质子泵抑制剂致胰岛素自身免疫综合征一例

胰岛素自身免疫综合征(IAS)是一种少见的自身免疫性内分泌疾病,是由于自身免疫、自身抗体作用引起的一组低血糖综合征。本文报道1例与质子泵抑制剂使用有关的IAS,旨在提醒临床医生在应用该类药物时患者若出现低血糖,需考虑到IAS发生的可能,减少误诊率,使患者得到快速有效的治疗。     

氯吡格雷致胰岛素自身免疫综合征一例

患者老年男性,因“发作性出汗、心悸22d”就诊,否认严重肝、肾功能不全病史,否认外源性胰岛素用药史,否认胰腺占位及手术史,有氯吡格雷服药史。多次查随机血浆葡萄糖<2.8 mmol/L,血清胰岛素>1000 mIU/L,胰岛素自身抗体(IAA)(+)。人类白细胞抗原分型:DRB1*0403与0701,DQB1*0302与0202。停用氯吡格雷,调节饮食结构,口服阿卡波糖后低血糖症状逐渐缓解,出院5个月后复查血清胰岛素及C-肽明显下降,IAA转阴,遂停用阿卡波糖,减少进餐次数,发作性出汗及心悸未再发生。     

胰岛素自身免疫综合征一例

患者,男性,40岁.因反复意识障碍、烦躁1天于2012月5日入住我院ICU科.入院查体:体温37.2℃,血压145/95mm Hg,脉搏120次/分,SpO296％,意识模糊,呈谵妄状态,查体不合作,呼吸平顺,平卧位,体型瘦,皮肤稍热、干燥.巩膜无黄染,双眼球结膜无水肿,双侧瞳孔等大等圆,直径约3mm,对光反射迟钝,颈可疑抵抗,气管居中,双侧甲状腺I°肿大,质软,表面光滑,未扪及结节,未闻及血管杂音.双肺呼吸音粗,未闻及干湿性啰音.心界无扩大,心率120次/分,律齐,无病理性杂音.腹平软,全腹无压痛反跳痛,肝脾肋下未触及,腹水征阴性,肠鸣音正常.四肢肌张力升高,肌力检查欠合作,约3级以上,双膝反射可引出,双巴氏征阴性.患者既往有甲状腺功能亢进症(简称甲亢)病史3年,曾口服药物(具体用药不详)治疗3个月后自行停药,未定期复诊.3个月前患者出现心悸、怕热多汗、消瘦等症状加重,于当地医院治疗,口服他巴唑10mg,1日3次,甲亢灵胶囊2粒,1日3次,心得安10 mg,1日3次至今.否认糖尿病、高血压等病史和手术外伤史.10月5日急查血糖1.09 mmol/L,头颅CT检查未见明显脑血管疾患.     

胰岛素自身免疫综合征一例

胰岛素自身免疫综合征(IAS)是以空腹低血糖或反应性低血糖及内在胰岛素自身抗体(IAA)为特征的罕见自身免疫性疾病,该病国内少见.     

他巴唑致胰岛素自身免疫综合征一例

患者女性 ,5 0岁。甲状腺功能亢进 (甲亢 )病史 6个月 ,病初血清促甲状腺激素 (ＴＳＨ) 0 0 1ｍＩＵ/Ｌ ,游离Ｔ39 6ｐｍｏｌ/Ｌ ,游离Ｔ4 5 1 2ｐｍｏｌ/Ｌ ,他巴唑 (ＭＭＩ)治疗 4个月。 2 2ｄ前起连续 3ｄ晨起饥饿感 ,伴心悸、多汗 ,进食后缓解 ,未介意。 19ｄ前晨家人发现其昏迷 ,当地医院测血糖低 (具体不详 ) ,静点 10 %葡萄糖 4ｈ后清醒如常人。此后连续 3ｄ发作低血糖 ,均为凌晨 ,发作时血糖分别为 1 1、1 8、1 6ｍｍｏｌ/Ｌ ,葡萄糖治疗有效。否认糖尿病史 ,从未用过口服降糖药和胰岛素 ;无高血压史。因低血糖原因不明于 2 0 0 0…     

胰岛素自身免疫综合征的诊治

胰岛素自身免疫综合征(IAS)为少见病.通过报道1例IAS并结合国内近20年报道的50例IAS病例,讨论IAS的诊治.临床上对伴有Graves病、服用他巴唑的高胰岛素性低血糖症患者,应检测胰岛素自身抗体,以避免误诊和不必要的手术.     

胰岛素自身免疫综合征

胰岛素自身免疫综合征是由血中非外源性胰岛素诱导的胰岛素自身抗体及高浓度免疫活性胰岛素所致的自发性低血糖症。其与伴发自身免疫性疾病及应用含巯基药物有关,并与人白细胞抗原高度相关,DRB1*0406可能是主要易感基因;不同人群的发病机制存在异质性。临床上主要特征为未使用外源性胰岛素情况下,出现反复发作性严重低血糖、胰岛素自身抗体滴度明显升高及游离胰岛素升高;主要应与胰岛素瘤鉴别。治疗以停用诱发药物为主,辅以少量多餐、低糖和高纤维饮食,多数患者可自行缓解。必要时应用小剂量泼尼松。     

胰岛素自身免疫综合征一例

患者,男性,27岁.因"反复意识不清20余天"入院.患者既往有甲状腺功能亢进(简称甲亢)病史3年,曾口服丙硫氧嘧啶治疗后出现皮疹,遂调整为他巴唑治疗,患者间断服药,2个月前开始规律口服"他巴唑10 mg,每日3次"进行抗甲亢治疗.服药20天后患者突发意识不清,呼之不应,至当地医院检查提示血糖低,给予静脉推注高糖后患者意识恢复;次日早晨患者再次出现意识不清,急查血糖1.9 mmol/L,给予高糖静脉推注后患者意识恢复.患者住院期间仍反复出现晨起意识不清,多次测血糖均＜2 mmol/L,给予葡萄糖静脉注射后症状可缓解.     

胰岛素自身免疫综合征三例

自身免疫性低血糖症（AIH）是低血糖的一种少见原因,其临床特点为自发性低血糖发作、高胰岛素血症及胰岛素抗体或胰岛素受体抗体阳性.根据自身抗体的不同可以分为两种类型：（1）在无外源性胰岛素应用时出现针对内源性胰岛素的抗体（IAA）阳性,称为胰岛素自身免疫综合征（IAS）,1970年由日本Hirata等首次报道,又称Hirata病[1];（2）是针对靶细胞表面的胰岛素受体的抗体（IRA）阳性,称为B型胰岛素抵抗综合征（TBIRS）,较罕见[2],部分可出现低血糖.我院自2009年报道1例IAS后[3],陆续出现数例,现再报告3例IAS患者,以提高临床认识.     

胰岛素自身免疫综合征合并Graves病1例及文献分析

胰岛素自身免疫综合征(IAS)是指从未使用过胰岛素的患者发生的严重自发性低血糖,由遗传因素和环境因素共同作用,大部分患者携带DRB1* 0406基因,多合并Graves病等自身免疫性疾病,以服用甲巯咪唑等药物为诱因,以血浆高胰岛素水平、高C肽水平、高滴度的胰岛素自身抗体(IAA)为主要特征.IAS具有自限性,停用诱发药物,辅以低碳水化合物、高蛋白、高纤维饮食,必要时给予小剂量糖皮质激素及免疫抑制剂,多数可缓解.     

Hypersensitivity to proton pump inhibitors: lansoprazole-induced Kounis syndrome

Proton pump inhibitors are commonly used in clinical practice for the treatment of peptic ulcer and gastroesophageal reflux and are well tolerated by the patients. Their use is rarely associated with hypersensitivity and anaphylactic reactions. According to the reports in the Uppsala Monitoring Center database the frequency of hypersensitivity reactions out of all reported adverse reactions for proton pump inhibitors and H2-histamine receptor antagonists was between 0.2% and 0.7%. A few cases of hypersensitivity to lansoprazole have been reported. We report a patient who developed Kounis syndrome after taking 30 mg of lansoprazole. This is the first report of Kounis syndrome associated with lansoprazole administration in the world literature.     

胰岛素自身免疫综合征一例报告

胰岛素自身免疫综合征 (ＩＡＳ)是诱发低血糖的一种少见疾病 ,容易误诊 ,兹将我们发现一例报道如下 :患者女性 ,36岁 ,农民 ,1998年因怕热多汗、心悸、消瘦被诊为“甲亢” ,不规则服药治疗 ,其间连续服过他巴唑 3个月 ,好转后间断服过中草药。 1999年 8月 2 8日上午 ,无明显诱因突感头昏心悸 ,但无抽搐及昏迷。急送某院查血糖为1.5 2ｍｍｏｌ/Ｌ ,经注射葡萄糖后缓解。 9月 2日 12 :0 0及19 :30又先后两次低血糖发作 (血糖分别为 1.42、2 .10ｍｍｏｌ/Ｌ) ,均经注射高渗葡萄糖后缓解 ,后转来我院。既往无注射胰岛素史 ,家族成员未发现同类患…     

Cushing syndrome caused by topical corticosteroid: a case report

Development of iatrogenic Cushing syndrome from topical steroid therapy is very rare in adults. A 48-year-old woman with a diagnosis of Cushing syndrome caused by long-term topical clobetasol propionate application was presented. Laboratory studies were consistent with adrenal suppression that improved after discontinuation of the use of topical glucocorticoids. Patients who will take treatment with steroids, even with topical steroids, should be offered information about the dose, duration, and type of the treatment and its systemic side-effects.     

Agranulocytosis induced by proton pump inhibitors

We report the first published case of agranulocytosis induced by omeprazole and its recurrence with esomeprazole, the S-isomer form of omeprazole. Interestingly, we found an homozygotous mutation of CYP2C19*17, responsible for the metabolism of proton pump inhibitors.     

Intravenous proton pump inhibitors

Intravenous (IV) administration of a proton pump inhibitor (PPI) is a faster way to achieve gastric acid suppression than oral administration of the same agent. Peak suppression after IV administration occurs within hours, compared with several days later after oral administration. Thus the IV route of administration offers a faster onset of gastric suppression, achievement of intragastric pH closer to neutrality, and better bioavailability. The PPIs that have IV formulations in the United States (esomeprazole, lansoprazole, and pantoprazole) are approved for different indications; the key differences among them relate to their ability to reach specific gastric pH, time to maintain a specific gastric pH, and ease of use of the IV formulation (eg, reconstitution, requirement of inline filters, infusion times).     

Case report of proton pump inhibitor responsive esophageal eosinophilia: why 2 months of proton pump inhibitors is required

Eosinophilic esophagitis (EoE) is a chronic inflammatory disease defined by the 2nd EoE consensus panel as: ‘symptoms related to esophageal dysfunction, ≥15 eosinophils per high‐power field, eosinophilia that persists after a trial of proton pump inhibitor (PPI) therapy, and exclusion of other secondary causes of esophageal eosinophilia’. After Ngo et al. first reported a case series of 3 patients initially diagnosed with eosinophilic esophagitis responding endoscopically and histologically to PPI therapy, the term PPI‐responsive esophageal eosinophilia has evolved. Several studies have since confirmed the existence of this entity. Although recent ACG guidelines call for a 2‐month course of PPI followed by endoscopy biopsies this recommendation is classified as a strong recommendation with ‘low evidence’, and has not been proven in the literature. We present a case of PPI‐REE treated with rabeprazole 20 mg BID for 2 months, and describe simultaneous symptom resolution with histological and endoscopic remission of disease. This unique case with serial endoscopy and histology at baseline and monthly suggests the current recommendation of at least two months therapy with PPIs dosed twice daily is appropriate. Future studies will need to address duration of high dose therapy, whether patients can be stepped down to once a day PPI, and therapeutic strategy for transient responders.     

Pharmacology of proton pump inhibitors

The gastric H,K-ATPase is the primary target for the treatment of acid-related diseases. Proton pump inhibitors (PPIs) are weak bases composed of two moieties, a substituted pyridine with a primary pK_a of about 4.0, which allows selective accumulation in the secretory canaliculus of the parietal cell, and a benzimidazole with a second pK_a of about 1.0. PPIs are acid-activated prodrugs that convert to sulfenic acids or sulfenamides that react covalently with one or more cysteines accessible from the luminal surface of the ATPase. Because of covalent binding, their inhibitory effects last much longer than their plasma half-life. However, the short half-life of the drug in the blood and the requirement for acid activation impair their efficacy in acid suppression, particularly at night. PPIs with longer half-life promise to improve acid suppression. All PPIs give excellent healing of peptic ulcers and produce good results in reflux esophagitis. PPIs combined with antibiotics eradicate Helicobacter pylori.