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   2016| May-August  | Volume 2 | Issue 2  
    Online since January 5, 2017

 
 
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ORIGINAL ARTICLES
Inflammatory bowel disease severity and activity are correlated to thyroid gland nodularity, chronic nonthyroidal illness, and thyroid autoantibodies but not thyroid dysfunction
Mohamed K Ghitany, Hanan Nouh, Tamer M Elsherbiny, Reham I Elsayed
May-August 2016, 2(2):67-80
DOI:10.4103/2356-8062.197574  
Introduction An association between inflammatory bowel disease (IBD) and autoimmune thyroid disease (AITD) exists. The aim of the present study was to evaluate thyroid nodules, function, and antibodies in patients with IBD. Patients and materials The study included 50 patients with established diagnosis of IBD either ulcerative colitis (UC) or Crohn’s disease and 25 healthy controls. They were classified into two groups: group I included 25 patients with UC, and group II included 25 patients with Crohn’s disease; the control group included 25 healthy individuals. They were subjected to history taking, complete physical examination, and laboratory investigations that included evaluation of erythrocyte sedimentation rate (ESR), C-reactive protein, fecal calprotectin, free T3, free T4, thyroid-stimulating hormone, antithyroid peroxidase (TPO), antithyroglobulin (TG), and TSH receptor antibodies. Ileocolonoscopic and histopathological examination with assessment of IBD activity and thyroid ultrasonography were carried out. Results There were no statistically significant differences between the three groups as regards anti-TG antibodies (P=0.075), anti-TPO (P=0.190), AITD assessed serologically or by means of ultrasound (P=1.000), or as regards thyroid status (P=0.528). IBD patients had significantly more thyroid nodules compared with controls (P<0.001), and there was a positive correlation between IBD markers of activity (ESR and fecal calprotectin) and the presence of nodules. A significant negative correlation existed between free T3 and fecal calprotectin, ESR, and C-reactive protein, as well as between free T4 and ESR and fecal calprotectin. A significant positive correlation between anti-TG antibodies and fecal calprotectin as well as between anti-TPO antibodies and histological activity assessment of UC patients also existed. We found a significant negative correlation between free T3 and free T4 and several indices of IBD activity/severity. Conclusion AITD and altered thyroid function were the same among IBD patients and controls. However, IBD patients had significantly more nodules; indices of activity/severity of IBD correlated negatively with free T3 and T4, and positively with anti-TPO, anti-TG, and nodularity.
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A study on the role of calcium homeostasis and vitamin D deficiency in premenopausal systemic lupus erythematosus patients and its relation with disease activity
Manal Y Tayel, Ashraf I El-Zawawy, Mohamed I Said, Eman A Soliman, Mohamed K Mohamed
May-August 2016, 2(2):95-107
DOI:10.4103/2356-8062.197571  
Introduction Systemic lupus erythematosus (SLE) is an inflammatory autoimmune disorder that may affect multiple organ systems. Vitamin D levels and its role in lupus inflammation is still a matter of debate. Objective The aim of this study was to assess the role of calcium homeostasis and vitamin D deficiency in premenopausal SLE patients and its relation with disease activity. Patients and methods We assessed serum 25-hydroxyvitamin D [25(OH)D] level in 60 (SLE) patients and 20 age and sex-matched healthy controls. We also assessed different clinical, immunological, and laboratory disease parameters in SLE patients − namely, erythrocyte sedimentation rate, C-reactive protein, antinuclear antibody, antidouble stranded DNA, C3, and C4–and disease activity score using the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) score. We correlated serum 25(OH)D with disease activity and different environmental parameters that might affect 25(OH)D level. Results A significantly lower 25(OH)D level was found in SLE patients compared with controls (P=0.033). Serum 25(OH)D was inversely correlated to SLEDAI score (P=0.043), antidouble stranded DNA (P<0.001), and erythrocyte sedimentation rate (P<0.001), but directly correlated to C3 and C4 levels (P=0.029). There was an inverse correlation between vitamin D supplementation and SLEDAI score (MCP=0.030), but there was no significant correlation with both calcium supplementation (P=0.861) and ionized calcium (P=0.681). Conclusion Vitamin D insufficiency and deficiency is highly prevalent in SLE patients than in healthy controls, and is prevalent among SLE patients with higher disease activity, which suggests an important role of vitamin D3 in the pathogenesis of SLE disease activity and flares. The therapeutic effect of vitamin D in SLE should be further assessed in interventional studies.
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Association of fibroblast growth factor 23, parathyroid hormone, and vitamin D with acute kidney injury
Montasser M Zeid, Akram A.M Deghady, Hesham K Elsaygh, Heba S El Shaer, Rasha I.A Gawish
May-August 2016, 2(2):88-94
DOI:10.4103/2356-8062.197589  
Introduction Fibroblast growth factor 23 (FGF23) plays an important role in regulating phosphate and vitamin D homeostasis. Elevated levels of FGF23 are independently associated with mortality in patients with chronic kidney disease and End stage renal disease (ESRD). Whether FGF23 levels are elevated and associated with adverse outcomes in patients with acute kidney injury (AKI) has not been studied so far. Objective The aim of this study was to determine the relationship between FGF23 levels in patients with AKI and morbidity, mortality, and/or the need for renal replacement therapy. Patients and methods The study included two groups: group 1, which included 30 AKI patients from the general medical ward and ICUs [identified in accordance with the criteria established by Acute Kidney Injury Network (AKIN) grading of AKI]; and group 2, which included 30 healthy controls matched with the patients as regards age and sex. Plasma levels of C-terminal FGF23, 1,25-dihydroxy vitamin D [1,25(OH)2D], and intact parathyroid hormone (iPTH) were measured within 24 h of AKI onset and 5 days later. The composite end point was death or need for renal replacement therapy. Results FGF23 levels on day 1 were significantly higher among participants with AKI than among controls (mean level: 278.20 ± 220.58 vs. 14.60 ± 9 pg/ml). There was a statistically significant negative correlation between FGF23 and vitamin D on day 1, with a P-value of less than 0.023, whereas there was no statistically significant negative correlation between FGF23 and vitamin D on day 5, with a P-value of 0.102. There was a statistically significant positive correlation between FGF23 on day 1 and both Acute Physiology and Chronic Health Evaluation and Sequential Organ Failure Assessment scores, with a P-value of less than 0.001. FGF23 proved to be a good predictor of mortality (sensitivity: 100%, specificity: 85%) at a cutoff value of 280 pg/ml. Conclusion FGF23 levels are elevated in AKI patients and are associated with increased mortality. AKI is also associated with significant reduction in the level of 1,25(OH)2D and with significant elevation of PTH.
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Study of chronic periodontitis in rheumatoid arthritis patients and its relation to serum anticitrulinated peptide antibody levels
Ragaa A Mahmoud, Amina H Hassab, Mona H Abdel Magid, Eiman A Soliman, Rania A Fahmy, Mona M Ashraf
May-August 2016, 2(2):108-116
DOI:10.4103/2356-8062.197573  
Background Recently discovered evidence suggests that periodontitis might have a direct role in initiating and sustaining the immunoinflammatory responses in rheumatoid arthritis (RA), besides the risk factors that are common to both conditions. Aim The aim of this study was to determine the prevalence of chronic periodontitis in a cohort of Egyptian RA patients and their first-degree relatives and siblings compared with a control group and its relation to serum anticitrulinated peptide antibody (ACPA) levels. Patients and methods This study was carried out on three groups: group I included 100 patients with RA who fulfilled the 2010 ACR/EULAR classification criteria for RA and had less than 5 years’ disease duration. They were recruited from the Rheumatology Unit and Rheumatology Outpatient Clinic at Alexandria Main University Hospital. Group II included 50 first-degree relatives and siblings of RA patients who were free of clinical joint disease, and group III included 50 age-matched and sex-matched healthy subjects referred for general dental treatment at the Dental Clinic of Alexandria Main University Hospital. RA disease activity was assessed by applying Disease Activity Score 28, and the functional state of the patients was assessed by applying the Health Assessment Questionnaire. All subjects underwent a dental examination, including Probing Pocket Depth (PPD), Clinical Attachment Loss (CAL), Plaque Index (PI), and modified Gingival Index. The ACPA levels in serum were evaluated in group I, group II, and group III participants with periodontitis. Results Group I patients had significantly more periodontitis than group II (P<0.001) and group III (P<0.001). There was a statistically significant difference between group I and group II in PPD (P<0.001), CAL (P<0.001), and PI (P<0.001) and a statistically significant difference between group I and group III in PPD (P=0.001), CAL (P=0.006), and PI (P=0.002). In group I, 82 (82%) patients had positive serum ACPA (320 U/ml), compared with only four (8%) subjects in group II and none of the controls in group III. There was a statistically significant difference between group I and group II in serum ACPA level (P<0.001), as well as between group I and group III (P<0.001). Conclusion Our study shows an association between RA and chronic periodontitis. Individuals with RA are more likely to experience periodontitis.
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Evaluation of different biochemical markers and imaging modalities in type 2 diabetes mellitus patients with and without albuminuria
Amr Mohamed Ebeid, Doaa Ibrahim Hashad, Mohamed Ahmed Sadaka, Mohamed Mahmoud Elshafie, Mohamed Mohamed Sakr, Samah Ibrahim Idris
May-August 2016, 2(2):81-87
DOI:10.4103/2356-8062.197572  
Objective The aim of this study was to evaluate the effects of albuminuria on different biochemical markers, different target organs, and subclinical atherosclerosis in patients with type 2 diabetes mellitus (T2DM). Patients and methods Sixty T2DM patients were divided into three equal groups according to their levels of albuminuria − namely, normoalbuminuria, microalbuminuria, and macroalbuminuria. Renal function tests, glycemic status markers, serum electrolytes, high-sensitivity C-reactive protein, fibroblast growth factor 23, vitamin D, intact parathyroid hormone, and fractional excretion of phosphate (FePO4) were measured. Patients also underwent renal arterial duplex, Doppler echocardiography, and estimation of the carotid intima–media thickness. Results Blood urea nitrogen and creatinine clearance were significantly higher in patients with albuminuria. Fasting blood glucose, postprandial blood glucose, and glycosylated hemoglobin levels were significantly higher in patients with albuminuria. There were no statistically significant differences among the studied groups as regards serum electrolytes. Fibroblast growth factor 23 levels were significantly higher in patients with albuminuria. In patients with macroalbuminuria, vitamin D levels were significantly lower, whereas intact parathyroid hormone and high-sensitivity C-reactive protein levels were significantly higher. There were no statistically significant differences among the studied groups as regards FePO4. There were no statistically significant differences between the studied groups as regards renal resistive indices, presence or absence of left ventricular hypertrophy, or carotid intima–media thickness. Left ventricular ejection fraction was significantly lower in patients with albuminuria. Conclusion In T2DM patients with albuminuria (especially macroalbuminuria), several markers of renal complications are elevated, denoting a high-risk population for the development of end-stage renal disease. Moreover, markers of asymptomatic left ventricular systolic dysfunction were observed, denoting a higher risk for cardiovascular morbidity and mortality.
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Interleukin-33 in systemic sclerosis: correlation with clinical manifestations and disease subset
Magdy A Zohairy, Anna N.A Raya, Akram M Deghady, Riham A Soliman
May-August 2016, 2(2):123-129
DOI:10.4103/2356-8062.197578  
Background Systemic sclerosis (SSc) is a generalized connective tissue disorder characterized by sclerotic changes in the skin and internal organs. Interleukin-33 (IL-33) is a newly reported cytokine of the IL-1 family. Aim of the work The aim of this study was to determine serum levels of IL-33 in SSc patients and evaluate its association with clinical manifestations and disease subset. Patients and methods The patients in this study were divided into group A and group B. Group A included 30 adult patients with SSc, which was subdivided into diffuse systemic sclerosis (dSSc) and limited systemic sclerosis (lSSc). All cases were diagnosed according to the American College of Rheumatology criteria for SSc. Group B included 15 healthy adults (age and sex matched) who served as controls. Serum IL-33 levels were examined by means of enzyme-linked immunosorbent assay in 30 patients with SSc and in 15 healthy individuals. Skin assessment was done using the modified Rodnan skin score. Results IL-33 was increased in all SSc patients compared with controls. The levels of IL-33 were significantly higher in the dSSc subset compared with the lSSc subset. IL-33 is highly correlated to the presence of pulmonary fibrosis, Raynaud’s phenomenon, pitting scars and ulcers, pulmonary hypertension, joint contracture, and modified Rodnan skin score. Thus, IL-33 levels were increased in SSc patients and correlated with the extent of skin sclerosis and the severity of pulmonary fibrosis. Therefore, IL-33 possibly plays a role in cutaneous and pulmonary fibrosis in SSc patients. Conclusion IL-33 may have a significant role in the pathogenesis of SSc. IL-33 serum levels paralleled the severity of the disease subset. Understanding of IL-33 functions is important for the development of new therapeutic approaches including IL-33 inhibitors and IL-33 receptor blockers as a therapeutic target.
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Interleukin-33 as a marker for disease activity in rheumatoid arthritis
Magdy A Zohairy, Anna N.A Raya, Akram M Deghady, Marwa R Amer
May-August 2016, 2(2):117-122
DOI:10.4103/2356-8062.197588  
Background Rheumatoid arthritis (RA) is a chronic systemic inflammatory disorder thought to be autoimmune in nature and predominately affects synovial joints. Interleukin-33 (IL-33) is a newly reported cytokine of the IL-1 family. Aim of the work The aim of this study was to assess the role of IL-33 in the pathogenesis of RA. Patients and methods Group A included 30 adult patients with RA; all cases were diagnosed according to the American College of Rheumatology criteria for RA. Group B included 20 healthy adult persons (age and sex matched) who comprised the control group. The serum IL-33 levels were examined by using the enzyme-linked immunosorbent assay for 30 patients with RA and 20 healthy individuals. Disease activity was assessed according to disease activity score 28–C-reactive protein (CRP) scale. Results IL-33 was increased in all RA patients compared with controls. IL-33 was highly correlated to erythrocyte sedimentation rate, CRP, rheumatoid factor, anti-cyclic citrullinated peptide, and disease activity score 28–CRP score. Therefore, IL-33 most probably has a significant role to play in the pathogenesis of RA. Conclusion IL-33 most probably has a significant role in the pathogenesis of RA. IL-33 serum levels paralleled the severity of the disease subset. Understanding the functions of IL-33 is important for the development of new therapeutic approaches including IL-33 inhibitors as a therapeutic target.
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