Dysfunctional elimination syndrome

Nonneurogenic bladder-sphincter dysfunction is thought to originate from behavioral factors that affect toilet training and inhibit the maturation of normal urinary control. Since the gastrointestinal tract plays a prominent role in lower urinary tract dysfunction, the term dysfunctional elimination syndromes (Koff et al.l998) is applied, if functional bowel disturbances are associated in terms of chronic constipation and encopresis. 

Dysfunctional elimination syndromes in childhood may have a negative impact on bladder and bowel function later in life. Women with urogyne-cological symptoms had significantly higher childhood dysfunctional elimination syndrome scores than normal women. 

Fecal and urinary incontinence are significantly more commonly observed in constipated than non-constipated children. Constipation and/or encopresis is commonly associated with nonneurogenic bladder-sphincter dysfunction. Comprehensive treatment is mandatory for successful management of affected children. Idiopathic urethritis might be a manifestation of underlying dysfunctional elimination syndromes. 

But children with VUR, nonneurogenic bladder-sphincter dysfunction and dysfunctional elimination syndromes remain at significant risk for a breakthrough UTI despite antibiotic prophylaxis, anticholinergic therapy, timed voiding and regular bowel evacuation (Koff et al. 1998). 

Chen JJ, Mao W, Homayoon K et al (2004) A multivariate analysis of dysfunctional elimination syndrome and its relationships with gender, urinary tract infection and vesicoureteral reflux in children. J Urol 171 1907-1910 Chiozza ML (2002) Dysfunctional voiding. Ped Med Chir 24 137-140... 

Koff SA, Wagner TT, Jayanthi VR (1998) The relationship among dysfunctional elimination syndromes, primary vesicoureteral reflux and urinary tract infections in children. JUrol 160 1019-1022... 

Lenalidomide was approved recently for the indication of myelodysplastic syndrome where the 5q deletion is present. Since lenalidomide is an analog of thalidomide, all the same precautions must be taken to prevent phocomelia. The time to maximum lenalidomide concentrations occurs 0.5 to 4 hours after the dose. The terminal half-life ranges from 3 to 9 hours. Approximately 65% of lenalidomide is eliminated unchanged in the urine, with clearance exceeding the glomerular filtration rate. To date, no pharmacokinetic studies have been done in patients with renal dysfunction. Lenalidomide is used in the treatment of myelodysplastic syndrome and multiple myeloma. Other side effects are neutropenia, thrombocytopenia, deep vein thrombosis, and pulmonary embolus. 

Haloperidol Blockade of D2 receptors >> 5HT2A receptors Some a blockade, but minimal M receptor blockade and much less sedation than the phenothiazines Schizophrenia (alleviates positive symptoms), bipolar disorder (manic phase), Huntington s chorea, Tourette s syndrome Oral and parenteral forms with metabolism-dependent elimination Toxicity Extrapyramidal dysfunction is major adverse effect... 

Toxicity and interactions Rifampin commonly causes light chain proteinuria and may impair antibody responses. Occasional side effects include skin rashes, thrombocytopenia, nephritis, and hver dysfunction. If given less often than twice weekly, rifampin may cause a flu-hke syndrome and anemia. Rifampin strongly induces liver dmg-metabolizing enzymes and enhances the elimination rate of many drugs including anticonvulsants, contraceptive steroids, cyclosporine, ketoconazole, methadone, and warfarin. 

The classification of the International Children s Continence Society should be used to eliminate confusion, to facilitate and enable comparative research and metaanalyses. This classification recognizes two main dysfunctions overactive bladder or unstable bladder (urge syndrome) and dysfunctional voiding. The common denominator of lower urinary tract dysfunction is bladder sphincter discoordination leading to chronic high intravesical pressure with resulting negative consequences for the urinary tract. 

---