Gross hematuria as the presentation of an inguinoscrotal hernia: a case report

<p>Abstract</p> <p>Introduction</p> <p>Several complications have been reported with inguinal hernias. Although hematuria and flank pain, either as the presentation or as a complication of inguinal hernia, are infrequent, this condition may lead to the development of obstructive uropathy, which can have diverse manifestations.</p> <p>Case presentation</p> <p>A 71-year-old Iranian man with Persian ethnicity presented with new onset episodes of gross hematuria and left-sided flank pain. A physical examination revealed a large and non-tender inguinal hernia on his left side. An initial workup included an abdominal ultrasound, an intravenous pyelogram and cystoscopy, which showed left hydronephrosis and a bulging on the left-side of his bladder wall. On further evaluation, computed tomography confirmed that his sigmoid colon was the source of the pressure effect on his bladder, resulting in hydroureteronephrosis and hematuria. No tumoral lesion was evident. Herniorrhaphy led to the resolution of his signs and symptoms.</p> <p>Conclusion</p> <p>Our case illustrates a rare presentation of inguinal hernia responsible for gross hematuria and unilateral hydronephrosis. Urologic signs and symptoms can be caused by the content of inguinal hernias. They can also present as complications of inguinal hernias.</p

Variability of 5-HT2C receptor cys23ser polymorphism among European populations and vulnerability to affective disorder.

Substantial evidence supports a role for dysfunction of brain serotonergic (5-HT) systems in the pathogenesis of major affective disorder, both unipolar (recurrent major depression) and bipolar.(1) Modification of serotonergic neurotransmission is pivotally implicated in the mechanism of action of antidepressant drugs(2) and also in the action of mood stabilizing agents, particularly lithium carbonate.(3) Accordingly, genes that code for the multiple subtypes of serotonin receptors that have been cloned and are expressed in brain,(4) are strong candidates for a role in the genetic etiology of affective illness. We examined a structural variant of the serotonin 2C (5-HT2C) receptor gene (HTR2C) that gives rise to a cysteine to serine substitution in the N terminal extracellular domain of the receptor protein (cys23ser),(5) in 513 patients with recurrent major depression (MDD-R), 649 patients with bipolar (BP) affective disorder and 901 normal controls. The subjects were drawn from nine European countries participating in the European Collaborative Project on Affective Disorders. There was significant variation in the frequency of the HT2CR ser23 allele among the 10 population groups included in the sample (from 24.6% in Greek control subjects to 9.2% in Scots, chi(2) = 20.9, df 9, P = 0.01). Logistic regression analysis demonstrated that over and above this inter-population variability, there was a significant excess of HT2CR ser23 allele carriers in patients compared to normal controls that was demonstrable for both the MDD (chi(2) = 7.34, df 1, P = 0.006) and BP (chi(2) = 5.45, df 1, P = 0.02) patients. These findings support a possible role for genetically based structural variation in 5-HT2C receptors in the pathogenesis of major affective disorder.Comparative StudyJournal ArticleMulticenter StudyResearch Support, Non-U.S. Gov'tSCOPUS: ar.jinfo:eu-repo/semantics/publishe