Looking for:
Prednisone efectos secundarios |
Corticosteroid Adverse Effects - StatPearls - NCBI Bookshelf - Reacciones adversas de los corticoides
Prednisone efectos secundarios. Prednisone EG
Impossibile parlare con un settore di security. Muro di gomma: instra. Zoe e Anna bravissime a spiegare in modo semplice, concreto ed efficace nozioni importantissime.
❾-50%}Prednisone efectos secundarios
La hiperglicemia inducida por esteroides se define como un aumento anormal de la glicemia asociada con el uso de glucocorticoides GC en un paciente con o sin antecedentes de diabetes mellitus.
Se utilizan tanto en pacientes internados como en pacientes en forma ambulatoria 3. Debido a las diferencias en la dosis de esteroides y el esquema utilizado, el enfoque del tratamiento de la hiperglicemia esteroidea siempre debe ser individualizado Las variables laboratoriales fueron: glicemias basales, glicemias postprandiales, HbA 1C , urea y creatinina,.
Figura 1 Hemoglobina glicada en pacientes con corticoterapia n Figura 2 Antecedente de diabetes mellitus en pacientes con corticoterapia n Figura 3 Indicaciones de corticoterapia n GC: paradigma de medicina traslacional.
Medicina B. Suh S, Park MK. Glucocorticoid-Induced diabetes mellitus: An important but Overlooked problem. Endocrinol Metab Seoul. Diabetes e hiperglicemia inducida por corticoides. Med La Paz. Steroid-induced insulin resistance and impaired glucose tolerance are both associated with a progressive decline of incretin effect in first-degree relatives of patients with type 2 diabetes.
Novel insights into glucocorticoid-mediated diabetogenic effects: towards expansion of therapeutic options?. Eur J Clin Invest. Acute and 2-week exposure to prednisolone impair different aspects of beta-cell function in healthy men. Eur J Endocrinol. Acta Med Iran. Ghrelin directly stimulates glucagon secretion from pancreatic alpha-cells.
Before initiating long-term systemic glucocorticoid therapy, the clinician should perform a thorough history and physical examination to assess for risk factors or preexisting conditions that may potentially be exacerbated by glucocorticoid therapy, such as above. In children, the clinician should also examine nutritional and pubertal status. American College of Rheumatology has published specific guidelines addressing this issue to help prevent and manage GiOp.
The HPA axis should undergo assessment if the patient has received systemic corticosteroids for more than two consecutive weeks or more than three cumulative weeks in the last six months or if the patient has persistent symptoms of adrenal suppression. Screening is by measuring early morning salivary cortisol after tapering off the dose of cortisol.
If morning cortisol is normal, but the patient has symptoms of adrenal suppression, perform a low-dose ACTH stimulation test to confirm the diagnosis. Consider endocrinology referral for confirmation of diagnosis. Growth in children and adolescents on chronic glucocorticoid therapy shall be monitored every six months and plotted on a growth curve.
Lipid profile shall be monitored one month after glucocorticoid initiation and then every 6 to 12 months. Glycemic control requires assessment via screening for classic symptoms at every visit: polyuria, polydipsia, weight loss.
Monitor glucose parameters for at least 48 hours after glucocorticoids initiation, then every 3 to 6 months for the first year and annually afterward. In children, an annual oral glucose tolerance test merits consideration if the child is obese or has risk factors for diabetes.
An annual ophthalmological examination shall be considered, especially for those with symptoms of cataracts, and early referral for intraocular pressure assessment should occur if there is a personal or family history of open-angle glaucoma, diabetes mellitus, or high myopia.
Patients who also require concomitant treatment with non-steroidal anti-inflammatory drugs NSAIDs or anticoagulants shall receive therapy with proton pump inhibitors PPI. Patients who require an extended course of glucocorticoids, especially high doses, shall receive appropriate immunizations before the institution of therapy. Prophylaxis for opportunistic infection with Pneumocystis jirovecii pneumonia PCP is also recommended in patients receiving prednisone at a dose of 20 mg or more for more than two weeks.
The prophylaxis can stop once the dose of prednisone is below 20 mg daily dose. Concomitant use of other medications also merits attention before initiating therapy as significant drug interactions exist between glucocorticoids and several drug classes. Abrupt cessation of chronic glucocorticoid therapy can be dangerous as there is a risk of HPA axis suppression. Withdrawal of glucocorticoid therapy needs tapering over the period. In general, patients who are given acute corticosteroid therapy for less than 14 to 21 days do not develop HPA axis suppression, and treatment can stop with no need for any tapering regime in them.
If the therapy has been ongoing for greater than three weeks, tapering is needed e. Acute psychosis can develop in patients receiving high-dose glucocorticoids. Immediate cessation of the drug on the appearance of symptoms is the first step. Although many drugs, including antipsychotics, antidepressants, benzodiazepines, and hydrocortisone, have been tried with variable success, currently, there is no consensus on the ideal therapeutic remedy to stop and reverse the corticosteroid-induced neuropsychiatric adverse effects in adults or children.
Their specific adverse effects further limit the use of the medications mentioned above. Physiologic doses of hydrocortisone have shown to improve mild to moderate psychosocial disturbances and insomnia experienced by children who developed severe behavioral problems with dexamethasone-based treatment regime administered to treat ALL.
No adverse effects were found with oral KCl supplementation. Glucocorticoids are widely used to manage many acute and chronic inflammatory disorders. The adverse effects of glucocorticoids are extensive and can involve many organ systems.
While short-term use of corticosteroids is associated with mild side effects, long-term use can result in several severe adverse effects, some of which are irreversible. This is why an interprofessional team approach to corticosteroid therapy and subsequent monitoring is necessary. Clinicians shall consider adverse effects and patients' underlying comorbidities before prescribing glucocorticoids and use glucocorticoids judiciously.
The clinician should use the lowest possible dose for the shortest possible. Patient education is vital in recognizing the adverse effects early. Children are particularly vulnerable to the side effects of corticosteroids, and parents need to understand the benefits and adverse effects of glucocorticoids.
Pharmacists shall alert physicians about possible drug interactions, check dosing and duration, and answer patient questions. The nursing team can play a crucial role in communication with the patient, early detection of adverse effects, and regular monitoring.
Close communication with other health professionals is necessary to ensure that the patient is not left unmonitored. This book is distributed under the terms of the Creative Commons Attribution 4. Turn recording back on. Help Accessibility Careers. StatPearls [Internet]. Search term. Continuing Education Activity Corticosteroids are hormone mediators produced by the cortex of adrenal glands that further categorize into glucocorticoids, mineralocorticoids, and androgenic sex hormones.
Indications Corticosteroids are hormone mediators produced by the cortex of adrenal glands that are further categorized into glucocorticoids major glucocorticoid produced by the body is cortisol , mineralocorticoids major mineralocorticoid produced in the body is aldosterone , and androgenic sex hormones.
As a Replacement Therapy Adrenocortical insufficiency Addison disease. Acute exacerbation of autoimmune diseases such as multiple sclerosis, vitiligo, uveitis, rheumatoid arthritis, SLE, etc.
Cerebral edema: Recommended only in specific conditions like elevated intracranial pressure due to the neoplasm or central nervous system CNS infection; generally avoided in moderate to severe brain injury.
Chronic inflammatory diseases asthma, chronic obstructive pulmonary disease, inflammatory bowel disease. Local symptomatic treatment: anterior uveitis, steroid-responsive dermatoses SRD , tenosynovitis, and osteoarthritis or juvenile idiopathic arthritis. Mechanism of Action Anti-Inflammatory and Immunosuppressive Effects The anti-inflammatory and immunosuppressive effects of glucocorticoids are dose-dependent, with immunosuppressive effects seen mostly at higher doses.
Genomic Mechanisms Being small, lipophilic substances, glucocorticoids readily pass the cell membrane by diffusion and enter the cytoplasm of the target cells, where most of their action is mediated by binding to the intra-cytoplasmic glucocorticoid receptors.
Non-Genomic Mechanisms The immediate effects of high dose-glucocorticoids are mediated via non-genomic mechanisms. The downstream effects of glucocorticoids are summarized below: Inhibition of neutrophil adhesion to endothelial cells and demargination of neutrophils from the marginal pool of blood vessels causing neutrophilic leukocytosis.
A decrease in the number of lymphocytes, macrophages, monocytes, eosinophils, and basophils decreased myelopoiesis and release from bone marrow, and increased apoptosis. Reduction in the formation of arachidonic acid derivatives by the promotion of synthesis of lipocortin-A that inhibits phospholipase A2. Inhibition of metalloproteinases collagenase and stromelysin, which are otherwise responsible for cartilage degradation.
Administration Several preparations of glucocorticoids are available, each with varying efficacy. Intravenous Administration Parenteral intravenous administration of high doses of glucocorticoids may be warranted in emergencies, such as septic shock, COPD exacerbation, and severe acute asthma.
Oral Administration Oral preparations are usually useful in both acute and chronic indications. Local Administration Glucocorticoid administration can be via several non-systemic routes, including intra-articular joint injections for joint inflammation, inhalational for asthma, topical for dermatological problems, ocular drops for eye conditions, and intra-nasal for seasonal rhinitis. Adverse Effects Factors Influencing the Adverse Effects of Glucocorticoids Given the diversity in the mechanism of action of glucocorticoids, they can cause a wide array of adverse effects ranging from mild to severe, some of which are unavoidable.
Musculoskeletal Adverse Effects Glucocorticoids induced Osteoporosis is one of the well-known and devastating adverse effects of long-term use of glucocorticoids. Metabolic and Endocrine Adverse Effects Systemic glucocorticoids cause a dose-dependent increase in fasting glucose levels and a more significant increase in postprandial values in patients without preexisting diabetes mellitus, but the development of de novo diabetes in a patient with initially normal glucose tolerance is uncommon.
Infections Moderate to high dose use of glucocorticoids poses a significant risk of infections, including common mild infections as well as serious life-threatening infections. Cardiovascular Adverse Effects Mineralocorticoid effects, especially as seen with cortisol and cortisone, can lead to fluid retention, edema, weight gain, hypertension, and arrhythmias by increasing renal excretion of potassium, calcium, and phosphate.
Ophthalmologic Adverse Effects The risk of cataracts is significantly high in patients taking prednisone more than 10 mg daily for more than one year, with a dose-dependence in a linear fashion. Neuropsychiatric Adverse Effects Patients receiving glucocorticoids often experience an improved sense of well-being within several days of starting the medications; mild euphoria or anxiety may also occur.
Contraindications General contraindications include hypersensitivity. Systemic Systemic fungal infections. Concomitant live or live attenuated virus vaccination if using glucocorticoids in immunosuppressive doses. Ophthalmic: Acute untreated purulent ocular infections, fungal or mycobacterial ocular infections, viral conjunctivitis, or keratitis. Glucocorticoids administered topically, by aerosol, or by intra-articular or bursal injection, provided that there is no clinical or laboratory evidence of immunosuppression.
Monitoring Baseline Assessment and Monitoring Preexisting conditions that should be assessed for and treated when starting glucocorticoids include: Diabetes mellitus. All adults receiving prednisone 2. Clinical fracture risk reassessment shall be performed at baseline and every 12 months in patients receiving long-term glucocorticoids. Bone mineral density BMD measurement via DEXA scan shall be performed ideally before or within six months after the initiation of glucocorticoid therapy in all adults 40 years of age or more, and in adults younger than 40 years of age if there is a history of osteoporotic fractures or other risk factors for osteoporosis.
In adults 40 years of age or more, the year fracture risk assessment is necessary using the FRAX tool a diagnostic tool that incorporates clinical factors and bone mineral density at the femoral neck. Based on the above data, in addition to the dose and duration of glucocorticoid therapy, patients fall into three fracture risk categories: low risk, moderate risk, and high risk.
Their fracture risk category shall dictate further management. Bisphosphonates, teriparatide, or denosumab shall be recommended in patients less than 40 years of age but in the moderate or high fracture risk category.
Bisphosphonates, teriparatide, denosumab, or raloxifene shall be recommended in patients 40 years of age or more in the moderate or high fracture risk category. Lateral spine X-ray shall be considered in adults 65 years of age or older to evaluate for vertebral fractures. Use of the lowest dose of glucocorticoids for the shortest period needed to achieve the treatment goals. Toxicity Acute psychosis can develop in patients receiving high-dose glucocorticoids.
Enhancing Healthcare Team Outcomes Glucocorticoids are widely used to manage many acute and chronic inflammatory disorders. Review Questions Access free multiple choice questions on this topic. Comment on this article. References 1. The effect of a hormone of the adrenal cortex hydroxydehydrocorticosterone; compound E and of pituitary adrenocorticotropic hormone on rheumatoid arthritis.
Proc Staff Meet Mayo Clin. Chikanza IC. Mechanisms of corticosteroid resistance in rheumatoid arthritis: a putative role for the corticosteroid receptor beta isoform. Ann N Y Acad Sci. Mechanisms involved in the side effects of glucocorticoids. Pharmacol Ther. Low dose long-term corticosteroid therapy in rheumatoid arthritis: an analysis of serious adverse events.
Am J Med. Ann Rheum Dis, 58 , pp. Maillefert, B. Combe, P. Goupille, A. Cantagrel, M. Long term structural effects of combination therapy in patients with early rheumatoid arthritis: five year follow up of a prospective double blind controlled study.
Ann Rheum Dis, 62 , pp. Goekoop-Ruiterman, J. De Vries-Bouwstra, C. Allaart, D. Van Zeben, P. Kerstens, J.
Hazes, et al. Clinical and radiographic outcomes of four different treatment strategies in patients with early rheumatoid arthritis the BeSt study. Arthritis Rheum, 52 , pp. Hansen, J. Podenphant, A. Florescu, M. Stoltenberg, A. Borch, E. Kluger, et al. A randomised trial of differenciated prednisolone treatment in active rheumatoid arthritis.
Clinical benefits and skeletal side effects. Paulus, D. Di Primeo, M. Sanda, J. Lynch, B. Schwartz, J. Sharp, et al. Progression of radiographic joint erosion during low dose corticosteroid treatment of rheumatoid arthritis. J Rheumatol, 27 , pp. Rau, S. Wassenberg, H. Low dose prednisolone therapy LDPT retards radiographically detectable destruction in early rheumatoid arthritis. Z Rheumatol, 59 ,. Zeidler, T. Kvien, P.
Hannoven, F. Wollheim, O. Forre, H. Geidel, et al. Progression of joint damage in early active severe rheumatoid arthritis during 18 months of treatment: Comparison of low-dose cyclosporin and parenteral gold.
Van Everdingen, J. Jacobs, D. Siewertsz van Reesema, J. Low-dose prednisone therapy for patients with early active rheumatoid arthritis: Clinical efficacy, disease-modifying properties, and side effects. Ann Intern Med, , pp. Van Everdingen, D. Jacobs, J. The clinical effect of glucocorticoids in patients with rheumatoid arthritis may be masked by decreased use of additional therapies.
Arthritis Rheum, 51 , pp. Jacobs, A. Van Everdingen, M. Verstapen, J. Followup radiographic data on patients with rheumatoid arthritis who participated in a two-year trial of prednisone or placebo. Arthritis Rheum, 54 , pp. Capell, R. Madhok, J. Hunter, D. Porter, E. Morrison, J. Lack of radiological and clinical benefit over two years of low dose prednisolone for rheumatoid arthritis: results of a randomised controlled trial.
Ann Rheum Dis, 63 , pp. Svensson, A. Boonen, K. Albertsson, D. Van der Heijde, C. Keller, I. Low-dose prednisolone in addition to the initial disease-modifying antirheumatic drug in patients with early active rheumatoid arthritis reduces joint destruction and increases the remission rate. Wassenberg, R. Rau, P. Steinfeld, H. Very low-dose prednisolone in early rheumatoid arthritis retards radiographic progression over two years.
Gotzsche, H. Short-term low-dose corticosteroids vs placebo and nonsteroidal antiinflammatory drugs in rheumatoid arthritis. Cochrane Database Syst Rev, , pp. Bijlsma, A. Huisman, R. De Nijs, J. Glucocorticoids in rheumatoid arthritis. Effects on erosions and bone. Ann NY Acad Sci, , pp. Sambrook, N. Best Pract Res Clin Rheumatol, 15 , pp. Luengo, C. Picado, L. Montserrat, J.
Vertebral fractures in steroid dependent asthma and involutional osteoporosis: a comparative study. Thorax, 46 , pp. Peel, D. Moore, N. Barrington, D.
Freddy Javier Bruno 1. Facultad de Medicina. Postgrado en Medicina Interna. Hospital Nacional. La prednisona fue el glucocorticoide utilizado con mayor frecuencia. Corticosteroid-induced hyperglycemia is a well-known adverse effect of glucocorticoid GC treatment. It can occur in both diabetic and non-diabetic patients. Observational, descriptive, longitudinal, prospective study carried out in men and women, older than 18 years old, who received enteral or parenteral corticotherapy and attended the outpatient clinical services of the Hospital Nacional in The autoimmune pathologies that most frequently required corticotherapy were systemic lupus erythematosus and rheumatoid arthritis.
Prednisone was the glucocorticoid used most frequently. No patient presented acute decompensation such as ketoacidosis or hyperosmolar state. The most frequent indication for the use of corticosteroids was autoimmune diseases and the most frequently used corticosteroid was prednisone. Keywords: corticosteroids - adverse effects; corticosteroids - therapeutic use; hyperglycemia; diabetes mellitus.
La hiperglicemia inducida por esteroides se define como un aumento anormal de la glicemia asociada con el uso de glucocorticoides GC en un paciente con o sin antecedentes de diabetes mellitus.
Se utilizan tanto en pacientes internados como en pacientes en forma ambulatoria 3. Debido a las diferencias en la dosis de esteroides y el esquema utilizado, el enfoque del tratamiento de la hiperglicemia esteroidea siempre debe ser individualizado Las variables laboratoriales fueron: glicemias basales, glicemias postprandiales, HbA 1Curea y creatinina.
Figura 1 Hemoglobina glicada en pacientes con corticoterapia n Figura 2 Antecedente de diabetes mellitus en pacientes con corticoterapia n Figura 3 Indicaciones de corticoterapia n GC: paradigma de medicina traslacional. Medicina B. Suh S, Park MK. Glucocorticoid-Induced diabetes mellitus: An important but Overlooked problem.
Endocrinol Metab Seoul. Diabetes e hiperglicemia inducida por corticoides. Med La Paz. Steroid-induced insulin resistance and impaired glucose tolerance are both associated with a progressive decline of incretin effect in first-degree relatives of patients with type 2 diabetes.
Novel insights into glucocorticoid-mediated diabetogenic effects: towards expansion of therapeutic options?. Eur J Clin Invest. Acute and 2-week exposure to prednisolone impair different aspects of beta-cell function in healthy men.
Eur J Endocrinol. Acta Med Iran. Ghrelin directly stimulates glucagon secretion from pancreatic alpha-cells. Mol Endocrinol.
Steroid hyperglycemia: Prevalence, early detection and therapeutic recommendations: A narrative review. World J Diabetes. Glucocorticoid-induced diabetic ketoacidosis in acute rheumatic fever. J Cardiovasc Pharmacol Ther. Management of hyperglycemia in the non-intensive care patient: Featuring subcutaneous insulin protocols.
Endocr Pract. Glucocorticoid-induced hyperglycemia. J Diabetes. Dipeptidyl peptidase-4 inhibitor for steroid-induced diabetes. World J Diabetes ;1 3 Intern Med. Indian J Endocrinol Metab. Glucocorticoid-induced Hyperglycemia.
Am J Med Sci ; 4 Incidence and risk factors of steroid-induced diabetes in patients with respiratory disease. J Korean Med Sci. Uso y abuso de los corticoides en las enfermedades respiratorias. Rev Chil Enf Respir ;29 2 [ Links ]. Short term use of oral corticosteroids and related harms among adults in the United States: population based cohort study. BMJ ;j A practical guide to the monitoring and management of the complications of systemic corticosteroid therapy. Allergy Asthma Clin Immunol.
Autor correspondiente: Dr. Services on Demand Journal. Cited by SciELO. Similars in SciELO. Material and methods: Observational, descriptive, longitudinal, prospective study carried out in men and women, older than 18 years old, who received enteral or parenteral corticotherapy and attended the outpatient clinical services of the Hospital Nacional in Rev Chil Enf Respir ;29 2 [ Links ] Recibido: 15 de Enero de ; Aprobado: 04 de Agosto de How to cite this article.
localhost › salud › medicina › estos-son-los-efectos-adversos-de-l. ¿Qué efectos secundarios puedo tener al utilizar este medicamento? Corticosteroids are hormone mediators produced by the cortex of adrenal glands that further categorize into glucocorticoids. Most often, patients receiving short-term corticosteroid therapy present with euphoria or hypomania, whereas long-term therapy tends to engender depressive. La prednisona es una hormona esteroide y un medicamento de venta con receta que tiene muchos Con frecuencia, la prednisona causa efectos secundarios. Take the steroid mediation after a full meal or with antacidsas this may help reduce irritation of the stomach.Published studies are primarily clinical and epidemiological research but also basic. SRJ is a prestige metric based on the idea that not all citations are the same. SJR uses a similar algorithm as the Google page rank; it provides a quantitative and qualitative measure of the journal's impact.
SNIP measures contextual citation impact by wighting citations based on the total number of citations in a subject field. Los glucocorticoides GC son un elemento fundamental en el tratamiento de la artritis reumatoide AR. Glucocorticoids GC are a mainstay of the therapy in rheumatoid arthritis RA. Currently, and despite their extensive use, the discussion about the benefits and adverse effects of low dose GC in the management of RA persists.
In recent years, a number of clinical trials have attempted to establish the benefits of long-term GC use as a disease-modifying antirheumatic drug in RA, and to define their side effects. Results of these clinical trials provide solid evidence that low-dose GC can inhibit radiographic damage in early RA, and that side effects of GC, when used in that clinical framework, are limited to hyperglycaemia, cataracts, and transient weight gain..
ISSN: Instructions for authors - Submit an article. Open Access Option. Previous article Next article. Issue 6.
Pages November - December Export reference. More article options. DOI: Uso de glucocorticoides en la artritis reumatoide. Use of Glucocorticosteroids in Rheumatoid Arthritis. Download PDF. Corresponding author. Hospital Universitario Puerta de Hierro. This item has received. Article information.
Palabras clave:. Artritis reumatoide. Results of these clinical trials provide solid evidence that low-dose GC can inhibit radiographic damage in early RA, and that side effects of GC, when used in that clinical framework, are limited to hyperglycaemia, cataracts, and transient weight gain. Key words:. Rheumatoid arthritis. Full text is only aviable in PDF. A comparison of cortisone and aspirin in the treatment of early cases of rheumatoid arthritis. Br Med J, 29 , pp.
A comparison of prednisolone with aspirin or other analgesics in the treatment of rheumatoid arthritis. Ann Rheum Dis, 18 , pp. Harris Jr, R. Emkey, J. Nichols, A.
Low dose prednisone therapy in rheumatoid arthritis: a double blind study. J Rheumatol, 10 , pp. The effect of glucocorticoids on joint destruction in rheumatoid arthritis. N Engl J Med, , pp.
Hickling, R. Jacoby, J. Joint destruction after glucocorticoids are withdrawn in early rheumatoid arthritis. Br J Rheumatol, 37 , pp. Van Gestel, R. Laan, C. Haagsma, L.
Van de Putte, P. Van Riel. Oral steroids as bridge therapy in rheumatoid arthritis patients starting with parenteral gold. A randomized double-blind placebo-controlled trial. Br J Rheumatol, 34 , pp. Saag, L. Criswell, K. Sems, M. Nettleman, S. Low-dose corticosteroids in rheumatoid arthritis. A meta-analysis of their moderateterm effectiveness.
Arthritis Rheum, 39 , pp. Boers, A. Verhoeven, H. Markusse, M. Van de Laar, R. Westhovens, J. Van Denderen, et al. Randomised comparison of combined stepdown prednisolone, methotrexate and sulphasalazine with sulphasalazine alone in early rheumatoid arthritis. Lancet, , pp. Landewe, M. Verhoeven, R. Westhovens, M. Van de Laar, H. Markusse, et al. COBRA combination therapy in patients with early rheumatoid arthritis: long-term structural benefits of a brief intervention. Arthritis Rheum, 46 , pp.
Haagsma, P. Van Riel, A. De Jong, L. Van de Putte. Combination of sulphasalazine and methotrexate versus the single components in early rheumatoid arthritis: a randomized, controlled, double blind, 52 week clinical trial. Br J Rheumatol, 36 , pp. Dougados, B. Combe, A. Cantagrel, P. Goupille, P. Olive, M. Schattenkirchner, et al. Combination therapy in early rheumatoid arthritis: a randomised, controlled, double blind 52 week clinical trial of sulphasalazine and methotrexate compared with the single components.
Ann Rheum Dis, 58 , pp. Maillefert, B. Combe, P. Goupille, A. Cantagrel, M. Long term structural effects of combination therapy in patients with early rheumatoid arthritis: five year follow up of a prospective double blind controlled study.
Ann Rheum Dis, 62 , pp. Goekoop-Ruiterman, J. De Vries-Bouwstra, C. Allaart, D.
No comments:
Post a Comment