Vol 43 # 3 September 2011 - Kma.org.kw

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220 KUWAIT MEDICAL JOURNAL September 2011 Original Article Evaluation of Insulin Resistance by the Homeostasis Model Assessment in Female Patients with Primary Sjogren’s Syndrome Gonca Karabulut 1 , Fulden Sarac 2 , Gul Kitapcioglu 3 , Candeger Yılmaz 2 , Yasemin Kabasakal 1 1 Department of Rheumatology, Ege University Faculty of Medicine, Izmir, Turkey 2 Department of Endocrinology and Metabolism, Ege University Faculty of Medicine, Izmir, Turkey 3 Department of Biostatistics and Medical Informatics, Ege University Faculty of Medicine, Izmir, Turkey ABSTRACT Kuwait Medical Journal 2011; 43 (3): 220-223 Objective: To evaluate insulin resistance in Primary Sjogren’s Syndrome (pSS) using homeostasis model assessment (HOMA) method Design: Cross-sectional study conducted between January 2006 and December 2008 Setting: Ege University Faculty of Medicine, Izmir, Turkey Subjects: Thirty-five female patients with pSS fulfilling the US-European Consensus Criteria Interventions: A brief clinical history, demographic, anthropometric, clinical and laboratory profiles were recorded Main Outcome Measures: HOMA-IR and serum lipid levels Results: Mean level of HOMA-IR was 1.8 ± 0.7 in patients with pSS. Mean levels of plasma fasting glucose and insulin were 90.6 ± 7.1 mg/dl, 7.8 ± 2.5 microU/l, respectively. A statistically significant difference was detected between ANA positivity and HOMA-IR values (p = 0.016). Four patients with pSS had high HOMA values (> 2.7) and all these patients had ANA positivity. A statistically significant positive correlation was detected between HOMA-IR values and HDL-C levels (R = 0,450 p = 0.009). However, a statistically significant difference was detected between extraglandular involvement and LDL-C (p = 0.01) and total cholesterol levels (p = 0.01). Patients who had no extraglandular involvement had higher levels of total cholesterol and LDL- C levels. Lower triglyceride levels were seen in patients with anti-La antibodies (p = 0.01) but not other antibodies (p > 0.05). Patients with ANA positivity and pSS had lower LDL- C levels (p = 0.009). Conclusion: Autoimmune mechanisms may play a role in insulin resistance in pSS. Metabolic alterations should be taken into account in their management. KEY WORDS: HOMA, insulin resistance, Sjogren’s syndrome INTRODUCTION Insulin resistance is a common metabolic state defined as a subnormal biologic response to given physiological levels of insulin, and plays an important role in the pathogenesis of several metabolic diseases such as obesity and diabetes mellitus (DM) [1] . There are several mechanisms that could contribute to altered insulin sensitivity that may be important in patients with rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE), and they provide insights into pathogenesis of insulin resistance associated with inflammation. These include obesity, the medications used to treat inflammatory diseases, and inflammatory mediators. The adipose tissue functions as an endocrine organ and produces several inflammatory mediators, thus contributing to a proinflammatory state and increased cardiovascular risk [2] . There are two types of insulin resistance syndrome; type A results from genetic defects in the insulin signaling mechanism and type B is caused by an autoimmune phenomenon associated with insulin receptor autoantibody formation [3] . Sjogren’s syndrome (SS) is a slowly progressive, inflammatory autoimmune disease affecting primarily the exocrine glands which then leads to clinical features of dry eyes and dry mouth. Extraglandular involvement including arthritis, pulmonary disease, renal disease and vasculitis may also occur in SS. In isolation, SS is termed as “primary” and when in combination with another autoimmune disease, it is termed as “secondary” [4-5] . Address correspondence to: Gonca Karabulut, MD, Division of Rheumatology, Department of Internal Medicine, Ege University School of Medicine, Izmir, Turkey. Tel: +90 232 3904235; Fax: +90 232 3423289, E-mail: gonca4us@yahoo.com
September 2011 KUWAIT MEDICAL JOURNAL 221 Primary Sjogren’s syndrome (pSS) can occur at all ages, but it affects primarily females during fourth and fifth decades of life, with a female / male ratio of 9 : 1, and its prevalence estimates range from approximately 0.5 to 2% [6,7] . There are a number of tests available for evaluating insulin sensitivity or resistance. Homeostasis model assessment (HOMA), the most commonly used method in clinical practice is used to assess insulin resistance using the fasting glucose and insulin concentrations [8] . There are a few studies up to date investigating the relationship of insulin resistance with systemic inflammatory rheumatic diseases such as RA and SLE [9-11] . There are a few studies up to date investigating the clinical significance of metabolic alterations in patients with pSS [12-14] . However, there is no study related to insulin resistance in pSS. Therefore, the aim of the study was to evaluate the insulin resistance in pSS by using the HOMA method. SUBJECTS AND METHODS This cross-sectional study was conducted by enrollment of 35 female patients with pSS who fulfilled the US-European Consensus Criteria [15] and were followed up by the Department of Rheumatology of Ege University. They were fully examined clinically. Patients with renal dysfunction (serum creatinine ≥ 1.2 mg/dl), DM or known glucose metabolism disturbances, hypothyroidism or any other inflammatory or malignant diseases were excluded. There were no patients on glucocorticoid, metformin, acorbose and antihypertensive treatment. Twenty of the patients with pSS were taking hydroxychloroquine (54.3%). This study was performed according to the principles of the Declaration of Helsinki and an informed consent was obtained from all patients. A brief clinical history, demographic, anthropometric and clinical profiles were recorded in all patients. Serum concentrations of glucose, triglyceride, total cholesterol, and high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) were determined by enzymatic procedures and insulin was measured by chemiluminance. Insulin resistance (IR) was estimated using the HOMA formula from fasting glucose and insulin concentrations as follows: HOMA - IR = (fasting plasma insulin [μU/ml] x fasting plasma glucose [mmol/l]) / 22.50 HOMA – IR values < 2.7 were considered normal. Statistical analysis The statistical analysis was performed using the statistical package program (SPSS 18.0). Mann– Whitney U test and correlation analysis were used for statistical analysis and a p-value less than 0.05 was accepted as significant. RESULTS Thirty-five pSS female patients were included this study. The mean age of the participants was 53.5 ± 9.2 years. Mean disease duration time was 8.0 ± 4.2 years. The clinical and laboratory features of the patients are shown in Table 1 and Table 2. Table 1: Characteristics of pSS patients Clinical and Laboratory Features n % Subjective Symptoms Dry mouth Dry eyes Extraglandular Manifestations Eye Findings Positive Schirmer-I test Immunological Features ANA positivity Anti Ro/SS-A positivity Anti La/SS-B positivity RF positivity Minor Salivary Gland Biopsy Chisholm III Chisholm IV Characteristics Laboratory Characteristics HOMA-IR Fasting insulin (pmol/l) Fasting glucose (mmol/l) HbA1c (%) Total Cholesterol (mmol/l) LDL-C (mmol/l) HDL-C (mmol/l) Triglyceride (mmol/l) Physical Examination Weight (kg) Waist circumference (cm) Body Mass Index (kg/m2) Systolic blood pressure (mmHg) Diastolic blood pressure (mmHg) 32 30 17 Mean levels of plasma fasting glucose and insulin were 5.03 ± 4.22 mmol/l, 54.17 ± 17.37 pmol/l respectively. Only one person had impaired glucose tolerance test by OGTT in pSS group (Table 2). In the pSS patient group, the extraglandular involvement rate was 48.6% (17 / 35). There was no association between the presence of extraglandular involvement and HOMA-IR values in patients with pSS (p = 0.523). There were no statistically significant differences between SS related symptoms such as dry eyes (p = 0.925), dry mouth (p = 0.860), parotid swelling (p = 0.525), Schirmer test (p = 0.881) results and minor 20 32 29 16 17 15 20 Mean ± SD 1.8 ± 0.7 54.17 ± 17.37 5.03 ±4.22 5.2 ± 0.4 5.28 ± 0.95 3.16 ± 0.76 1.58 ± 0.41 1.23 ± 0.38 73.44 ± 12.44 93.82 ± 14.29 26.41 ± 2.97 127.49 ± 18.24 69.58 ± 17.24 91.4 85.7 48.6 57.1 91.4 82.9 45.7 51.5 42.9 57.1 Table 2: Laboratory and physical examination characteristics of pSS patients
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