Kleptomania is the inability to resist the urge to steal items, usually for reasons other than personal use or financial gain. First described in 1816, kleptomania is classified in psychiatry as an impulse control disorder. Some of the main characteristics of the disorder suggest that kleptomania could be an obsessive-compulsive spectrum disorder, but also share similarities with addictive and mood disorders.The disorder is frequently under-diagnosed and is regularly associated with other psychiatric disorders, particularly anxiety, eating disorders, alcohol and substance use. Patients with kleptomania are typically treated with therapies in other areas due to the comorbid grievances rather than issues directly related to kleptomania.Over the last 100 years, a shift from psychotherapeutic to psychopharmacological interventions for kleptomania has occurred. Pharmacological treatments using selective serotonin reuptake inhibitors (SSRIs), mood stabilizers and opioid receptor antagonists, and other antidepressants along with cognitive behavioral therapy, have yielded positive results. However, there have also been reports of kleptomania induced by selective serotonin reuptake inhibitors (SSRIs). Signs and symptoms
Some of the fundamental components of kleptomania include recurring intrusive thoughts, impotence to resist the compulsion to engage in stealing, and the release of internal pressure following the act. These symptoms suggest that kleptomania could be regarded as an obsessive-compulsive type of disorder.People diagnosed with kleptomania often have other types of disorders involving mood, anxiety, eating, impulse control, and drug use. They also have great levels of stress, guilt, and remorse, and privacy issues accompanying the act of stealing. These signs are considered to either cause or intensify general comorbid disorders.
Increased gene expression following increased histone acetylation is an expected effect of an HDAC inhibitor. Increased hemoglobin F (another surrogate marker for gene-expression changes resulting from HDAC inhibition) was also detected in blood after romidepsin administration, and persistent histone acetylation was inversely associated with drug clearance and directly associated with patient response to therapy. Dosage and administration
The approved dosage of romidepsin in both CTCL and PTCL is a four-hour i.v. administration of 14 mg/m2 on days 1, 8, and 15 of a 28-day treatment cycle. This cycle should be repeated as long as the patient continues to benefit and tolerate the therapy. A dose reduction to 10 mg/m2 is possible in some patients who experience high-grade toxicities. Pharmacokinetics
In trials involving patients with advanced cancers, romidepsin exhibited linear pharmacokinetics across doses ranging from 1.0 to 24.9 mg/m2 when administered intravenously over four hours. Age, race, sex, mild-to-severe renal impairment, and mild-to-moderate hepatic impairment had no effect on romidepsin pharmacokinetics. No accumulation of plasma concentration was observed after repeated dosing. Mechanism of action
Romidepsin acts as a prodrug with the disulfide bond undergoing reduction within the cell to release a zinc-binding thiol. The thiol binds to a zinc atom in the binding pocket of Zn-dependent histone deacetylase to block its activity. Thus it is an HDAC inhibitor. Many HDAC inhibitors are potential treatments for cancer through the ability to epigenetically restore normal expression of tumor suppressor genes, which may result in cell cycle arrest, differentiation, and apoptosis. Adverse effects
The use of romidepsin is uniformly associated with adverse effects.