一例持续高钠血症伴渴感减退患者的临床研究

采用禁水和水负荷试验对一例高钠血症伴渴感减退患者进行临床研究,观察血钠、血尿渗透压等变化。显示其仍有调节ADH释放机制,但其阈值增高,符合原发性高钠血症。口服双氢克尿噻和醋酸去氨加压素可部分改善上述异常。     

醋酸去氨加压素联合奥昔布宁治疗儿童单症状性夜遗尿疗效观察

目的观察醋酸去氨加压素联合奥昔布宁口服治疗儿童单症状性夜遗尿的临床疗效。方法选取148例儿童单症状性夜遗尿患儿,随机分为观察组76例和对照组72例。两组均给予基础治疗并且口服常规剂量醋酸去氨加压素,观察组加用奥昔布宁。治疗3个月后观察疗效,停药后随访3个月观察复发情况。结果观察组显效52例,有效19例,无效5例;对照组显效30例,有效26例,无效16例。观察组疗效优于对照组(P0.01)。观察组停药后复发率为11.84%,低于对照组的25.00%,差异具有统计学意义(P0.05)。结论醋酸去氨加压素联合奥昔布宁治疗儿童单症状性夜遗尿比单独使用醋酸去氨加压素疗效更好,而且停药后复发率更低,值得在临床上推广应用。     

去氨加压素治疗咯血的疗效研究

目的探讨去氨加压素治疗咯血的疗效。方法将196例咯血患者随机分为对照组94例及去氨加压素组102例,对照组予垂体后叶素治疗,去氨加压素组给予醋酸去氨加压素持续静脉滴注,观察两组的疗效及副作用。结果两组患者治疗咯血的总有效率分别为,两者差异无统计学意义P〉0．05,加压素组各项副作用明显少于对照组两者有显著差别P〈0．05。结论去氨加压素可用于治疗咯血,其副作用比垂体后叶素少。     

醋酸去氨加压素治疗食管胃底静脉曲张破裂出血疗效观察

目的探讨醋酸去氨加压素治疗食管胃底静脉曲张破裂出血的治疗作用。方法将64例食管胃底静脉曲张破裂出血的患者随机分为两组,治疗组32例,醋酸去氨加压素15μg加入生理盐水100ml静脉滴注,每日2次;对照组予垂体后叶素以0.3～0.4u/min微泵持续静脉注射,同时予硝酸甘油静滴0.8mg/h,维持72h。两组患者均予以禁食、抑酸、维生素K1、输液或输血等治疗措施。结果治疗组显效22例,有效7例,无效2例,总有效率90.63%;对照组显效11例,有例6例,无效15例,总有效率53.13%。治疗组效果明显优于对照组（P〈0.05）。不良反应少于对照组（P〈0.05）。结论醋酸去氨加压素治疗食管胃底静脉曲张破裂出血的疗效明显优于垂体后叶素,且副作用少,值得临床广泛应用。     

醋酸去氨加压素治疗120例结核咯血的临床分析

目的探讨去氨加压素治疗结核咯血的疗效。方法咯血病人240例,在抗结核治疗基础上,予醋酸加压素12μg或垂体后叶素12U加入生理盐水500 ml中静脉滴注,3~7日为一疗程,观察两组的疗效及副作用。结果两组患者治疗咯血的显效率分别为67.5%和55%,差异有统计学意义(P0.05);总有效率分别为89.17%和86.67%,差异无统计学意义(P0.05);加压素组血压升高、心悸、胸闷副作用显著少于垂体后叶素组(P0.05)。结论去氨加压素可用于治疗结核咯血,其副作用较垂体后叶素少。     

内镜下注射去氨加压素治疗上消化道溃疡出血37例

上消化性溃疡出血是临床常见急症,常表现为急性、大量出血,需及时止血,减少机体血容量的损失,防止疾病进一步发展,避免造成严重后果[1].近年来,尽管抑制胃酸分泌的药物治疗上消化道出血取得一定疗效,尤其是质子泵抑制剂;但仍有小部分患者出血凶猛,在药物发挥作用之前已出现休克症状[2].随着内镜技术不断发展,目前急诊内镜下治疗急性上消化道出血已成为首选方法[3].2010年7月～2012年7月,我们在内镜下于溃疡出血部位注射去氨加压素治疗上消化道出血37例,效果较好.现报告如下.     

沙培林联合5-FU腹腔注射治疗癌性腹水28例疗效观察

恶性胸腹水是癌症患者常见的严重并发症之一,如不及时控制,将严重影响患者生命和生存质量。2006年6月-2008年2月,我们对28例胃癌术后并腹腔积液患者采用沙培林联合5-FU腹腔内注射治疗,效果良好。现报告如下。     

可达龙治疗心肌梗死并发室性心律失常40例疗效观察及护理体会

急性心肌梗死后心室肌细胞形成电重构。缺血区心肌细胞动作电位时程缩短，缺血区与非缺血区之间不同部位的心室肌之间可产生电不均一性，易致折返激动，使室性心律失常的发生率增加，此为心肌梗死后发生猝死的主要原因之一。可达龙是一种苯比呋喃类的衍生物，属于第3类抗心律失常药，对控制室性早搏及室性心动过速、预防室颤有显著效果。近年来，我们应用可达龙治疗心肌梗死并发室性心律失常40例。效果满意。现将护理体会报告如下。     

尿激酶、低分子肝素钙及奥扎格雷钠联合治疗进展性脑梗死49例疗效观察

尿激酶、低分子肝素钙及奥扎格雷钠目前均己广泛用于急性脑梗死的治疗,并取得一定疗效,但三者联用治疗进展性脑梗死的报道少见。2005年1月～2007年1月,我们应用尿激酶、低分子肝素钙及奥扎格雷钠联合治疗进展性脑梗死49例,取得较满意效果。现报告如下。     

原发性高钠血症的临床病例分析

为探讨原发性高钠血症的治疗方案,对4例原发性高钠血症患者分别采用两种不同方案治疗.2例先给予垂体前叶激素的治疗,再给予垂体后叶激素补充治疗,另2例同时给予垂体前叶和后叶激素治疗,结果发现:4例患者治疗后临床症状及血渗透压均正常,使用垂体前叶和后叶激素同时治疗的患者治疗时间缩短,而且治疗方案安全.     

Clinical presentation of hypernatremia in elderly patients: a case control study

OBJECTIVES: To assess early clinical signs and their prognostic value in elderly patients with hypernatremia. DESIGN: Prospective, case control study of 150 patients with hypernatremia matched to 300 controls. SETTING: Multicenter study including seven short- and long-term geriatric care facilities. MEASUREMENTS: Clinical assessment of hydration status at bedside, such as abnormal skin turgor or dry oral mucosa. Secondary outcome measures: 30-day mortality rate and clinical indicators (assessed at the peak of natremia) associated with mortality. RESULTS: Patients and controls were comparable in terms of drugs and underlying diseases, except for history of dementia, which was more frequent in patients than in controls. Patients were significantly more likely than controls to have low blood pressure, tachycardia, dry oral mucosa, abnormal skin turgor, and recent change of consciousness. Only three clinical findings were found in at least 60% of patients with hypernatremia: orthostatic blood pressure and abnormal subclavicular and forearm skin turgor. The latter two signs were significantly more frequent in patients with hypernatremia. Four other signs (tachycardia, abnormal subclavicular skin turgor, dry oral mucosa, and recent change of consciousness) had a specificity of greater than 79%. Using logistic regression, four signs were significantly and independently associated with hypernatremia: abnormal subclavicular and thigh skin turgor, dry oral mucosa, and recent change of consciousness. The mortality rate was 41.5% and was significantly higher in patients with hypernatremia. The status of consciousness when hypernatremia was diagnosed was the single prognostic indicator associated with mortality (odds ratio=2.3, 95% confidence interval=1.01-5.2). CONCLUSION: Most of the classical signs of dehydration are irregularly present in patients with hypernatremia. Caregivers should carefully screen any variations in consciousness, because they may reveal severe hypernatremia.     

Myelodysplastic syndrome with central diabetes insipidus manifesting hypodipsic hypernatremia and dehydration

Central diabetes insipidus (DI) is a rare but recognized complication of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) that is caused by leukemic infiltration to the hypothalamo-neurohypophyseal system. In rare patients in whom a wide region of the hypothalamus is involved, central DI results in hypodipsic hypernatremia and dehydration. Typical DI symptoms such as polydipsia, polyuria, and marked thirst are concealed in these cases, because the hypothalamic "thirst center" cannot send thirst stimuli to the cerebral cortex. Herein we describe a patient with MDS developing into AML, who presented with hypodipsic hypernatremia and dehydration. A diagnosis of central DI was made on the ground of a low level of serum anti-diuretic hormone (ADH) despite high serum osmolality. A magnetic resonance imaging study revealed attenuation of a physiological "bright spot" of the neurohypophysis. An induction course chemotherapy including regular-dose cytarabine and daunorubicin produced a rapid improvement of hypernatremia. The bone marrow aspirate after two courses of chemotherapy showed complete remission. At that point, ADH release and the "bright spot" were recovered. In order to correctly diagnose central DI in association with hematological malignancies, we should not overlook this atypical type of DI.     

Congenital nephrogenic diabetes insipidus presenting as osmotic demyelination syndrome in infancy: A case report

Rationale:Almost 90% of congenital nephrogenic diabetes insipidus (NDI) cases are caused by mutations in the arginine vasopressin receptor 2 gene, which has X-linked recessive inheritance. Although NDI is commonly diagnosed in early infancy based on its characteristic findings, clinical diagnosis can be delayed when no other family members have been diagnosed with NDI because several findings of NDI are nonspecific.Patient concerns:A 3-month-old boy diagnosed with NDI presenting with osmotic demyelination syndrome (ODS) was admitted for poor weight gain after birth and poor feeding during the week prior to admission.Diagnosis:On admission, the initial blood examination showed hypernatremia (158 mmol/L), and treatment with intravenous fluids over the next 2 days further elevated the serum sodium level (171 mmol/L). After admission, polyuria was recognized, and polyuria in his grandmother and mother since childhood without a diagnosis of NDI was found. Magnetic resonance imaging showed multifocal, symmetrical lesions, including the lateral pons, on diffusion- and T2-weighted imaging, which led to a diagnosis of ODS.Intervention:The infusion was stopped, and the patient was fed milk diluted 2-fold with water.Outcomes:The serum sodium level gradually decreased to 148 mmol/L over the course of 1 week. Low-sodium milk was started at 4 months of age and maintained a serum sodium level of approximately 140 mmol/L, which was within the normal range. The developmental quotient was 94 at 4 years of age.Lessons:ODS is an encephalopathy resulting from extreme fluctuations in serum sodium concentration and plasma osmolality. ODS due to hypernatremia has been reported in several patients, although it usually occurs during rapid correction of hyponatremia. Consequences of the central nervous system are a critical complication of NDI that affects prognosis. These consequences can be avoided with treatment. Early blood examination or polyuria in the patient, mother, or another family member and hypernatremic dehydration with good urine output should lead to an early diagnosis and prevent central nervous system consequences.     

上消化道大出血继发暂时性尿崩症1例报道

上消化道大出血患者继发暂时性尿崩症少见,因大出血而导致的失血性休克状态,不能保证重要脏器的供血供氧,再加上交感神经的反射性兴奋引起动脉痉挛甚至闭塞,进而导致脑垂体大面积坏死,出现尿崩症。一旦发生应及时处理原发病,补充血容量及减少出血,必要时抗利尿激素替代治疗。目前部分继发性暂时性尿崩症患者症状较轻,且不典型,需临床医生提高警惕,早期预防尿崩症的发生。     

连续性血液净化治疗脓毒症所致高钠血症41例效果观察

目的观察连续性血液净化治疗脓毒症所致高钠血症的临床疗效。方法将65例脓毒症所致高钠血症患者按照治疗方法分为观察组41例及对照组24例,两组均予脓毒症的相关治疗,观察组在此基础上采用连续性血液净化（CBP）治疗,对照组采取胃肠道补水的传统方法治疗,观察两组治疗前、后血钠（Na）、血尿素氮、血肌酐及血浆渗透压变化,比较其高钠治愈率和病死率。结果观察组治疗后血Na、血浆渗透压、病死率均明显低于对照组,治愈率明显高于对照组,P〈0.05;其余各指标比较无统计学差异。结论 CBP治疗高钠血症效果显著,能明显改善患者预后;优于胃肠道补水的传统治疗方法。     

以中枢性尿崩为首发表现的朗格汉斯细胞组织细胞增生症的临诊应对

报道3例以中枢性尿崩为首发表现的朗格汉斯细胞组织细胞增生症(LCH)患者,总结其临床表现、实验室检查、影像学检查、病理结果、诊断过程和治疗反应。3例患者早期均以中枢性尿崩症起病,垂体磁共振成像(MRI)均表现为垂体柄增粗,垂体后叶正常高信号消失。2例患者表现为孤立性下丘脑-垂体病变,1例表现为垂体和甲状腺多系统受累。病理结果显示典型的朗格汉斯细胞,免疫组织化学示S-100、CD1a、Langerin阳性。LCH临床表现呈现明显的异质性,容易误诊和漏诊。确诊依赖病理结果,孤立性下丘脑-垂体病变活检难度较大,建议积极筛查其他器官增加活检概率。LCH导致的神经垂体损害通常需要终生激素替代治疗。     

幼年皮肌炎35例临床分析及文献复习

目的 探讨幼年皮肌炎的发病原因、诊治方法及预后.方法 分析我院35例幼年皮肌炎的临床特点、病理、实验室检查、诊治过程及预后情况,并结合文献复习.结果 幼年皮肌炎合并肿瘤及引起重要内脏器官损伤少见.治疗首选激素,疗效明显.对于病情控制不理想或泼尼松减量困难的病例,可加用免疫抑制剂.4例重者加用静脉注射人免疫球蛋白(IVIG)等.35例患儿中25例痊愈,10例有效,后者经维持治疗,最终停药.一般用药时间为2～3年或更长.8例患儿在停药后1～4年病情反复,再给予治疗,仍有效.本组患儿酶学指标在治疗3～5周后降低或正常,肌力在1～6个月(平均2.6个月)恢复,肌力恢复从4～5级需1.5～3个月,从3～5级需6～12个月.结论 幼年皮肌炎早期诊断、早期治疗,预后良好.     

对2型糖尿病患者启动胰岛素治疗的思考

在2型糖尿病的治疗中尽早启动胰岛素治疗,是血糖达标的需要,也是保护胰岛β细胞、恢复其功能,从而延缓糖尿病进展的需要。初诊2型糖尿病患者经过3个月的生活方式干预和优化的口服降糖药物治疗血糖仍不能达标时,即应启动胰岛素治疗。对代谢紊乱严重、血糖水平较高的患者,应及时启动胰岛素强化治疗。可供选择的胰岛素治疗方案很多,各有优缺点和适应人群,临床上应当因患者而异地选择适宜的起始治疗方案。如何依据糖化血红蛋白（Hb）A1c选择起始治疗方案,目前尚无定论。推荐当HbA1c≤8．5％时主要选择基础胰岛素,HbA1c〉8．5％时选择预混胰岛素或基础—餐时或持续皮下胰岛素输注（CSII）作为起始胰岛素治疗方案。