Neuroleptic malignant syndrome after the use of venlafaxine in a patient with generalized anxiety disorder.

Neuroleptic malignant syndrome (NMS) is a potentially lethal adverse reaction to neuroleptics, which is characterized by hyperthermia, extrapyramidal symptoms, altered consciousness and autonomic dysfunction. Although NMS is most commonly induced by the high-potency neuroleptics, its development has also been associated with the use of non-neuroleptic agents that block central dopamine pathways. A 68-year-old man with generalized anxiety disorder and depressive symptoms presented at the emergency department (ED) with high fever, tremor, muscle rigidity, rhabdomyolysis and altered mental status. NMS was considered to have been caused by the recent addition and subsequent dose increase in his treatment regimen of venlafaxine, a serotonin norepinephrine reuptake inhibitor. He was successfully treated with bromocriptine, lorazepam, and fluid hydration in the ED and intensive care unit.     

Prolonged extracorporeal membrane oxygenation support for acute respiratory distress syndrome.

When all conventional treatments for respiratory failure in patients with acute respiratory distress syndrome (ARDS) have failed, extracorporeal membrane oxygenation (ECMO) can provide a chance of survival in these desperately ill patients. A 49-year-old male patient developed septic shock and progressive ARDS after liver abscess drainage. Venovenous ECMO was given due to refractory respiratory failure on postoperative day 6. Initially, two heparin-binding hollow-fiber microporous membrane oxygenators in parallel were used in the ECMO circuit. Twenty-two oxygenators were changed in the first 22 days of ECMO support because of plasma leak in the oxygenators. Each oxygenator had an average life of 48 hours. Thereafter, a single silicone membrane oxygenator was used in the ECMO circuit, which did not require change during the remaining 596 hours of ECMO. The patient's tidal volume was only 90 mL in the nadir and less than 300 mL for 26 days during the ECMO course. The patient required ECMO support for 48 days and survived despite complications, including septic shock, ARDS, acute renal failure, drug-induced leukopenia, and multiple internal bleeding. This patient received an unusually long duration of ECMO support. However, he survived, recovered well, and was in New York Heart Association functional class I-II, with a forced expiratory volume in 1 second of 81% of the predicted level 18 months later. In conclusion, ECMO can provide a chance of survival for patients with refractory ARDS. The reversibility of lung function is possible in ARDS patients regardless of the severity of lung dysfunction at the time of treatment.     

Time-dependent inhibition and tetrahydrobiopterin depletion of endothelial nitric-oxide synthase caused by cigarettes.

Smoking causes a dysfunction in endothelial nitric-oxide synthase (eNOS), which is ameliorated, in part, by administration of tetrahydrobiopterin (BH(4)). The exact mechanism by which the nitric oxide deficit occurs is unknown. We have previously shown that aqueous extracts of chemicals in cigarettes (CE) cause the suicide inactivation of neuronal NO synthase (nNOS) by interacting at the substrate-binding site. In the current study, we have found that CE directly inactivates eNOS by a process that is not affected by the natural substrate l-arginine and is distinct from the mechanism of inactivation of nNOS. We discovered that CE causes a time-, concentration-, and NADPH-dependent inactivation of eNOS in an in vitro system containing the purified enzyme, indicating a metabolic component to the inactivation. The CE-treated eNOS but not nNOS was nearly fully reactivated upon incubation with excess BH(4), suggesting that BH(4) depletion is a potential mechanism of inactivation. Moreover, in the presence of CE, eNOS catalyzed the oxidation of BH(4) to dihydrobiopterin and biopterin by a process attenuated by high concentrations of superoxide dismutase but not catalase. We speculate that a redox active component in CE, perhaps a quinone compound, causes oxidative uncoupling of eNOS to form superoxide, which in turn oxidizes BH(4). The discovery of a direct inactivation of eNOS by a compound(s) present in tobacco provides a basis not only for further study of the mechanisms responsible for the biological effects of tobacco but also a search for a potentially novel inactivator of eNOS.     

Pyometra as a lower abdominal doughnut sign on a Ga-67 scan

A 77-year-old woman was referred for Ga-67 scan to evaluate intermittent fever and chills that had lasted more than 20 days. The Ga-67 whole-body scan revealed a doughnut-shaped Ga-67 accumulation in the lower abdominal region. Combined Ga-67 and Tc-99m MDP bone scan confirmed that this activity was in the uterus, because the shape of the urinary bladder on bone scan was different from that of the Ga-67-avid lesion. Pyometra was proved during operation, and pus culture was performed.     

闭角型青光眼患者红细胞免疫功能与EPO和ET-1的相关性

目的：探讨闭角型青光眼患者红细胞免疫功能与血清促红细胞生成素(EPO)和血浆内皮素-1(ET-1)的相关性。

方法：选取2017-06/10期间我院收治的闭角型青光眼患者30例(病例组)与眼部正常者30例(对照组)为研究对象。测定并比较两组受试者红细胞免疫功能、血清EPO和血浆ET-1浓度,分析之间的相关性。

结果：病例组受试者红细胞C3b受体花环率明显低于对照组(10.81%±2.01% vs 18.06%±3.44%),红细胞免疫复合物花环率明显高于对照组(17.21±3.49% vs 11.74±2.14%),血清EPO浓度明显高于对照组(26.10±5.22 mU/mL vs 22.68±4.06mU/mL),血浆ET-1浓度明显高于对照组(70.85±7.16ng/L vs 58.43±5.09ng/L)。闭角型青光眼患者红细胞C3b受体花环率与血清EPO浓度呈显著正相关(r=0.271,P<0.05),与血浆ET-1浓度无明显相关性。

结论：闭角型青光眼患者红细胞免疫功能与血清EPO浓度呈正相关。     

The Butterfly Fragment in Wedge‐Shaped Femoral Shaft Fracture: Comparison of Two Different Surgical Methods

ObjectiveOur study compared the results of wedge‐shaped femoral shaft fracture following intramedullary (IM) nailing with or without fixation of the third fragment.MethodsWe retrospectively reviewed patients presenting with femoral shaft fracture with AO/OTA type 32‐B from 2011 to 2016. Patients were divided into two groups: closed reduction without touching the third fragment and open reduction with fixation of the third fragment. The fragment ratio, fragment length, nail size, dynamization or not, mRUST scores, union rate, and union time were compared between the two groups. Risk factors of non‐union were also investigated, including sex, age, fracture pattern, fracture location, dynamization, nail size, fragment ratio, fragment size, and postoperative fragment displacement.ResultsA total of 80 patients met inclusion criteria, 20 patients with wedge‐shaped shaft femoral fracture were managed with IM nailing and open reduction with fixation of the third fragment. Sixty patients were treated with IM nail without touching the third fragment. The union rate for the fixation and non‐fixation groups were 60.0% and 81.7%, respectively. The mean union time for the fixation group was 19 months vs 14 months for the non‐fixation group. Multi‐regression analysis showed larger nail size (odds ratio: 2.26) and fixation of the third fragment (odds ratio: 0.18) influenced fracture healing.ConclusionsFixation of the third fragment in wedge‐shaped shaft femoral fracture results in a longer union time and lower union rate. In the management of femoral fracture with a third fragment, a larger nail size is recommended and fixation should be performed in a closed manner. Fixation of the fragment may achieve better fracture reduction. However, disruption of the vasculature and surrounding structures may further result in nonunion of the fracture site.     

A new isoquinolinone derivative with noble vasorelaxation activity

The pharmacological effects of BDPBI (7-bromo-1,4-dihydro-2-phenyl-4,4-bis(4-pyridinylmethyl)2H-isoquinolin-3-one dihydrochloride) were tested on isolated endothelium-containing or denuded aorta of the guinea pig. BDPBI with the formula C(27)H(24)BrCl(2)N(3)O was synthesized starting with 3-isochromanone. In the endothelium-containing preparations of the aortic rings, phenylephrine (PHE; 10 micromol/l) elicited contracture and acetylcholine (ACh; 10 micromol/l) or BDPBI (0.01-10 micromol/l) elicited relaxation effects on the PHE-precontracted preparations. The BDPBI-elicited effect on the PHE-precontracted aortic rings was not altered in the presence of adrenergic blockers (propranolol or yohimbine; 1 micromol/l) or pretreated preparations with aspirin, indomethacin (10 micromol/l) or L-NAME (1 mmol/l). However, the relaxation effects of BDPBI were blocked if the preparations were pretreated with diphenhydramine (10 micromol/l) or chloropheniramine maleate (10 micromol/l). In contrast to lower concentrations of atropine (1 micromol/l), higher concentrations of atropine (30 micromol/l) did block the effects of BDPBI on the PHE-precontracted aortic rings. HTMT dimaleate (0.01-10 micromol/l), a histamine H(1) receptor agonist, also elicited relaxation effects on the PHE-precontracted preparation, and the effects were blocked if the preparations were pretreated with diphenhydramine or chloropheniramine maleate. On isolated denuded aorta of the guinea pig, BDPBI did not elicit relaxation effects on the PHE-precontracted aortic rings. These results demonstrated that the vasorelaxation effect of BDPBI on PHE-precontracted aortic rings is partly dependent on the activation of a histaminergic receptor from the vascular endothelium. We suggested that BDPBI would be an effective vasorelaxant for cardiovascular systems.     

Genetic alterations of HOXA10 and their effect on the severity of endometriosis in a Taiwanese population

Endometriosis is one of the most common gynaecological diseases and evidence has suggested that it may be inherited as a complex genetic trait. HOXA10, a homeobox gene, is expressed in the developing uterus and participates in endometrium development and may contribute to endometriosis. In this study, the HOXA10 gene was analysed in 112 patients with endometriosis and in 54 women without endometriosis, as diagnosed laparoscopically. The entire HOXA10 gene was amplified using polymerase chain reaction followed by single-strand conformation polymorphism analysis and sequencing. Association between the polymorphism and the clinical parameters of endometriosis were examined. There were 7.23% patients with HOXA10 genetic alterations; however, there was no significant increase in the endometriosis patients compared with the controls. Most of these DNA variants were found to be novel mutations that reside within the HOXA10 homeobox domain. Six variants generate amino acid changes in the protein and one harbours a premature stop codon. It was found that patients with HOXA10 polymorphism were associated with a lower serum cancer antigen-125, a lower American Fertility Society score and less severe obliterated cul-de-sac. It is postulated that genetic alterations in the homeobox domain might lead to less specificity for HOXA10 protein binding to a DNA molecule.