Background: Systemic lupus erythematosus (SLE) is a systemic autoimmune inflammatory disease characterized by abnormal production of autoantibodies and proinflammatory cytokines. Both Th1 and Th2 responses have been implicated in the pathogenesis of SLE. IL-33 is involved in the pathogenesis of chronic inflammatory arthritis like as family members, IL-1 and IL-18. IL-33 induce production of IL-5, IL-13 and hypergammaglobulinaemia.Objective: To estimate serum levels of IL-33 in SLE and if levels correlated with disease activity and clinical presentation. Methods:This study was carried out on 24 patients diagnosed according to the American College of Rheumatology (ACR) classification criteria for SLE and 18 apparently healthy persons as control, clinical examination and laboratory investigations were done and measurment of IL-33 level in the serum by ELISA. Results:The most frequent clinical finding in SLE patients was arthritis (87.5%). A significant increase in serum IL-33 levels was found in SLE patients than control persons (P<0.001). Positive significant correlation was found between IL-33 and ESR, CRP, serum creatinine and SLE disease activity index (P<0.001). No significant correlation was detected between IL-33 and RBCs, WBCs, platelet count, haemoglobin and serum urea nitrogen. Conclusion:The serum IL-33 level was significantly higher in SLE patients than control group and its level was significantly related to disease activity. IL-33 may play a role in the inflammatory (flare) phase of SLE and may have a role in local inflammation of tissues as arthritis and lupus nephritis. Table 2: Clinical findings of SLE patients.Laboratory findings of studied groups: The most frequent laboratory abnormalities were ANA positivity found in all patients (100%) and Anti-ds DNA positivity found in 83.3% of patients. In group B, ANA and Anti-ds DNA were negative. Active lupus nephritis was detected by the presence of proteinuria (<0.5gm/day) in 17 patients (70.8%), Citation: Toama MA, Kandil AH, Mourad MH, Soliman MI, Esawy AM (2017) Serum Level of Interleukin 33 and its Relation with Disease Activity and Clinical Presentation in Systemic Lupus Erythematosus. J Clin Exp Dermatol Res 8: 390.
Hepatocellular carcinoma (HCC) is a grave primary liver cancer that has a limited therapeutic option because it is generally diagnosed later in an advanced stage due to its aggressive biologic behavior. The early detection of HCC has a great impact on the treatment efficacy and survival of patients at high risk for cancer. Potential host, environmental, and virus-related risk factors have been introduced. Hepatitis B virus (HBV) is a major cause of end-stage liver diseases such as liver cirrhosis or HCC in endemic areas, and its serologic or virologic status is considered an important risk factor. HCC risk prediction derived from the identification of major risk factors is necessary for providing adequate screening/surveillance strategies to high-risk individuals. Several risk prediction models for HBV-related HCC have been presented recently with simple, efficient, and readily available to use parameters applicable to average- or unknown-risk populations as well as high-risk individuals. Predictive scoring systems of risk estimation to assess HCC development can provide the way to an evidence-based clinical approach for cost- and effort-effective outcomes, capable of inducing a personalized surveillance program according to risk stratification. In this review, the concepts and perspectives of the risk prediction of HCC are discussed through the analysis of several risk prediction models of HBV-related HCC.
Introduction: Urinary and Fecal Control depends on two factors, the first is an inherent, and the second is an acquired. The inherent factor is the presence of an intact sound IUS and IAS. The acquired factor is, through toilet training, having and maintaining high sympathetic tone at the IUS and the IAS. This keeps the sphincters contracted and the urethra and the anal canal empty and closed all the time. Laceration of the collagen chassis of the IUS leads to its weakness and subsequent stress urinary incontinence (SUI) and/or over active bladder (OAB). Similarly, lacerations of the collagen chassis of the IAS lead to its weakness and subsequent fecal incontinence (FI). The lacerations in one/or both sphincters are mainly caused by childbirth trauma (CBT). The pelvic collagen is hormone dependent and drop in the estrogen level causes further weakness of the sphincters. In men senile prostatic enlargement compress the upper part of the urethra leading to irregular dilatation of the bladder neck allowing some urine to enter the urethra on increases of abdominal pressure causing frequent desire to void. The start of voiding may take some time (hesitancy) because of the effort to open the urethra which is compressed by the enlarged prostate. Reconstructive surgery: In women the commonest cause of incontinence is traumatic lacerations of the collagen chassis of the IUS and/or the IAS from CBT. Reconstructive surgery is to restore the normal anatomy and it will restore the function. A new operation "urethra-ano-vaginoplasty" is introduced where mending the torn collagen chassis of the IUS and overlapping the anterior vaginal wall flaps over the mended IUS; and mending the torn chassis of the IAS, overlapping the posterior vaginal wall flaps over the mended sphincter, approximate the two levator ani muscles and repair of the perineum is done.
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