Aripiprazole for drug-induced sexual dysfunction in schizophrenic males / 中华男科学杂志

Objective@#To investigate the clinical effects of aripiprazole on sexual dysfunction induced by amisulpride or risperidone in male patients with schizophrenia.@*METHODS@#This study included 75 male patients with drug-induced secondary sexual dysfunction after treated with amisulpride or risperidone for first-episode schizophrenia between October 2014 and October 2016. We substituted aripiprazole for amisulpride or risperidone, gradually increased the dose from 10 to 30 mg/d within 2 weeks, and maintained 30 mg/d from the 3rd week. At 4 and 8 weeks after medication, we evaluated the sexual function of the patients, measured the levels of serum prolactin (PRL) and testosterone (T), obtained the scores of the Positive and Negative Symptoms Scale (PANSS), recorded adverse reactions, and compared the parameters with those before aripiprazole administration.@*RESULTS@#Compared with pre-aripiprazole administration, the patients showed significant increases after 4 weeks of medication in the sexual function score (24.3 ± 2.1 vs 32.6 ± 3.6, P 0.05). In comparison with pre-aripiprazole administration, the PANSS score was significantly decreased at 4 weeks after medication (62.1 ± 4.9 vs 57.2 ± 5.5, P <0.05) and even lower at 8 weeks (51.2 ± 5.2) (P <0.05). The incidence rates of medication-related excitation, dizziness, insomnia, and loss of appetite were 6.7%, 5.3%, 4.0% and 1.3% respectively, and no other serious adverse reactions were observed.@*CONCLUSIONS@#Aripiprazole is effective for the treatment of drug-induced sexual dysfunction in schizophrenic men by continuously alleviating their positive and negative symptoms and meanwhile improving their sexual function and restoring their sexual hormone levels.

High extracellular potassium ion concentration attenuates the blockade action of ketanserin on Kv1.3 channels expressed in xenopus oocytes / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Ketanserin (KT), a selective serotonin (5-HT) 2-receptor antagonist, reduces peripheral blood pressure by blocking the activation of peripheral 5-HT receptors. In this study electrophysiological method was used to investigate the effect of KT and potassium ion on Kv1.3 potassium channels and explore the role of blocker KT in the alteration of channel kinetics contributing to the potassium ion imbalances.</p><p><b>METHODS</b>Kv1.3 channels were expressed in xenopus oocytes, and currents were measured using the two-microelectrode voltage-clamp technique.</p><p><b>RESULTS</b>KCl made a left shift of activation and an inactivation curve of Kv1.3 current and accelerated the activation and inactivation time constant. High extracellular [K(+)] attenuated the blockade effect of KT on Kv1.3 channels. In the presence of KT and KCl the activation and inactivation time constants were not influenced significantly no matter what was administered first. KT did not significantly inhibit Kv1.3 current induced by tetraethylammonium (TEA).</p><p><b>CONCLUSIONS</b>KT is a weak blocker of Kv1.3 channels at different concentrations of extracellular potassium and binds to the intracellular side of the channel pore. The inhibitor KT of ion channels is not fully effective in clinical use because of high [K(+)](o) and other electrolyte disorders.</p>

Changes of blood lipids in colorectal cancer patients with coronary heart disease and value of lipid-lowering therapy with statins / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the changes of blood lipid in patients with colorectal cancer complicated by coronary heart disease (CHD) and the effect of lipid-lowering therapy with statins in these patients.</p><p><b>METHODS</b>In 32 pathologically confirmed colorectal cancer patients with CHD, the concentrations of total cholesterol (TC), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C) and lipoprotein (a) (Lp(a)) were detected at the baseline, before and after the operation, and at 6 months of postoperative atorvastatin treatment. Thirty patients with TC over 5.70 mmol/L and established coronary artery disease served as the control group.</p><p><b>RESULTS</b>TC, TG and LDL-C in the 30 control patients were significantly decreased after 6 months of 20 mg atorvastatin treatment, and even further decreased till 12 months (P<0.01), but no significant changes occurred in HDL-C and Lp(a). The baseline level of TC, TG, LDL-C and HDL-C were significantly decreased (P<0.01), while Lp(a) increased (P<0.05) in the 32 cancer patients with CHD. Continuing atorvastatin treatment further decreased TC, TG and LDL-C (P<0.05) and increased HDL-C (P<0.05) without affecting Lp(a). The cancer patients had significantly lower TC and LDL-C levels than the control group (P<0.05), but had significantly increased Lp(a) (P<0.05). Six months of atorvastatin treatment further decreased LDL-C and HDL-C in the cancer patients (P<0.05), while TC and Lp(a) had no significant changes.</p><p><b>CONCLUSIONS</b>Increased Lp(a) in colorectal cancer patients can be associated with its anti-tumor effect. Alterations in the blood lipid profile raises a new issue concerning the safety of lipid-lowering therapy in colorectal cancer patients complicated by CHD.</p>