Subject(s)
Adenosine Deaminase/deficiency , Adenosine Deaminase/genetics , Intercellular Signaling Peptides and Proteins/deficiency , Intercellular Signaling Peptides and Proteins/genetics , Leg Ulcer/genetics , Skin Diseases, Genetic/diagnosis , Adult , Chronic Disease , Consanguinity , Humans , Leg Ulcer/pathology , Male , Pedigree , Skin Diseases, Genetic/geneticsABSTRACT
Lower-limb ulcers in systemic sclerosis patients are rarely reported. The aim of this study was to describe the main causes and outcomes of lower-limb ulcers in systemic sclerosis patients and to assess factors associated with ischaemic causes (arterial disease and/or microvascular impairment). A retrospective, multicentre, case-control study was conducted in 2013 and 2014, including 45 systemic sclerosis patients presenting lower-limb ulcers between 2008 and 2013. The estimated prevalence of lower-limb ulcers among systemic sclerosis patients was 12.8%. Ulcers were related to venous insufficiency in 22 cases (49%), ischaemic causes in 21 (47%) and other causes in 2 (4%). Complete healing was observed in 60% of cases in a mean time of 10.3 months; 59% relapsed during a mean follow-up of 22 months. Ischaemic lower-limb ulcer outcomes were poor, with a 28.6% amputation rate. Logistic-regression multivariate analyses between ischaemic lower-limb ulcer cases and matched systemic sclerosis-controls identified past or concomitant digital ulcer and cutaneous sclerosis of the feet as independent risk factors associated with ischaemic lower-limb ulcers.
Subject(s)
Ischemia/epidemiology , Leg Ulcer/epidemiology , Scleroderma, Systemic/epidemiology , Adult , Aged , Aged, 80 and over , Amputation, Surgical , Chi-Square Distribution , Disease Progression , Female , France/epidemiology , Humans , Ischemia/diagnosis , Ischemia/therapy , Leg Ulcer/diagnosis , Leg Ulcer/therapy , Limb Salvage , Logistic Models , Male , Middle Aged , Multivariate Analysis , Odds Ratio , Prevalence , Recurrence , Retrospective Studies , Risk Factors , Scleroderma, Systemic/diagnosis , Scleroderma, Systemic/therapy , Time Factors , Treatment Outcome , Wound Healing , Young AdultSubject(s)
Fibrosarcoma/etiology , Jewelry/toxicity , Neoplasms, Radiation-Induced/pathology , Soft Tissue Neoplasms/etiology , Thorax/pathology , Aged, 80 and over , Fatal Outcome , Fibrosarcoma/pathology , Humans , Male , Neoplasm Metastasis , Sclerosis/etiology , Soft Tissue Neoplasms/pathology , Thorium/toxicity , Uranium/toxicityABSTRACT
OBJECTIVES: The broader and prolonged use of anti-tumor necrosis factor (TNF) agents in inflammatory bowel disease (IBD) could expose patients to an increased risk of adverse reactions, including dermatological complications. We assessed the cumulative incidence of anti-TNF-induced cutaneous adverse reactions in IBD patients, their risk factors, their dermatological management, and their outcome in a large cohort of IBD patients. METHODS: In a single-center observational retrospective study, including all consecutive adult IBD patients treated with an anti-TNF agent between 2001 and 2014, all patients with dermatological complications under anti-TNF therapy were identified in a well-defined cohort of IBD patients. We conducted a survival analysis to determine the cumulative incidence of dermatological complications and risk factors for developing any dermatological complications, cutaneous infections, and psoriasiform lesions. Survival curves were estimated by the Kaplan-Meier method, and we used a Cox proportional hazards model to test the association between parameters and time to each event: any dermatological complication, cutaneous infections, and psoriasis lesions. RESULTS: Among 583 IBD patients, 176 dermatological complications occurred, involving 20.5% of patients. Median duration of follow-up was 38.2 months (range: 1-179). Psoriasiform lesions (10.1%; 59/583) and cutaneous infections (11.6%, 68/583) were the most frequently observed, with a cumulative incidence of, respectively, 28.9% and 17.6% at 10 years. They led to anti-TNF discontinuation, respectively, in 18.6% and 2.9% of patients. In case of switching to another anti-TNF agent for psoriasiform lesions, recurrence occurred in 57% of patients. Ulcerative colitis was associated with a lower risk of developing cutaneous infections than Crohn's disease (hazard ratio (HR)=0.25; 95% confidence interval (CI)=0.09-0.68; P=0.007). Higher dosing of anti-TNF agent was associated with a higher risk of developing cutaneous infections (HR=1.99; 95% CI=1.09-3.64; P=0.025). A younger age at time of anti-TNF initiation was associated with a higher risk of dermatological complications (HR=2.25; 95% CI=1.39-3.62; P<0.001). CONCLUSIONS: Dermatological complications involve one of five patients treated with anti-TNF therapy after a 14-year follow-up. Association of cutaneous infections with higher anti-TNF dosing suggests a dose-dependent effect. Discontinuation of anti-TNF therapy due to dermatological complications is required in one out of five patients with psoriasiform lesions, but specific dermatological treatment allows to continue anti-TNF therapy in half of them.
Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Colitis, Ulcerative/drug therapy , Crohn Disease/drug therapy , Drug Eruptions/epidemiology , Psoriasis/epidemiology , Skin Diseases, Infectious/epidemiology , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Adalimumab , Adolescent , Adult , Age Factors , Aged , Aged, 80 and over , Anti-Inflammatory Agents, Non-Steroidal/administration & dosage , Antibodies, Monoclonal/administration & dosage , Antibodies, Monoclonal/adverse effects , Antibodies, Monoclonal, Humanized/administration & dosage , Antibodies, Monoclonal, Humanized/adverse effects , Child , Dose-Response Relationship, Drug , Drug Eruptions/etiology , Drug Eruptions/pathology , Female , Humans , Incidence , Infliximab , Kaplan-Meier Estimate , Male , Middle Aged , Prevalence , Proportional Hazards Models , Psoriasis/chemically induced , Psoriasis/drug therapy , Retrospective Studies , Risk Factors , Skin Diseases, Infectious/chemically induced , Skin Diseases, Infectious/drug therapy , Young AdultSubject(s)
Blepharitis/etiology , Breast Neoplasms/secondary , Conjunctival Neoplasms/secondary , Conjunctivitis/etiology , Eyelid Neoplasms/diagnosis , Aged , Biopsy , Blepharitis/diagnosis , Breast Neoplasms/diagnosis , Conjunctival Neoplasms/diagnosis , Conjunctivitis/diagnosis , Diagnosis, Differential , Eyelid Neoplasms/complications , Female , HumansABSTRACT
BACKGROUND: Modern dressings (MDs) may have a low sensitization rate, but there is a lack of prospective studies in patients with chronic leg ulcers (CLUs) to evaluate this. OBJECTIVES: To determine the rate of sensitization (contact allergy) to MDs and substances present in dressings. PATIENTS AND METHODS: A prospective multicentre study was carried out in patients with CLUs at five French dermatology departments; patch tests were performed with the European baseline series and with an additional 27 individual allergens and 10 MDs. RESULTS: Among 354 patients (226 women and 128 men) with CLUs, 59.6% had at least one positive patch test reaction to an MD and 19% had at least one sensitization to an MD. The number of positive test reactions per patient was correlated with the duration of ulcerative disease, but not with ulcer duration, the cause of the ulcer, or the presence of surrounding eczematous lesions. For 11 of 45 patients sensitized to Ialuset cream®, more detailed information could be obtained with sensitization to sodium dehydroacetate (5 cases) or Lanette SX® (3 cases). CONCLUSIONS: Sensitization to MDs is not rare. It is absolutely necessary to label all components of MDs on their packaging and to avoid some sensitizing molecules, such as colophonium derivatives or any strong sensitizers.
Subject(s)
Bandages/adverse effects , Dermatitis, Allergic Contact/etiology , Leg Ulcer/therapy , Aged , Chronic Disease , Female , Humans , Male , Patch Tests , Prospective StudiesABSTRACT
Nicorandil, a nicotinamide ester, was first reported to be involved in the induction of oral ulcers in 1997. Since then, many reports of single or multiple nicorandil-induced ulcerations (NIUs) have been reported. We hypothesised that in the case of high-dosage nicorandil or after an increased dosage of nicorandil, nicotinic acid and nicotinamide (two main metabolites of nicorandil) cannot appropriately merge into the endogenous pool of nicotinamide adenine dinucleotide/phosphate, which leads to abnormal distribution of these metabolites in the body. In recent or maintained trauma, nicotinamide increases blood flow at the edge of the raw area, inducing epithelial proliferation, while nicotinic acid ulcerates this epithelial formation, ultimately flooding the entire scar. We demonstrate, by comparison to a control patient non-exposed to nicorandil, an abnormal amount of nicotinic acid (×38) and nicotinamide (×11) in the ulcerated area in a patient with NIUs. All practitioners, especially geriatricians, dermatologists and surgeons, must be aware of these serious and insidious side effects of nicorandil. It is critical to rapidly reassess the risk-benefit ratio of this drug for any patient, and not only for those with diverticular diseases.
Subject(s)
Niacin/metabolism , Niacinamide/metabolism , Nicorandil/adverse effects , Skin Ulcer/chemically induced , Skin Ulcer/metabolism , Vasodilator Agents/adverse effects , Aged, 80 and over , Female , Humans , Nicorandil/metabolism , Skin Ulcer/pathologySubject(s)
Antibodies, Monoclonal, Humanized/therapeutic use , Dermatologic Agents/therapeutic use , Psoriasis/drug therapy , Adult , Antibodies, Monoclonal, Humanized/adverse effects , Dermatologic Agents/adverse effects , Female , Humans , Psoriasis/complications , Renal Dialysis , Renal Insufficiency, Chronic/complications , Renal Insufficiency, Chronic/therapy , Severity of Illness Index , UstekinumabSubject(s)
Anti-Inflammatory Agents/adverse effects , Attention/drug effects , Candidiasis, Oral/drug therapy , Clobetasol/adverse effects , Dermatologic Agents/adverse effects , Headache/chemically induced , Irritable Mood/drug effects , Lichen Planus, Oral/drug therapy , Pemphigoid, Bullous/drug therapy , Sleep Initiation and Maintenance Disorders/chemically induced , Absorption , Administration, Cutaneous , Administration, Topical , Aged , Aggression/drug effects , Anti-Inflammatory Agents/administration & dosage , Anti-Inflammatory Agents/pharmacokinetics , Anti-Inflammatory Agents/therapeutic use , Candidiasis, Oral/complications , Clobetasol/administration & dosage , Clobetasol/pharmacokinetics , Clobetasol/therapeutic use , Dermatologic Agents/administration & dosage , Dermatologic Agents/pharmacokinetics , Dermatologic Agents/therapeutic use , Drug Overdose , Humans , Lichen Planus, Oral/complications , Male , Mouth Mucosa/drug effects , Pemphigoid, Bullous/complications , Skin AbsorptionABSTRACT
Lichen sclerosus et atrophicus (LSA) is an inflammatory disease that affects the genitals, which was first described by Hallopeau in 1887 and is of unknown etiology. Only 15% of patients have an associated extra-genital form, and 2.5% have an isolated extra-genital form. LSA treatment remains poorly codified and mostly empirical. Here, we report a case of LSA, of mainly cutaneous form, which was effectively treated using extracorporeal photochemotherapy (ECP). Remission was achieved quickly, after the fourth session, with excellent treatment tolerance. ECP is now recognized as an effective treatment for erosive lichen planus, graft-versus-host disease (GVHD), and scleroderma. Thus, we began ECP treatment for our cases of LSA based on clinical and/or anatomopathological similarities between LSA and these commonly ECP-treated disorders. The fact that ECP is effective in LSA, GVHD, erosive lichen planus, and scleroderma strengthen the hypothesis that there is a common link between these four conditions.
Subject(s)
Lichen Sclerosus et Atrophicus/therapy , Photopheresis , Female , Humans , Lichen Sclerosus et Atrophicus/pathology , Middle Aged , Remission InductionSubject(s)
Acute Generalized Exanthematous Pustulosis/pathology , Hashimoto Disease/pathology , Acute Generalized Exanthematous Pustulosis/drug therapy , Adult , Antithyroid Agents/therapeutic use , Carbimazole/therapeutic use , Colchicine/therapeutic use , Diagnosis, Differential , Female , Hashimoto Disease/drug therapy , Humans , Thyroxine/therapeutic use , Tubulin Modulators/therapeutic useSubject(s)
Granuloma Annulare/diagnosis , Penile Diseases/diagnosis , Administration, Topical , Aged, 80 and over , Anti-Inflammatory Agents/administration & dosage , Clobetasol/administration & dosage , Diagnosis, Differential , Granuloma Annulare/drug therapy , Humans , Male , Penile Diseases/drug therapySubject(s)
Foot Dermatoses/drug therapy , Photochemotherapy , Warts/drug therapy , Female , Humans , Immunocompromised Host , Middle AgedABSTRACT
Mutations in two genes encoding cell cycle regulatory proteins have been shown to cause familial cutaneous malignant melanoma (CMM). About 20% of melanoma-prone families bear a point mutation in the CDKN2A locus at 9p21, which encodes two unrelated proteins, p16(INK4a) and p14(ARF). Rare mutations in CDK4 have also been linked to the disease. Although the CDKN2A gene has been shown to be the major melanoma predisposing gene, there remains a significant proportion of melanoma kindreds linked to 9p21 in which germline mutations of CDKN2A have not been identified through direct exon sequencing. The purpose of this study was to assess the contribution of large rearrangements in CDKN2A to the disease in melanoma-prone families using multiplex ligation-dependent probe amplification. We examined 214 patients from independent pedigrees with at least two CMM cases. All had been tested for CDKN2A and CDK4 point mutation, and 47 were found positive. Among the remaining 167 negative patients, one carried a novel genomic deletion of CDKN2A exon 2. Overall, genomic deletions represented 2.1% of total mutations in this series (1 of 48), confirming that they explain a very small proportion of CMM susceptibility. In addition, we excluded a new gene on 9p21, KLHL9, as being a major CMM gene.