小儿七珍丸致成人慢性砷中毒2例

中药小儿七珍丸含有雄黄和朱砂等成分,用于治疗小儿急性惊风和便秘等症.本文报道2例成人长期大量服用小儿七珍丸致慢性砷中毒.例1,女,36岁.因便秘服用小儿七珍丸40～80粒,1;K/d,共3年.在开始服药2～3个月后,患者出现乏力、纳差、腹部皮肤黑变.近1年来出现头晕、头痛、失眠、肢端麻木.入院后,查体示:面部、躯干及四肢色素沉着、手掌及足底皮肤增厚,血砷为7.3μg/L,尿砷为0.117 mg/L.诊为慢性砷中毒.患者经用二巯丙磺钠治疗3个疗程后症状明显减轻.例2,男,40岁.因便秘服用小儿七珍丸20～80粒,每天1～2次,共7年.用药后患者逐渐出现乏力、纳差、恶心、腹胀、全身皮肤色素沉着、皮肤过度角化、手足麻木、肝脾肿大、贫血,尿砷为4.28 mg/L.诊为慢性砷中毒.患者经用二巯丙磺钠治疗5个疗程后,症状明显减轻出院.     

Immunotherapy in acute arsenic poisoning

We investigated the use of immunotherapy on the treatment of sodium arsenite toxicity. Female balb/c mice injected with arsanilic acid conjugated to a carrier protein (ovalbumin) were shown to produce antibodies (arsenic reactive serum, ARS) reactive with arsanilic acid and sodium arsenite. Serum was tested for anti-ARS antibodies using a solid phase radioimmunoassay. The antisera bound to ARS conjugated to the synthetic copolymer glutamic acid60 tyrosine30 when diluted as high as 1:4096. Following multiple injections of 100 micrograms of arsanilic acid--ovalbumin compound, mortality on injection with sodium arsenite 0.87 mg/kg i.p. one week later decreased to 0 deaths in 22 pretreated mice vs 9 deaths in 29 untreated mice (31% mortality; p less than .005). No decrease in mortality was noted at higher challenges (1.15 mg/kg) of sodium arsenite. Antisera from pretreated mice was injected 0.1 cc i.p. into 12 week old female balb/c mice followed by an injection of sodium arsenite 0.87 mg/kg i.p. at 10 minutes. Again a protective effect was observed with 0 deaths in 18 mice vs eight deaths in 21 mice (38%; p less than .005). Seventeen additional mice were given an injection of 0.87 mg/kg i.p. of sodium arsenite. After 30 minutes, all mice became symptomatic whereupon antisera 0.1 cc i.p. was given. The one day mortality (2/17, 12%) was possibly lower than the combined control mortality (17/50, 34%; p less than 0.07). There was no change in mortality noted when antisera was administered to mice acutely exposed to 5 mg/kg HgCl2.     

含雄黄中成药致慢性砷中毒2例

例1女。22岁。因便秘于1999年6月开始不规则服用(长期间断性)健儿药片(别名:郑州肥儿丸,内含雄黄、甘草、使君子仁、蜂蜡、郁金等成分。),2000年6月患者开始出现乏力、月经不调等症状(不明原因),2002年症状加重,在当地(山西运城)血研所诊断为MDS(骨髓异常增生综合征),2002年下半年出现皮肤反应:躯干点状色素减退斑,斑周围出现色素沉着,呈雨滴状。2004年4月患者来我院就诊,检查:面部、躯干、双上臂、双股部散在绿豆大小色素减退斑,周围色素沉着,呈雨滴状改变,双手前臂、手背、双小腿、足背弥漫性色素沉着,掌跖点状角化。实验室检查砷含量:…     

Clinical manifestations and arsenic methylation after a rare subacute arsenic poisoning accident

One hundred and four workers ingested excessive levels of arsenic in an accident caused by leakage of pipeline in a copper-smelting factory. Clinical examinations were performed by physicians in a local hospital. Excreted urinary arsenic species were determined by cold trap hydride generation atomic absorption spectrometry. In the initial toxic phase, gastrointestinal symptoms were predominant (83 people, 79.8%). Most patients showed leucopenia (72 people, 69.2%), and increased serum alanine aminotransferase (84 people, 80.8%) and aspartate aminotransferase (58 people, 55.8%). Thirty-five patients (33.6%) had elevated red blood cells in urine. After 17 days of admission, many subjects (45 people, 43.3%) developed peripheral neuropathy and 25 of these 45 patients (24.0%) showed a decrease in motor and sensory nerve conduction velocity. In the comparison of urinary arsenic metabolites among subacute arsenic-poisoned, chronic high arsenic-exposed and control subjects, we found that subacute arsenic-poisoned patients had significantly elevated proportions of urinary inorganic arsenic (iAs) and methylarsonic acid (MMA) but reduced proportion of urinary dimethylarsinic acid (DMA) compared with chronic high arsenic-exposed and control subjects. Chronic exposed subjects excreted higher proportions of iAs and MMA but lower proportions of DMA in urine compared with control subjects. These results suggest that gastrointestinal symptoms, leucopenia, and hepatic and urinary injury are predominant in the initial phase of subacute arsenic poisoning. Peripheral neuropathy is the most frequent manifestation after the initial phase. The biomethylation of arsenic decreases in a dose rate-dependent manner.     

由过量服用牛黄解毒片(丸)引发砷中毒的反思

过量长期服用含砷制剂有可能造成砷中毒,对此保持足够的警惕,对于临床医务工作具有重要的意义.兹将近年来有关砷制剂的相关资料作一报道.     

Lack of effectiveness of D-penicillamine in experimental arsenic poisoning

Based on some anecdotal case reports D-penicillamine (DPA) has been advocated for the treatment of arsenic poisoning. Experimental evidence, however, supporting that recommendation is lacking. In the present experiments the effectiveness of DPA was compared with dimercaprol (British Antilewisite, BAL), dimercaptopropanesulfonate (DMPS), and dimercaptosuccinic acid (DMSA) using different controlled experimental settings. In one study mice received As2O3 (9-14 mg/kg sc). Treatment with DMSA after 30 min afforded almost complete protection against the lethal effects of arsenic whereas DPA was not effective. In a second study, mice and guinea pigs were injected sc with 8.4 mg/kg As2O3 (containing a tracer dose of 74As). Thirty min later 0.7 mmol/kg of DPA or one of the other antidotes was injected ip. As determined 4 and 12 h after the arsenic injection, DPA was unable to reduce the 74As content in any of the organs investigated (blood, liver, kidneys, lungs, heart, brain, testes, spleen, skeletal muscle, and skin). On the other hand, BAL, DMPS, and DMSA markedly reduced the tissue content of 74As with respect to controls. Finally, the ability of the antidotes to reverse biochemical effects of arsenic was investigated in vitro using suspensions of incubated renal tubulus cells. The marked inhibition of gluconeogenesis induced by 30 mumol/L As2O3 was almost completely reversed upon addition of 90 mumol of either BAL, DMPS, or DMSA. In this experimental model, too, DPA was ineffective. It was concluded that the use of DPA in arsenic poisoning needs to be reevaluated.     

亚慢性砷中毒大鼠血脂的变化

砷及其化合物广泛地存在于自然界中,并被应用于工业、农业及医药等领域。砷中毒已成为一严重的公共卫生问题,在我国的山西、内蒙古、新疆、台湾及美国和加拿大等地区及国家发现了大面积的地方性砷中毒病区[1]。砷的毒性及其防治也因此受到学者们的普遍关注。大量文献报道砷可引     

Family aggregation in a population of chronic arsenic poisoning associated with high arsenic coal burning

About 2600 cases of chronic arsenic poisoning (CAP) in Southwest China-Guizhou Povince represent a unique case of CAP in the world associated with indoor high As coal burning.An epidemiological investigation in 4 clans (694 subjects,male 299,female 395) was launched in one Cun(village) in JL area(21000 residents,about 2000 CAP cases).(1)Clan G(possible Hanized Yi origin).The ancestors,a couple settled here in Qing dynasty.CAP prevalence was 43.3%(93/215).It was found that in 9 of 25 brotherhood groups all the members suffered with CAP.(2) An non-consanguinous branch of family G.The ancestor,a boy was adopted by family G in 1890s.The incidence rate was 20.8%(11/53) which was lower than that in clan G(consanguineous)(P=0.00261,r=0.344),though both clans have been living in the same family for 4 generations.(3)Clan B(Han origin).The ancestor moved the family from Nanjing in Ming dynasty.The CAP prevalence is 45.5%(75/165).(4)Clan P(ethnic Miao).The CAP prevalence is 3.9(9/232),far less than other ethnic clans,for example,less than clan G (consanguineous)(P=3.706E=23,r=0.052944).The observation suggests possible family aggregation of CAP in high As coal using area.further work is required.     

过量服用牛黄解毒片引起慢性砷中毒1例

患者,女,29岁.因砷中毒引起的肝硬化腹水来东直门医院内科门诊就诊.     

Chronic arsenic intoxication diagnostic score (CAsIDS)

Arsenic and its compounds are well‐established, potent, environmentally widespread and persistent toxicants with metabolic, genotoxic, mutagenic, teratogenic, epigenetic and carcinogenic effects. Arsenic occurs naturally in the Earth's crust, but anthropogenic arsenic emissions have surmounted the emissions from important natural sources such as volcanism. Inorganic arsenicals exhibit acute and chronic toxicities in virtually all cell types and tissues, and hence arsenic intoxication affects multiple systems. Whereas acute arsenic intoxication is rare and relatively easy to diagnose, chronic arsenic intoxication (CAsI) is common but goes often misdiagnosed. Based on a review of the literature as well as our own clinical experience, we propose a chronic arsenic intoxication diagnostic score (CAsIDS). A distinctive feature of CAsIDS is the use of bone arsenic load as an essential criterion for the individual risk assessment of chronic arsenic intoxication, combined with a systemic clinical assessment. We present clinical examples where CAsIDS is applied for the diagnosis of CAsI, review the main topics of the toxicity of arsenic in different cell and organ systems and discuss the therapy and prevention of disease caused or aggravated by chronic arsenic intoxication. CAsIDS can help physicians establish the diagnosis of CAsI and associated conditions.