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      Paronychia with Pyogenic Granuloma in a Child Treated with Indinavir: The Retinoid-Mediated Side Effect Theory Revisited

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          Abstract

          Background: The introduction of HIV-1 protease inhibitors into the treatment of patients infected with HIV-1 has had a major influence on clinical practice. However, the use of protease inhibitors is frequently associated with the development of resistance and several side effects and interactions with other drugs have been reported. Observations: We present the first pediatric patient with paronychia with pyogenic granuloma associated with the administration of the protease inhibitor indinavir. Clinical findings are discussed in view of a possible interference of indinavir with endogenous retinoid metabolism. Conclusion: Considerable evidence advocates the mediation of indinavir side effects by impaired oxidative metabolism of retinoic acid through the inhibition of cytochromes P450 3A by indinavir rather than by impaired formation of 9-cis-retinoic acid.

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          Diagnosis, prediction, and natural course of HIV-1 protease-inhibitor-associated lipodystrophy, hyperlipidaemia, and diabetes mellitus: a cohort study.

          A. Carr, K Samaras, A Thorisdottir … (1999)
          The prevalence and severity of lipodystrophy syndrome with long-term therapy for HIV-1 infection that includes a protease inhibitor is unknown. We studied the natural course of the syndrome to develop diagnostic criteria and identifying markers that predict its severity. We assessed 113 patients who were receiving HIV-1 protease inhibitors (mean 21 months) and 45 HIV-1-infected patients (28 with follow-up) never treated with a protease inhibitor. Lipodystrophy was assessed by questionnaire (including patients' rating of severity), physical examination, and dual-energy x-ray absorptiometry. Body composition and fasting lipid and glycaemic variables were compared with data obtained 8 months previously. Oral glucose tolerance was investigated. There was 98% concordance between patients' reports of the presence or absence of lipodystrophy (reported by 83% of protease-inhibitor recipients and 4% of treatment-naïve patients; p=0.0001) and physical examination. Patients' ratings of lipodystrophy were significantly associated with declining total body fat (p=0.02). Lower body fat was independently associated with longer duration of protease-inhibitor therapy and lower bodyweight before therapy, and more severe lipodystrophy was associated with higher previous (p < 0.03) and current (p < or = 0.01) triglyceride and C-peptide concentrations, and less peripheral and greater central fat (p=0.005 and 0.09, respectively). Body fat declined a mean 1.2 kg over 8 months in protease-inhibitor recipients (p=0.05). The prevalence of hyperlipidaemia remained stable over time (74% of treated patients vs 28% of naïve patients; p=0.0001). Impaired glucose tolerance occurred in 16% of protease-inhibitor recipients and diabetes mellitus in 7%; in all but three patients these abnormalities were detected on 2 h post-glucose load values. Diagnosis and rating severity of lipodystrophy is aided by the combination of physical examination, patient's rating, and measurement of body fat, fasting triglycerides, and C-peptide. Weight before therapy, fasting triglyceride, and C-peptide concentrations early in therapy, and therapy duration seem to predict lipodystrophy severity. Lipodystrophy was common and progressive after almost 2 years of protease inhibitor therapy, but was not usually severe. Hyperlipidaemia and impaired glucose tolerance were also common.
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            Pathogenesis of HIV-1-protease inhibitor-associated peripheral lipodystrophy, hyperlipidaemia, and insulin resistance.

            Andrew G. Carr, Katherine Samaras, Donald J. Chisholm … (1998)
            HIV-1 protease-inhibitor treatments are associated with a syndrome of peripheral lipodystrophy, central adiposity, breast hypertrophy in women, hyperlipidaemia, and insulin resistance. The catalytic region of HIV-1 protease, to which protease inhibitors bind, has approximately 60% homology to regions within two proteins that regulate lipid metabolism: cytoplasmic retinoic-acid binding protein type 1 (CRABP-1) and low density lipoprotein-receptor-related protein (LRP). We hypothesise that protease inhibitors inhibit CRABP-1-modified, and cytochrome P450 3A-mediated synthesis of cis-9-retinoic acid, a key activator of the retinoid X receptor; and peroxisome proliferator activated receptor type gamma (PPAR-gamma) heterodimer, an adipocyte receptor that regulates peripheral adipocyte differentiation and apoptosis. Protease-inhibitor binding to LRP would impair hepatic chylomicron uptake and triglyceride clearance by the endothelial LRP-lipoprotein lipase complex. The resulting hyperlipidaemia contributes to central fat deposition (and in the breasts in the presence of oestrogen), insulin resistance, and, in susceptible individuals, type 2 diabetes. Understanding the syndrome's pathogenesis should lead to treatment strategies and to the design of protease inhibitors that do not cause this syndrome.
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              Multiplicity generates diversity in the retinoic acid signalling pathways.

              Mark Leid, Philippe Kastner, Pierre Chambon (1992)
              Complexity in the retinoid signalling system arises from a combination of several forms of retinoic acid, multiple cytoplasmic binding proteins and nuclear receptors, and the existence of polymorphic retinoic acid response elements. Additional diversity appears to be generated by heterodimeric interactions between two families of nuclear retinoic acid receptors, and between nuclear retinoic acid receptors and other members of the nuclear receptor superfamily. Thus, a complex array of combinatorial effects is beginning to emerge which may account for the pleiotropic effects of retinoids.
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                Author and article information

                Journal
                Journal ID (publisher-id): DRM
                Journal ID (nlm-ta): Dermatology
                Journal ID (doi): 10.1159/issn.1018-8665
                Title: Dermatology
                Publisher: S. Karger AG
                ISSN (Print): 1018-8665
                ISSN (Electronic): 1421-9832
                Publication date Subscription-year: 2000
                Publication date (Print): 2000
                Publication date (Electronic): 11 February 2000
                Volume: 200
                Issue: 1
                Pages: 40-42
                Affiliations
                Universitätskliniken für aKinder- und Jugendheilkunde und bDermatologie und Venerologie, Innsbruck, Österreich; cTzimas-Dimolios Co., Thessaloniki, Greece
                Article
                Publisher ID: 18313 Other ID: Dermatology 2000;200:40–42
                DOI: 10.1159/000018313
                PubMed ID: 10681612
                SO-VID: 81cb641c-8ed4-495a-99e5-9c6519b4531f
                Copyright © © 2000 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Page count
                Figures: 1, References: 20, Pages: 3
                Categories
                Subject: Short Communication

                ScienceOpen disciplines: Oncology & Radiotherapy,Pathology,Surgery,Dermatology,Pharmacology & Pharmaceutical medicine
                Keywords: Retinoid,Acitretin,Paronychia,Pyogenic granuloma,HIV-1 protease inhibitor,Indinavir,Vitamin A,Retinoic acid,Etretinate,Isotretinoin
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy, Pathology, Surgery, Dermatology, Pharmacology & Pharmaceutical medicine
                Keywords: Retinoid, Acitretin, Paronychia, Pyogenic granuloma, HIV-1 protease inhibitor, Indinavir, Vitamin A, Retinoic acid, Etretinate, Isotretinoin

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