传染性红斑一例

1病例介绍 患儿男,11岁。因发热3 d,全身红斑、丘疹伴瘙痒2 d于2012年3月19日入住我院。患者就诊前3 d无明显诱因出现发热伴寒颤,体温最高38.9℃,不伴咳嗽、恶心、咽喉疼痛等症状。患儿至当地医院予＂阿莫西林、布洛芬混悬液＂等治疗后体温降至正常（具体不详）。     

发热、咳嗽、咯血、声嘶

病历摘要（第一部分） 患者男性,22岁,因＂发热、咳嗽、咳痰1月余,加重10 d＂于2011年6月27日入住本院. 病史 患者2011年5月4日无明显诱因出现午后发热,体温39℃,伴畏寒寒战、咳嗽、咳少量白黏痰,无乏力、盗汗、咯血、胸闷、心悸.外院先后予头孢美唑、莫西沙星及阿奇霉素治疗后体温可降至37.5℃左右,改服中药,仍间断发热,体温38℃.     

成人麻疹误诊1例分析

对成人麻疹误诊1例分析如下。 1病历摘要 男,32岁。因发热4 d伴咽痛于2009-01-18T 19：30就诊。患者4 d前无明显诱因出现发热,咽痛,体温维持在39℃左右,伴寒战,无抽搐,无咳嗽、流涕、流泪等卡他症状,无畏光。     

骨髓形态学检查诊断黑热病1例

1临床资料 1.1一般资料患者,男,19岁,来自青海农村地区。10月前无明显诱因出现间断发热,体温38-39℃。发热时出汗明显且无明显规律。体温高于39℃时伴寒战无咳嗽咳痰,伴恶心呕吐乏力,于当地医院就诊发现＂血常规三系下降＂,生化检查乳酸脱氢酶升高,肝功能异常,     

系统性红斑狼疮合并组织细胞坏死性淋巴结炎一例

1 病历 患者,36岁,女性,因＂发热咳嗽2个月＂于2011年5月10日入本院呼吸科.患者2个月前无明显诱因出现发热,体温最高达39.5℃,呈持续高热,发热伴畏寒寒战,咳嗽伴少量白色非浓痰,伴膝关节疼痛.入当地医院,行CT检查,发现左下肺渗出性病变,双侧胸腔少量积液,考虑为肺部感染,给予＂氟康唑,头孢美唑,利巴韦林,亚胺培南西司他汀＂及规范四联诊断性抗痨治疗20 d,发热无好转.     

以巨噬细胞活化综合征为首发临床表现的系统性红斑狼疮1例并文献复习

1 临床资料 患者,女,30岁,因"反复发热1个月,腹痛2 d"入住我院.1个月前患者无诱因出现发热,体温38.4℃,伴咳嗽,咳少量白色黏痰,同时伴口、眼干燥,无口腔溃疡、光过敏、面部红斑、关节痛.当地医院诊断为肺部感染,给予抗感染治疗(具体用药、用法、用量不详),体温较前稍下降.入院前28 d再次出现高热,体温最高40.3℃,伴肌痛,继续抗感染治疗10 d,症状无好转,仍发热.     

淋巴瘤误诊成人Still病1例

患者,女,24岁,职员。因＂反复皮疹、发热、关节痛8天＂于2010年1月29日入院。入院前8天患者无明显诱因出现颈部、前胸、前臂及大腿内侧红色丘疹并搔痒,直径约2-5mm,融合成片,压之不退色。伴发热、咽痛、乏力,体温波动于37-38.5℃,伴全身多关节疼痛,以双肩、腕、膝关节明显,无畏寒、寒战。门诊拟＂发热、皮疹、关节痛查因＂收入我科。     

纵膈淋巴结结核治疗中出现类赫氏反应一例

1病例介绍患者女,48岁。因＂反复畏寒、发热,伴四肢关节疼痛10＋d＂入院。10＋d前无诱因出现畏寒,发热T39℃,无咽痛、咳嗽、咳痰、腹泻等不适,伴四肢大关节疼痛,无活动受限。     

以巨噬细胞活化综合征为首发临床表现的系统性红斑狼疮1例并文献复习

1临床资料患者,女,30岁,因"反复发热1个月,腹痛2 d"入住我院。1个月前患者无诱因出现发热,体温38.4℃,伴咳嗽,咳少量白色黏痰,同时伴口、眼干燥,无口腔溃疡、光过敏、面部红斑、关节痛。当地医院诊断为肺部感染,给予抗感染治疗(具体用药、用法、用量不详),体温较前稍下降。入院前28 d再次出现高热,体温最高40.3℃,伴肌痛,继续抗感染治疗10 d,症状无好转,仍发热。实验室检查示:血常规白细胞2.22×109/L,血小     

2例红霉素引起肌无力

患者男,3岁1个月.发热10 d,咳嗽7 d入院.入院前10 d发热,体温波动于37.5℃～39.2℃,伴流涕.人院前7 d咳嗽,逐渐加重,干咳、无咳痰.     

药物超敏反应综合征14例漏误诊原因分析

目的探讨药物超敏反应综合征(DIHS)的临床特点以及漏误诊原因。方法回顾性分析2014年1月—2018年10月住院诊断为重症药疹的患者,按照RegiSCAR评分系统筛选出DIHS的病例,将其他重症药疹患者纳入非DIHS组。记录2组的致敏药物、一般资料、临床症状、实验室检查等,并对相关数据进行统计分析。结果本次研究重症药疹37例,经RegiSCAR评分系统筛选DIHS 14例(漏误诊率37.84%)。DIHS患者中常见的致敏药物为抗生素类,其次为非甾体抗炎药。DIHS患者以发热(主要为高热)、嗜酸粒细胞升高、淋巴结肿大及肝功能损伤多见,可出现面部肿胀、异型淋巴细胞,且在糖皮质激素减量过程中易复发。DIHS组与非DIHS组白细胞异常、嗜酸粒细胞升高、天冬氨酸转氨酶>100 U/L患者比较差异有统计学意义(P<0.05,P<0.01)。14例DIHS经治疗后,7例好转出院,1例痊愈出院,1例自动出院失访,2例转上级医院,3例死亡;治疗有效率57.14%,病死率21.43%。3例死亡患者病情进展极为迅速,均出现内脏器官损伤,2例为多器官功能衰竭。结论重症药疹患者应进行RegiSCAR评分系统评分,提高该病的早期诊断率。DIHS病情进展快,病死率高,应加强对本病的认识,尽量避免漏诊及误诊,及时停用致敏药物,把握治疗时机,降低该病病死率。     

Neuroleptic Malignant Syndrome in a Child Treated with an Atypical Antipsychotic

Neuroleptic malignant syndrome (NMS) is an uncommon potentially fatal side effect of neuroleptic drugs, characterized by movement disorder, altered mental status and autonomic instability. A single dose of clotiapine was administered to an 11‐year old male with acute psychosis. The previously healthy child had signs consistent with NMS including hyperthermia, hypertension, motor and mental changes. Repeat examination performed two weeks later, demonstrated that while his hyperthermia subsided, his mental status deteriorated. Olanzapine was administered, after which the child had hyperthermia, dystonia and more pronounced restlessness, once again consistent with NMS. He developed respiratory failure and was intubated and mechanically ventilated. Lorazepam, dantrolene and bromocriptine were administered as treatment of possible NMS. His mental condition, movement disorder and autonomic dysfunction improved significantly. Two weeks later, the patient was discharged in good general condition without the need for any ongoing medical treatment. There are only few case reports of NMS in children treated with olanzapine, an atypical antipsychotic. In children, caution must be exercised when prescribing antipsychotics, particularly atypical antipsychotics as these drugs may cause NMS. Because of the low incidence of NMS, a high index of suspicion is needed to identify cases so prompt treatment can be undertaken.     

Inflammatory processes in schizophrenia: a promising neuroimmunological target for the treatment of negative/cognitive symptoms and beyond

Emerging evidence indicates that schizophrenia is associated with activated peripheral and central inflammatory responses. Such inflammatory processes seem to be influenced by a number of environmental and genetic predisposition factors, and they may critically depend on and contribute to the progressive nature of schizophrenic disease. There is also appreciable evidence to suggest that activated inflammatory responses can undermine disease-relevant affective, emotional, social, and cognitive functions, so that inflammatory processes may be particularly relevant for the precipitation of negative and cognitive symptoms of schizophrenia. Recent clinical trials of anti-inflammatory pharmacotherapy in this disorder provide promising results by showing superior beneficial treatment effects when standard antipsychotic drugs are co-administered with anti-inflammatory compounds, as compared with treatment outcomes using antipsychotic drugs alone. Given the limited efficacy of currently available antipsychotic drugs to ameliorate negative and cognitive symptoms, the further exploration of inflammatory mechanisms and anti-inflammatory strategies may open fruitful new avenues for improved treatment of symptoms undermining affective, emotional, social and cognitive functions pertinent to schizophrenic disease.     

Marked elevation of serum creatine kinase associated with olanzapine therapy.

OBJECTIVE: To report a case of marked elevation of serum creatine kinase (CK) associated with olanzapine therapy. CASE SUMMARY: A 39-year-old white Jewish schizophrenic man treated with olanzapine developed an elevated serum CK concentration with a peak concentration of 4000 IU/L (normal < 230). No other diagnostic criteria for neuroleptic malignant syndrome (NMS) were present. On discontinuation of the drug, serum CK concentrations returned to normal within eight days. DISCUSSION: Olanzapine, like other atypical antipsychotic drugs, may cause muscle injury with concomitant elevations of serum CK of muscle origin. We suggest that in patients treated with olanzapine, CK concentrations should be checked on initiation of therapy, within the first 48 hours, and weekly thereafter for at least one month. In addition, patients with clinical signs suggestive of NMS should be monitored more carefully. For those patients with a history of NMS, or even of isolated serum CK elevation during antipsychotic therapy, follow-up should be stricter. CONCLUSIONS: Marked elevation of serum CK may be a possible complication of olanzapine therapy.     

Ziprasidone: an atypical antipsychotic drug for the treatment of schizophrenia

BACKGROUND: Over the past decade, use of the atypical antipsychotic drugs clozapine, risperidone, olanzapine, and quetiapine has significantly changed the treatment of schizophrenia in the United States. The ability to make optimal drug choices will depend on determining whether there are clinically important differences between these drugs. OBJECTIVE: This review describes ziprasidone, the most recently introduced antipsychotic drug. Its mechanism of action, pharmacokinetics, and adverse-effect profile are discussed, and the results of clinical efficacy trials are summarized. METHODS: This review of ziprasidone is based on data from premarketing clinical efficacy and safety trials, a briefing document from the US Food and Drug Administration Psychopharmacological Drugs Advisory Committee, published studies, and abstracts presented at national and international meetings. International Pharmaceutical Abstracts and MEDLINE were searched for relevant citations, with no limitation on year. RESULTS: Ziprasidone has been reported to be an effective antipsychotic drug for both positive and negative symptoms of schizophrenia, and long-term use has been effective in preventing relapse. Its 5-hydroxytryptamine (HT)1D-antagonist and 5-HT(1A)-agonist activity are consistent with a potential for antidepressant and anxiolytic activity beyond its antipsychotic effects. Ziprasidone has been associated with a low incidence of sedative effects, a low likelihood of extrapyramidal symptoms and postural hypotension, and no anticholinergic effect, although it may cause transient hyperprolactinemia. Unlike most atypical antipsychotic drugs, ziprasidone is not associated with weight gain, hyperlipidemia, or elevated plasma glucose levels. It is, however, more likely than other atypical antipsychotic drugs to increase the QTc interval (QT interval corrected for heart rate). For acute psychotic symptoms in patients with schizophrenia, schizoaffective disorder, or acute mania, ziprasidone is administered twice daily at a usual daily dose of 80 to 160 mg, whereas 40 mg/d may be an effective maintenance dose. CONCLUSIONS: Differences in efficacy and tolerability between existing atypical antipsychotic drugs allow individualization of drug therapy for patients with schizophrenia or schizoaffective disorder. Ziprasidone differs from other atypical antipsychotic drugs in several clinically important ways, although further experience is necessary to clarify the significance of these differences.     

Indirect modulation of dopamine D2 receptors as potential pharmacotherapy for schizophrenia: II. Glutamate (Ant)agonists

OBJECTIVE: To summarize the published preclinical and clinical data that suggest the possible use of glutamate receptor agonists or antagonists as novel antipsychotic agents. DATA SOURCES: Primary and review articles were identified by MEDLINE search (from 1966 to December 1999) and through secondary sources. STUDY SELECTION AND DATA EXTRACTION: All of the articles identified from the data sources were evaluated and all information deemed relevant was included. DATA SYNTHESIS: The standard antipsychotic drugs, whose clinical activity correlates with affinity for dopamine D2 receptors, alleviate some of the positive symptoms of schizophrenia, but have limited impact on negative symptoms. Several lines of evidence implicate glutamate-receptor system dysfunction(s) in schizophrenia, either as causative or contributory factors. In addition, several standard antipsychotic drugs modulate glutamate or glutamate receptor activity, suggesting an alternative view of their mechanism of antipsychotic action. Preliminary studies have shown that drugs which modulate glutamate brain concentrations have positive effects in animal models of schizophrenia. CONCLUSIONS: A role for glutamate in the pathogenesis or pharmacotherapy of schizophrenia is suggested from anatomic (interactions between glutamatergic and dopaminergic systems in relevant brain regions), physiologic (implication of glutamate-receptor dysfunction), and pharmacologic (modulation of glutamate or glutamate receptors) evidence. Therefore, compounds that function at glutamate receptors might represent a novel approach to the treatment of the disease or to the amelioration of symptoms, either as monotherapy or as an adjunct to dopamine D2 receptor antagonists.     

Antipsychotic drug actions on gene modulation and signaling mechanisms

Schizophrenia is a debilitating chronic mental disorder characterized by significant lifetime risk and high social costs. Although its etiology remains unknown, many of its symptoms may be mitigated by treatment with antipsychotic drugs (APDs). These compounds, generally classified as first- or second-generation antipsychotics, have complex receptor profiles that may account for short-term clinical response and normalization of acute manifestation of the disease. However, APDs have additional therapeutic properties that may not be directly related to receptor mechanisms, but rather involve neuroadaptive changes in selected brain regions. Indeed the neurodevelopmental origin of schizophrenia suggests that the disease is characterized by neuroanatomical and pathophysiological impairments that, at molecular level, may reflect compromised neuroplasticity; the process by which the brain adapts to changes in a specific environment. Accordingly, it is possible that the long-term clinical efficacy of APDs might result from their ability in modulating systems crucially involved in neuroplasticity and cellular resilience. We have reviewed and discussed the results of several studies investigating the post-receptor mechanisms in the action of APDs. We specifically focused on intracellular signaling cascades (PKA, DARPP-32, MAPK, Akt/GSK-3, β arrestin-2), neurotrophic factors and the glutamatergic system as important mediators for antipsychotic drug induced-neuroplasticity. Altogether, these data highlight the possibility that post-receptor mechanisms will eventually be promising targets for the development of novel drugs that, through their impact on neuroplasticity, may contribute to the improved treatment of patients diagnosed with schizophrenia.     

吸烟行为与精神分裂症关系的研究进展

精神分裂症病人有很高的吸烟率,吸烟对精神分裂症病人的影响体现在多个维度,可对抗精神病药物的血药浓度、药物副反应、临床症状、体重、糖脂代谢、心脏以及认知功能产生影响,指出要提高精神分裂病病人的生活质量,应综合考虑以上因素,从而调整治疗方案。     

Aripiprazole in combination with other antipsychotic drugs may worsen psychosis

Aripiprazole is a new generation antipsychotic drug with a partial agonist effect on dopamine D2 and D3 receptors. We report the case of a schizophrenic patient whose symptoms worsened after adding aripiprazole to another antipsychotic drug (amisulpiride). The physiopathology of this process seems to be mediated through the dopaminergic effect of aripiprazole in hypodopaminergic environments, caused by the administration of antipsychotic drugs such as amisulpiride. Besides this, the chronic administration of neuroleptic drugs may induce a hypersensitivity to dopamine agonists. In this context, we consider that the dopaminergic effect of aripiprazole may have induced a worsening of psychotic symptoms. We conclude that clinicians should be cautious when adding aripiprazole to patients under treatment with dopamine antagonists with a high affinity for D2 and D3 receptors.     

Neuroleptic malignant syndrome

The neuroleptic malignant syndrome (NMS) is a potentially fatal complication of antipsychotic drugs. It is characterized by severe muscular rigidity, hyperthermia, and autonomic disturbances. Neuroleptic malignant syndrome is easily confused with other health problems; distinctions between it and malignant hyperthermia, heatstroke, and lethal catatonia are made. The relevant literature is reviewed; a case history is presented; and implications for nursing care (e.g., early detection) are discussed.