Tattoo complications in treated and non-treated psoriatic patients.

BACKGROUND: Tattooing is a widespread phenomenon, with an estimated prevalence of 10-30% in Western populations. For psoriasis patients, current recommendations are to avoid having a tattoo if the disease is active and they are receiving immunosuppressive treatments. Although scientific data supporting these recommendations are lacking, dermatologists are often reluctant to advocate tattooing in psoriasis patients. OBJECTIVE: We aimed to evaluate the frequency of tattoo complications in patients with psoriasis and determine whether the occurrence of complications was associated with psoriasis status and treatments received at the time of tattooing. METHODS: We performed a multicentre cross-sectional study. Adults with psoriasis were consecutively included and classified as tattooed or non-tattooed. Prevalence of complications associated with tattoos was then evaluated according to psoriasis onset and treatments. The study was divided into three parts, in which data were collected through a series of questionnaires filled in by the dermatologist. Complications included pruritus, oedema, allergic reaction/eczema, infection/superinfection, granuloma, lichenification, photosensitivity, Koebner phenomenon and psoriasis flare after tattooing. Diagnosis of complications was made retrospectively. RESULTS: We included 2053 psoriatic patients, 20.2% had 894 tattoos. Amongst non-tattooed patients, 15.4% had wished to be tattooed, with psoriasis being stated as a reason for not having a tattoo by 44.0% and 5.7% indicating that they planned to have a tattoo in the future. Local complications, such as oedema, pruritus, allergy and Koebner phenomenon, were reported in tattoos in 6.6%, most frequently in patients with psoriasis requiring treatment at the time of tattooing (P < 0.0001). No severe complications were reported. CONCLUSIONS: The rate of tattoo complications in psoriasis patients was low. Although the risk of complications was highest amongst patients with psoriasis requiring treatment at the time of tattooing, all the complications observed were benign. These results can be helpful for practitioners to give objective information to patients.

[Leg ulcers occurring under tyrosine kinase inhibitor therapy (sunitinib, nilotinib)]. / Ulcères des membres inférieurs développés sous inhibiteurs de tyrosine kinase (sunitinib, nilotinib).

BACKGROUND: Certain anticancer drugs are known to induce leg ulcers, mainly chemotherapy agents such as hydroxyurea. We report 2 cases of leg ulcers in cancer patients treated with the tyrosine kinase inhibitors, sunitinib and nilotinib, and we discuss the role of these treatments in the pathogenesis of leg ulcers. PATIENTS AND METHODS: Case 1. A 62-year-old patient on sunitinib for intrahepatic cholangiocarcinoma developed a lesion on her right foot. The vascular evaluation was negative. After progressive worsening, sunitinib was stopped and healing was observed within a few months. Case 2. A 83-year-old patient had been treated for chronic myeloid leukemia since 2005. Nilotinib was introduced in 2009. Peripheral arterial revascularization was required in May 2013. A few months later, worsening was noted with the onset of ulceration and necrosis of the third toe. Further revascularisation surgery was performed, and nilotinib was suspended and antiplatelets introduced. Healing occurred a few months later. DISCUSSION: Many skin reactions have been described in patients on nilotinib and sunitinib, but few publications report the development of de novo ulcers in patients without risk factors. The pathophysiology of the development of ulcers in patients receiving tyrosine kinase inhibitors is not clear, and probably involves several mechanisms of action. The increasing use of this type of treatment could lead to an upsurge in the incidence of vascular complications. CONCLUSION: We report two cases of leg ulcers developing in patients on tyrosine kinase inhibitors and raise the question of causal implication of these treatments in the pathogenesis of ulcers.

[Cutaneous tuberculosis and erythema induratum: a retrospective study of 13 cases in France]. / Tuberculose cutanée et érythème induré de Bazin: étude rétrospective de 13 cas.

BACKGROUND: Tuberculosis is the most common mycobacterial disease in the world. The cutaneous form is rare in low endemic countries. The occurrence of several cutaneous tuberculosis cases in our dermatology department during 2011-2012 led us to investigate whether there was a resurgence of cutaneous tuberculosis in France. The aim was to analyse changes in cutaneous tuberculosis and the related clinical, microbiological and therapeutic data. PATIENTS AND METHODS: We conducted a retrospective study in our hospital between 2005 and 2012 by querying the PMSI database (code: A 18.4). Epidemiological, clinical, paraclinical and therapeutic data were collected. Erythema induratum was regarded as a variety of cutaneous tuberculosis. RESULTS: Thirteen patients presented cutaneous tuberculosis between 2005 and 2012. The most frequent clinical forms were erythema induratum of Bazin (n=6) and scrofuloderma (n=3). Microbiological evidence was provided in only 4 cases. DISCUSSION: Diagnosis is difficult due to the varied clinical forms and to the relatively high frequency of paucibacillary forms. Further, the set of additional examinations is non-specific. In some cases, it is only therapeutic tests that allow diagnosis to be made. The place of new diagnostic tools must be clarified and a universally acceptable definition of erythema induratum devised.

[Subcutaneous calcinosis, a late and severe complication of radiotherapy: Three cases]. / La calcinose sous-cutanée, une complication rare et sévère de la radiothérapie: trois observations.

BACKGROUND: Radiation-induced subcutaneous calcinosis is a rare and special form of potentially severe subcutaneous calcinosis of late onset. Herein, we report three cases of this disease, occurring in each instance more than 10 years after use of radiotherapy as an adjuvant treatment in breast cancer. PATIENTS AND METHODS: Our report concerns 3 women aged 69-88 years consulting for pre-sternal ulcers (n=2) and/or subcutaneous nodules (n=2). These lesions developed on areas irradiated between 10 and 38 years earlier for breast cancer. In all three cases, radiological explorations showed extensive subcutaneous calcification. In one case, calcification extended into the mediastinum. In each patient, a diagnosis of radiation-induced subcutaneous calcinosis was made and symptomatic treatment was given. DISCUSSION: Radiation-induced subcutaneous calcinosis is an irreversible and rare complication of high-dose radiation that usually occurs several years after radiotherapy. Its severity is related to potential ulcerations, pain and a risk for in-depth extension up to the mediastina. This complication remains unclear and treatment has not been codified. The only option seems to be "heavy" plastic surgery.

[Acute finger ischemia: A retrospective study of 13 patients]. / Ischémie digitale aiguë : étude rétrospective de 13 cas.

BACKGROUND: Acute ischemia of the upper limbs is rare in comparison with ischemia of the lower limbs. The origins of this condition are varied. GOALS: We retrospectively analyzed cases of acute finger ischemia (Raynaud's phenomena was excluded) in a dermatology department between 2008 and 2013 in order to evaluate the etiology and management of this phenomenon. RESULTS: Thirteen cases of finger ischemia were reported. The mean age was 54 years. Active smoking was noted in 11 cases. Ischemia was acute in 9 cases and subacute in 4 cases. The location was unilateral in 10 cases and bilateral in 2. Etiologies were: dysplasia of the palmar arch, antiphospholipid antibody syndrome, frostbite, distal arteritis linked to smoking, paraneoplastic arteritis, Buerger's disease, polyarteritis nodosa, stenosis of the subclavian artery, and 3 cases of embolic origin (ulnar, cardiac, and paraneoplastic aneurysm). In the acute phase, antiplatelets were given in 6 cases, anticoagulants in 10 cases and ilomedin in 6 cases. Sympathectomy was performed in 1 case and amputation in 2 cases. DISCUSSION: This study illustrates the diversity of etiologies of finger ischemia. The etiological test battery should be broad and include immunological and thrombophilia tests, arterial and cardiac investigations, cervical radiography and CT scan (screening for cancer). Close collaboration between dermatologists, hematologists, vascular surgeons and radiologists is essential for the management of these patients.

Ca²âº signals promote GLUT4 exocytosis and reduce its endocytosis in muscle cells.

Elevating cytosolic Ca(2+) stimulates glucose uptake in skeletal muscle, but how Ca(2+) affects intracellular traffic of GLUT4 is unknown. In tissue, changes in Ca(2+) leading to contraction preclude analysis of the impact of individual, Ca(2+)-derived signals. In L6 muscle cells stably expressing GLUT4myc, the Ca(2+) ionophore ionomycin raised cytosolic Ca(2+) and caused a gain in cell surface GLUT4myc. Extra- and intracellular Ca(2+) chelators (EGTA, BAPTA-AM) reversed this response. Ionomycin activated calcium calmodulin kinase II (CaMKII), AMPK, and PKCs, but not Akt. Silencing CaMKIIδ or AMPKα1/α2 partly reduced the ionomycin-induced gain in surface GLUT4myc, as did peptidic or small molecule inhibitors of CaMKII (CN21) and AMPK (Compound C). Compared with the conventional isoenzyme PKC inhibitor Gö6976, the conventional plus novel PKC inhibitor Gö6983 lowered the ionomycin-induced gain in cell surface GLUT4myc. Ionomycin stimulated GLUT4myc exocytosis and inhibited its endocytosis in live cells. siRNA-mediated knockdown of CaMKIIδ or AMPKα1/α2 partly reversed ionomycin-induced GLUT4myc exocytosis but did not prevent its reduced endocytosis. Compared with Gö6976, Gö6983 markedly reversed the slowing of GLUT4myc endocytosis triggered by ionomycin. In summary, rapid Ca(2+) influx into muscle cells accelerates GLUT4myc exocytosis while slowing GLUT4myc endocytosis. CaMKIIδ and AMPK stimulate GLUT4myc exocytosis, whereas novel PKCs reduce endocytosis. These results identify how Ca(2+)-activated signals selectively regulate GLUT4 exocytosis and endocytosis in muscle cells.

[Two cases of severe pruritus revealing Hodgkin's disease in children]. / Prurit sévère révélant un lymphome de Hodgkin chez l'enfant : deux observations.

BACKGROUND: Pruritus in children is a frequent reason for consultation, most often related to a common dermatosis. Where dermatological investigation fails to reveal a dermatological cause, a general cause may be suspected. We report three cases of pruritus revealing Hodgkin's lymphoma in children. PATIENTS AND METHODS: Case 1: a 14-year-old girl presented pruritus with diffuse scratching lesions present for 6 months, associated with right cervical lymph nodes occurring after the onset of pruritus. Tomodensitometry revealed involvement of the supra- and sub-diaphragmatic lymph nodes as well as pulmonary involvement. Lymph node biopsy confirmed nodular sclerosing Hodgkin's lymphoma. Case 2: a 14-year-old boy was hospitalized for suspected psychogenic pruritus. He presented intense itching, predominantly in the lower extremities and at night, occurring over the previous 6 months as well as night sweats. Examination showed that the patient had lost 5kg in 1 month and had a low-grade fever of 38°C; he presented linear striated scratching lesions on both legs. Cervical and inguinal lymphadenopathy was seen. The chest scan also revealed supra-diaphragmatic adenomegalies. The biopsy confirmed Hodgkin's lymphoma. DISCUSSION: Systemic causes of pruritus in children are poorly described in the literature. In these two cases, pruritus allowed a diagnosis of Hodgkin's lymphoma to be made, emphasizing the important role of dermatologists in the early diagnosis of haematological malignancy.

[Phlegmasia cerulea dolens]. / La phlébite bleue.

BACKGROUND: Herein we report a case of phlegmasia cerulea dolens, a form of venous thrombosis complicated by arterial ischaemia. PATIENTS AND METHODS: A 69-year-old man presented a bilateral trophic condition of the lower limbs that had appeared 3 weeks earlier. The patient had a history of metastatic urothelial bladder carcinoma and arteritis. Clinical examination revealed right leg ulcers with massive bilateral oedema of the lower limbs, cyanosis and local ischaemia. Doppler ultrasound revealed bilateral and proximal deep vein thrombosis (sural and superficial femoral veins of the right leg; sural and iliac veins of the left leg) without any distal arterial flow. We concluded on a diagnosis of bilateral phlegmasia cerulea dolens. DISCUSSION: Phlegmasia cerulea dolens is a particular type of deep venous thrombosis in which a proximal venous thrombus is combined with arterial ischaemic signs due to brutal and massive oedema and slowing down of arterial flow. In most cases, the lower limbs are involved, with malignancy being the most common cause. It should be suspected in the presence of the classical triad of "pain, oedema and cyanosis", with confirmation by Doppler ultrasound. There is no general consensus regarding standard management. Traditionally, systemic anticoagulation has been the mainstay of treatment for this condition. Endovascular surgery may be a possibility in some cases. Prompt diagnosis and rapid treatment initiation are paramount in order to improve the prognosis of this severe condition with ominous prospects.

[Erythrokeratodermia variabilis]. / Érythrokératodermie variable.

BACKGROUND: Erythrokeratodermia variabilis (EKV) is a rare genodermatosis associated with keratinisation disorders. Mutations are found in genes encoding connexin 31 and 30.3 mapped to chromosome 1 p34-35. We report two cases of EKV, one of which presented dramatic improvement with oral retinoids. PATIENTS AND METHODS: A 15-month-old boy was referred to us with reddish-brown hyperkeratotic and well-demarcated plaques on the extremities, axillary space and face. The lesions started when he was 6months of age. Cutaneous histopathology showed acanthosis and papillomatosis associated with orthokeratotic hyperkeratosis. Anatomoclinical comparison confirmed the diagnosis of EKV. A second child aged 10years was referred to us with fixed, well-demarcated hyperkeratotic plaques associated with transient red patches. The lesions began when she was 1month old. Anatomoclinical comparison confirmed the diagnosis of EKV and the patient showed dramatic improvement after 2weeks on acitretin. DISCUSSION: EKV is characterized by the association of fixed well-demarcated plaques and transient erythematous patches. Although cutaneous histopathology is not specific, a typical physical examination and a compatible cutaneous histopathology can aid the diagnosis. Oral retinoids are often very rapidly effective.

Intracellular transport of the transmembrane glycoprotein G of vesicular stomatitis virus through the Golgi apparatus as visualized by electron microscope radioautography.

The intracellular migration of G protein in vesicular stomatitis virus-infected cells was visualized by light and electron microscope radioautography after a 2-min pulse with [3H]mannose followed by nonradioactive chase for various intervals. The radioactivity initially (at 5-10 min) appeared predominantly in the endoplasmic reticulum, and the [3H]mannose-labeled G protein produced was sensitive to endoglycosidase H. Silver grains were subsequently (at 30-40 min) observed over the Golgi apparatus, and the [3H]mannose-labeled G protein became resistant to endoglycosidase H digestion. Our data directly demonstrate the intracellular transport of a plasmalemma-destined transmembrane glycoprotein through the Golgi apparatus.

Protein kinase B/Akt participates in GLUT4 translocation by insulin in L6 myoblasts.

L6 myoblasts stably transfected with a GLUT4 cDNA harboring an exofacial myc epitope tag (L6-GLUT4myc myoblasts) were used to study the role of protein kinase B alpha (PKBalpha)/Akt1 in the insulin-induced translocation of GLUT4 to the cell surface. Surface GLUT4myc was detected by immunofluorescent labeling of the myc epitope in nonpermeabilized cells. Insulin induced a marked translocation of GLUT4myc to the plasma membrane within 20 min. This was prevented by transient transfection of a dominant inhibitory construct of phosphatidylinositol (PI) 3-kinase (Deltap85alpha). Transiently transfected cells were identified by cotransfection of green fluorescent protein. A constitutively active PKBalpha, created by fusion of a viral Gag protein at its N terminus (GagPKB), increased the cell surface density of GLUT4myc compared to that of neighboring nontransfected cells. A kinase-inactive, phosphorylation-deficient PKBalpha/Akt1 construct with the mutations K179A (substitution of alanine for the lysine at position 179), T308A, and S473A (AAA-PKB) behaved as a dominant-negative inhibitor of insulin-dependent activation of cotransfected wild-type hemagglutinin (HA)-tagged PKB. Furthermore, AAA-PKB markedly inhibited the insulin-induced phosphorylation of cotransfected BAD, demonstrating inhibition of the endogenous PKB/Akt. Under the same conditions, AAA-PKB almost entirely blocked the insulin-dependent increase in surface GLUT4myc. PKBalpha with alanine substitutions T308A and S473A (AA-PKB) or K179A (A-PKB) alone was a less potent inhibitor of insulin-dependent activation of wild-type HA-PKB or GLUT4myc translocation than was AAA-PKB. Cotransfection of AAA-PKB with a fourfold DNA excess of HA-PKB rescued insulin-stimulated GLUT4myc translocation. AAA-PKB did not prevent actin bundling (membrane ruffling), though this response was PI 3-kinase dependent. Therefore, it is unlikely that AAA-PKB acted by inhibiting PI 3-kinase signaling. These results outline an important role for PKBalpha/Akt1 in the stimulation of glucose transport by insulin in muscle cells in culture.

Opposite effects of insulin on focal adhesion proteins in 3T3-L1 adipocytes and in cells overexpressing the insulin receptor.

Insulin can regulate the abundance and organization of filamentous actin within cells in culture. Early studies using cell lines that overexpress the insulin receptor demonstrated that insulin caused a rapid reversible disassembly of actin filaments that coincided with the rapid tyrosine dephosphorylation of focal adhesion kinase. We have extended these studies by demonstrating that paxillin, another focal adhesion protein, and Src undergo tyrosine dephosphorylation in response to insulin in Chinese hamster ovary (CHO) and rat hepatoma (HTC) cells that overexpress the insulin receptor. This contrasted with the effect of insulin in parental CHO and HTC cells in which focal adhesion proteins were not dephosphorylated in response to the hormone. In addition, insulin caused a dispersion of focal adhesion proteins and disruption of actin filament bundles only in cells that overexpressed the insulin receptor. Moreover, in 3T3-L1 adipocytes, which are considered prototypic insulin-responsive cells, actin filament assembly was stimulated, and focal adhesion protein tyrosine phosphorylation was not altered. 3T3-L1 cells have more insulin receptors than either parental CHO or HTC cells but have fivefold less insulin receptors than the overexpressing cell lines. We hypothesize that a threshold may exist in which the overexpression of insulin receptors determines how insulin signaling pathways regulate the actin cytoskeleton.

VAMP2, but not VAMP3/cellubrevin, mediates insulin-dependent incorporation of GLUT4 into the plasma membrane of L6 myoblasts.

Like neuronal synaptic vesicles, intracellular GLUT4-containing vesicles must dock and fuse with the plasma membrane, thereby facilitating insulin-regulated glucose uptake into muscle and fat cells. GLUT4 colocalizes in part with the vesicle SNAREs VAMP2 and VAMP3. In this study, we used a single-cell fluorescence-based assay to compare the functional involvement of VAMP2 and VAMP3 in GLUT4 translocation. Transient transfection of proteolytically active tetanus toxin light chain cleaved both VAMP2 and VAMP3 proteins in L6 myoblasts stably expressing exofacially myc-tagged GLUT4 protein and inhibited insulin-stimulated GLUT4 translocation. Tetanus toxin also caused accumulation of the remaining C-terminal VAMP2 and VAMP3 portions in Golgi elements. This behavior was exclusive to these proteins, because the localization of intracellular myc-tagged GLUT4 protein was not affected by the toxin. Upon cotransfection of tetanus toxin with individual vesicle SNARE constructs, only toxin-resistant VAMP2 rescued the inhibition of insulin-dependent GLUT4 translocation by tetanus toxin. Moreover, insulin caused a cortical actin filament reorganization in which GLUT4 and VAMP2, but not VAMP3, were clustered. We propose that VAMP2 is a resident protein of the insulin-sensitive GLUT4 compartment and that the integrity of this protein is required for GLUT4 vesicle incorporation into the cell surface in response to insulin.

Replacement of mouse LM fibroblast choline by a sulfonium analog. Effects on membrane properties as determined by virus probes.

A sulfonium analog of choline ('sulfocholine', a natural phospholipid constituent of diatoms) was metabolically incorporated into mouse LM fibroblasts cultured in serum-free medium. Subconfluent cultures of LM cells were able to utilize sulfocholine as sole choline source and to increase in cell number for 3 days of incubation; thereafter a decrease in cell number was observed. In contrast, cultures of LM cells seeded to confluency showed no decrease in cell number up to at least 10 days when maintained, with daily medium changes, in medium containing either choline or the sulfonium analog. Such confluent cultures, maintained for 7 days in sulfocholine-containing medium, showed virtually complete replacement of cellular phosphatidylcholine and greater than 50% replacement of cellular sphingomyelin by their respective sulfonium analogs. The functional exchangeability of natural phosphatidylcholine and sphingomyelin with their sulfonium analogs to participate in normal cell membrane-mediated activities was demonstrated by comparatively assaying the abilities of sulfocholine- and choline-maintained cells to incorporate and replicate certain animal viruses known to possess membrane-dependent steps in various phases of their replication cycles. No difference was detected between the abilities of sulfocholine- and choline-maintained cells to take up vesicular stomatitis virus or mengo virus, or to replicate vesicular stomatitis virus, mengo virus or mouse hepatitis virus.

Reduction of insulin-stimulated glucose uptake in L6 myotubes by the protein kinase inhibitor SB203580 is independent of p38MAPK activity.

Insulin increases glucose uptake through translocation of the glucose transporter GLUT4 to the plasma membrane. We previously showed that insulin activates p38MAPK, and inhibitors of p38MAPKalpha and p38MAPKbeta (e.g. SB203580) reduce insulin-stimulated glucose uptake without affecting GLUT4 translocation. This observation suggested that insulin may increase GLUT4 activity via p38alpha and/or p38beta. Here we further explore the possible participation of p38MAPK through a combination of molecular strategies. SB203580 reduced insulin stimulation of glucose uptake in L6 myotubes overexpressing an SB203580-resistant p38alpha (drug-resistant p38alpha) but barely affected phosphorylation of the p38 substrate MAPK-activated protein kinase-2. Expression of dominant-negative p38alpha or p38beta reduced p38MAPK phosphorylation by 70% but had no effect on insulin-stimulated glucose uptake. Gene silencing via isoform-specific small interfering RNAs reduced expression of p38alpha or p38beta by 60-70% without diminishing insulin-stimulated glucose uptake. SB203580 reduced photoaffinity labeling of GLUT4 by bio-LC-ATB-BMPA only in the insulin-stimulated state. Unless low levels of p38MAPK suffice to regulate glucose uptake, these results suggest that the inhibition of insulin-stimulated glucose transport by SB203580 is likely not mediated by p38MAPK. Instead, changes experienced by insulin-stimulated GLUT4 make it susceptible to inhibition by SB203580.

Insulin-stimulated glucose transport in circulating mononuclear cells from nondiabetic and IDDM subjects.

The objectives of this study were 1) to evaluate glucose transport and its regulation by insulin in easily accessible human cells, 2) to investigate the glucose transporter isoforms involved, and 3) to establish whether a defect in glucose transport is associated with peripheral insulin resistance, which is common in insulin-dependent diabetes mellitus (IDDM) patients. We measured 2-deoxyglucose (2-DG) uptake in circulating mononuclear cells from 23 nondiabetic adults, 16 adults with IDDM, and 10 children with IDDM. Circulating mononuclear cells were separated from whole blood by Ficoll gradients and incubated with +/- 1 nM insulin. 2-DG uptake was measured after incubation with [3H]2-DG and cell separation through corn oil-phthalate. Cytochalasin B-inhibitable 2-DG uptake (basal and insulin stimulated) was higher in control than in IDDM subjects (P less than 0.001). Insulin significantly increased 2-DG uptake or 3-O-methylglucose uptake in both groups. Basal and insulin-stimulated 2-DG uptake was similar for adults and children with IDDM and did not correlate with age or body mass index in any group or disease duration, insulin dosage, or HbA1c in IDDM. In separated monocytes and lymphocytes, 2-DG uptake increased in response to insulin only in the monocyte population. Insulin dose-response curves indicated maximal stimulation of hexose uptake at 1-2 nM insulin for both control and diabetic subjects and demonstrated a significant decrease in maximal insulin response in the latter. Immunoblotting with specific antibodies revealed that circulating mononuclear cells and separated monocytes express the GLUT1 but not the GLUT4 isoform of the glucose transporter.(ABSTRACT TRUNCATED AT 250 WORDS)

[Crusted scabies induced by topical corticosteroids: A case report]. / Gale hyperkératosique favorisée par l'utilisation de dermocorticoïdes : à propos d'un cas.

The frequency of scabies is increasing in France. Crusted (or Norwegian) scabies is a very contagious form of scabies because of the huge number of mites in the skin. It is observed in patients suffering from immunodepression, motor or sensory deficiency, or mental retardation. The clinical presentation, except for the classic manifestation of scabies, is characterized by crusted lesions. Treatment is not easy and requires hospitalization. Topical corticosteroids are frequently used for children's dermatological diseases. Their long-term and inappropriate application in an infested scabies child can induce crusted scabies. We report on a case of an 8-year-old boy who developed crusted scabies induced by topical corticosteroid application. We discuss the therapeutic aspects of this severe form of scabies.

[Compression care for venous leg ulcers: Assessment of medical practices in 100 patients]. / La compression dans la prise en charge des ulcères veineux des membres inférieurs. Évaluation des pratiques professionnelles sur 100 patients.

INTRODUCTION: The etiologic treatment of venous ulcers is based on compression therapy in compliance with the new guidelines promulgated by the French National Authority for Health (HAS) in 2010. Prescriptions often originate from a request by the nurse delivering care in the patient's home. A recent French study demonstrated the positive impact of compression therapy on venous ulcer healing. The objective of this study was to evaluate medical practices in order to target corrective actions. MATERIALS AND METHODS: We conducted a single-center prospective observational study, using a standardized questionnaire from January to May 2014. Patients with venous ulcers who had an indication for compression therapy were included consecutively. The questionnaire collected demographic and clinical data and also recorded the results of complementary tests and the characteristics of the compression therapy. RESULTS: One hundred patients were included (61 women and 39 men). The average age was 76 years. Patients were recruited during consultations (n = 69), with a majority of patients living at home (n = 80) and receiving home care delivered by a nurse (n = 81). Thirteen patients were seen for the first time and 87 patients were receiving long-term care. The ulcers evolved for 5.7 years on average. Patients presented peri-lesional edema (n = 58), ankle ankylosis (n = 49), autonomous mobilization (n = 40) and walking problems (n = 60). Physical therapy was prescribed for 39 patients and was effectively carried out for 24. The two main causes were venous varices (n = 66) and post-phlebitis disease (n = 18). Compression therapy was prescribed for 97 patients and the products delivered by the pharmacy were consistent with the prescription for 74 patients. Compliance with compression therapy was faulty for 28 patients because of poor tolerance, misunderstanding, manipulation problems, or inappropriate footwear. At assessment, 66 patients were wearing the bands, but not always correctly (starting at the base of the toes [n = 61], heel included [n = 43], proper stretching [n = 43] up to below the knee [n = 57]). Proper footwear was noted in 70 patients. CONCLUSION: Data are scarce on compliance with compression banding. This study shows that further efforts are needed to ensure proper patient education and professional training for physicians and allied profession concerning the installation of compression therapy. Total compliance was observed in only 35% of patients. In addition, the products delivered by the pharmacy were not consistent with the prescription in 26% of cases. Many discrepancies were observed between what was prescribed and what the patients achieved. Patient adherence is a crucial issue for compression therapy.