxp3+ T cells.14 The results of this study are difficult to interpret

because conversion of Foxp3− to Foxp3+ T cells requires that the responsive T cell be stimulated through their TCR and TCR stimulation was not used in this paper.2,19 The goal of our studies was to examine the potential effects of statins on the conversion of mouse Foxp3− T cells to Foxp3+ Tregs. We used an in vitro model system in which highly purified Foxp3− T cells, obtained from TCR transgenic mice on a RAG−/− background, were cultured in the absence of antigen-presenting cells in the presence of a TCR stimulus, CD28-mediated co-stimulation and IL-2. Under these conditions the addition of simvastatin alone had a modest effect on the induction of Foxp3+ T cells that was partially independent of the presence of TGF-β. Importantly, simvastatin exerted a potent synergistic effect on Foxp3 induction when combined with low concentrations of TGF-β.

Serial measurements of sFlt-1/PlGF ratio suggested pre-eclampsia was unlikely. We compared the results to post partum specimens collected from previous women with varying HDP. The events would be consistent with PRES due to cerebral traction trauma secondary to spinal fluid leak. Conclusions: This case report highlights the utility of measuring circulating angiogenic markers in clarifying the cause of post partum seizures. This is the first case where post partum PRES secondary to epidural anaesthesia has been

described with the use of sFlt-1/PlGF to help reach the diagnosis. 300 PROPYLTHIOURACIL see more INDUCED ANTI-NEUTROPHIL CYTOPLASMIC ANTIBODY (ANCA) VASCULITIS V LIM, A DAVID, S TOOMBES, S VENUTHURUPALLI Renal Medicine, Toowoomba Hospital, Toowoomba, Queensland, Australia Aim: To present a case of Propylthiouracil induced anti-neutrophil cytoplasmic antibody vasculitis (AAV). Background: Propylthiouracil (PTU) is commonly used to treat hyperthyroidism. PTU is known to be associated with AAV. PTU induced vasculitis differs from primary AAV as being common in younger

patients with a milder course although fatal cases were described especially when diagnosis was delayed. Case Report: A 58 year old lady presented with one month history of haematuria, increasing polyarthralgia on a background of rheumatoid arthritis X-396 purchase for six years. She noticed progressive dyspnoea for the last eighteen months and skin lesions over three years. She was

diagnosed to have multinodular goitre with thyrotoxicosis in 2006. She was initially treated with Carbimazole but changed to PTU due to nausea since 2010. Her thyrotoxicosis was controlled successfully with PTU. She had normal renal functions during these years. Initial investigations revealed elevated serum creatinine Tau-protein kinase with proteinuria and haematuria, microcytic anaemia and raised inflammatory markers. She tested positive for both PR3 and MPO ANCAs, anti-nuclear antibody and anti-cyclic citrulline peptide antibody. High resolution computed tomography showed ground glass opacities in lungs fields. With her clinical presentation and investigations, PTU induced AAV involving skin, lungs and kidney was considered. PTU was ceased and she was commenced on Prednisolone and Cyclophosphamide. Kidney biopsy revealed features of acute tubular injury with red cell casts and minimal immunofluorescent reactivity for IgG and C3. There were no crescents or necrotising lesions. Electron microscopy is pending. Her renal function was stabilised following treatment with improvement of respiratory and cutaneous symptoms. Conclusions: ANCA-positive multisystem involvement can be observed following treatment of PTU and requires a high index of suspicion for early detection and treatment.