Functional mechanism underlying cyclooxygenase-2 expression in rat small intestine following administration of indomethacin: Relation to intestinal hypermotility

Background and Aim:  We recently reported that cyclooxygenase (COX)-2 is upregulated in the rat small intestine after administration of indomethacin, and this may be the key to non-steroidal anti-inflammatory drug (NSAID)-induced intestinal damage. The present study investigated the mechanism for COX-2 expression induced in the rat small intestine by indomethacin, in relation with ulcerogenic processes.
Methods:  Animals were given indomethacin or SC-560 p.o., and the intestinal mucosa was examined 24 h later.
Results:  Indomethacin caused hemorrhagic lesions in the small intestine, accompanied with an increase in intestinal motility, bacterial invasion and inducible nitric oxide synthase (iNOS) activity, as well as the expression of COX-2 mRNA in the mucosa. Although SC-560 did not cause any damage, this agent caused intestinal hypermotility, the bacterial invasion and the upregulation of COX-2 expression. The mucosal PGE₂ content was decreased by SC-560 at 3 h but recovered 12 h later, and this recovery of PGE₂ was attenuated by both atropine and ampicillin, in addition to rofecoxib. The intestinal hypermotility response to indomethacin was prevented by both 16,16-dimethyl PGE₂ and atropine, but not ampicillin. Yet all these agents inhibited not only the bacterial invasion but also the expression of COX-2 and iNOS activity in the intestinal mucosa following indomethacin treatment, resulting in the prevention of intestinal lesions.
Conclusion:  These results suggest that COX-2 expression in the intestinal mucosa following the administration of indomethacin is associated with intestinal hypermotility and bacterial invasion. The intestinal hypermotility caused by COX-1 inhibition may be a key to COX-2 expression after administration of NSAIDs and their intestinal ulcerogenic properties.     

Cardiovascular calcification in end-stage renal disease.

Cardiovascular diseases are common in patients with end-stage renal disease (ESRD) and cardiovascular morbidity and mortality among dialysis patients are substantially higher than in the general population. The reasons for this high incidence are multiple. They include traditional factors such as hypertension, diabetes, dyslipidaemia, sodium overload, and elevated homocysteine levels as well as disturbances of mineral metabolism, specifically abnormalities in phosphorus and calcium homeostasis. This review will describe the specific cardiovascular complications related to calcifications in ESRD, the implications of the abnormalities of mineral metabolism in its pathogenesis and the current imaging techniques available for the detection of cardiovascular calcifications. Excess of calcium load contributes to the development of cardiac calcifications; therefore, alternative strategies to diminish exogenous calcium load should be considered in patients with ESRD.     

糖化血红蛋白及糖化血清蛋白与糖尿病肾功能衰竭患者的血糖监测

糖化血红蛋白(Hb)A1c是血糖监测的苇要指标,反映检测前2～3个月的平均血糖水平.慢性肾功能衰竭(CRF)患者存在贫血、酸中毒、氧化应激、胰岛素抵抗、血液透析及促红细胞生成素(EPO)的应用等因素,对HbA1c的测定会造成影响.糖化血清蛋白(GSP)反映检测前2～3周的平均血糖水平,仅受血浆蛋白的影响,几乎不受血红蛋白和EPO治疗等以上因素的影响,且对短时间内的血糖变化更为敏感.将GSP作为糖尿病肾功能衰竭患者血糖监测指标可能比HbA1c更理想.     

职业性萘暴露工人的健康监护结果评价

目的：讨论萘对人体的慢性毒效应和亚临床客观检测指标。方法：对河南省萘暴露工人（环境接触萘浓度平均为８．２５～２６．４３ｍｇ／ｍ３）进行了健康监护和医学动态观察。结果：发现长期萘暴露工人的白细胞、血小板减少及眼晶体混浊检出率显著高于对照组（Ｐ＜０．００１）；血清ＳＯＤ同功酶、ＧＳＨ－ＰＸ活性显著低于对照组，而ＬＰＯ水平、神经元特异性烯醇化酶（ＮＳＥ）活性水平以及外周血染色体畸变和微核阳性检出率均显著高于对照组（Ｐ＜０．００１）。神经行为功能检查结果，主要为消极情绪增加，记忆力下降等。事件相关电位Ｐ３００峰潜伏期比对照组显著延长，与对照组差异显著（Ｐ＜０．０５）。结论：慢性低浓度萘暴露对工人主要损害部位（靶器官）有皮肤，眼、血液和神经组织等。ＮＣＴＢ、ＮＳＥ、Ｐ３００三项可作为早期神经受损的客观指标。     

肾综合征出血热患者T细胞亚群数量与白细胞介素2,4水平变化的关系

采用ABC免疫组化染色法及单克隆抗体夹心法ELISA，同步检测了34例肾综合征出血热（HFRS）患者外周血T细胞亚群数量和血清白细胞介素2和4（IL－2、IL－4）水平。发现HFRS病程中各T细胞亚群数量均有不同程度的升高，其中CDS阳性T细胞在各病期均有升高。IL－4水平升高仅见于发热期．而IL－2的升高主要在低血压期和少尿期。病程中有CD4／CD8比值的下降甚至倒置。这种比值的变化与IL－2和IL－4的动态变化有一定的相关性。结果揭示，在HFRS发病机理中存在Thl型和Th2型免疫反应等多种免疫病理机制。     

Neonatal renal failure due to obstructive candidal bezoars

Acute renal failure (ARF) developed in a 7-week-old infant due to bilateral candidal bezoars (fungal balls) causing obstruction at the pelviureteric junction. The baby was born at term with an appropriate birthweight, and had been treated with broad-spectrum antibiotics for respiratory distress and septicemia during the 1st week of life. Recovery from ARF followed renal decompression with bilateral nephrostomy tube placement and parenteral administration of amphotericin B and 5-flucytosine. Received August 21, 1996; received in revised form and accepted January 3, 1997     

Distal Penile Gangrene in a Patient with Chronic Renal Failure

To date, only 10 cases of distal penile gangrene in patients with chronic renal failure have been reported. This rare condition is believed to result from progressive vascular calcification due to secondary hyperparathyroidism in patients with chronic renal failure. We report an additional case of distal penile gangrene in a 41-year-old man who presented with chronic renal disease and pulmonary tuberculosis. Since some authors have emphasized that aggressive surgical treatment in such cases has a significant mortality rate, we took a more conservative approach to treatment.     

Cibenzoline-induced respiratory muscular paralysis in a hemodialysis patient

A 69-year-old man was admitted to our kidney center with endstage renal failure. We started intermittent peritoneal dialysis immediately because of severe azotemia, hyperkalemia, and metabolic acidosis. Two weeks after admission, he developed uremic pericarditis with frequent ventricular premature contractions and supraventricular premature contractions. The intermittent peritoneal dialysis was then replaced by intensive hemodialysis, and oral administration of 300 mg/d of cibenzoline was started. Four days later, he developed thirst, weakness, and dyspnea due to respiratory muscular paralysis. We initiated respiratory support with a respirator because analysis of his blood gases revealed marked hypercapnia and hypoxia. He also developed hypoglycemia and prolonged PQ and QRS intervals on the electrocardiogram, which we believed were due to cibenzoline intoxication; we discontinued the cibenzoline immediately. All symptoms improved, and he was extubated 5 days later. After 2 months, his pericardial effusion disappeared. He now continues maintenance hemodialysis as an outpatient. We suspect that the cibenzoline induced the respiratory muscular paralysis for 2 reasons: 1) the patient experienced the respiratory muscular paralysis, at the same time he also experienced thirst, weakness, hypoglycemia, and prolonged PQ and QRS intervals on electrocardiogram, and all of these symptoms improved after the discontinuation of cibenzoline, and 2) his plasma concentration of cibenzoline became remarkably elevated, to 20 times above the standard therapeutic level. This patient's clinical course indicates that hemodialysis might be superior to intermittent peritoneal dialysis for treatment of cibenzoline intoxication.     

腹膜透析对尿毒症患者肺功能的影响

目的　了解尿毒症患者腹膜透析治疗前后的肺功能变化。方法　分别测定 5 0例尿毒症患者及2 0例正常人的用力肺活量 (FVC)、最大通气量 (MBC)、1秒钟用力呼气容积 (FEV1 )、最大呼气流量 (PEF)、最大呼气中段流量 (MMEF)、2 5 %肺活量最大呼气流量 (·V2 5)和肺一氧化碳弥散量 (DL co)等参数 ,其中 30例尿毒症患者在透析治疗 2月后进行了上述参数的复查。结果　尿毒症患者的肺通气量和气道功能指标 FVC、MBC、FEV1 、PEF、MMEF、·V2 5以及肺弥散功能指标 DL co均明显低于正常人 ;透析治疗后 ,尿毒症患者的气道功能指标 FEV1 、PEF、MMEF和 ·V2 5明显改善 (P<0 .0 5 ) ,但肺通气量指标 FVC、 MBC和肺弥散功能指标 DL co无明显改善 (P>0 .0 5 )。结论　尿毒症患者存在肺通气功能及弥散功能的降低 ,伴气道阻塞 ;透析治疗能显著改善气道阻塞 ,但对肺弥散功能及肺通气量无明显改善 ,此现象往往反映患者已有继发性肺纤维化的存在