Acute thallium

Prussian blue s safety profile is superior to that of other proposed therapies, and that it should be considered the drug of choice in acute thallium poisoning. 

In cases of acute thallium intoxication in humans, similar distributions were observed (Weinig and Walz 1971, Arnold 1986), with specific thallium depot compartments being kidney and muscle. However, no correlation was found between the tissue distribution and particular sensitivity to the toxicodynamic effects of thallium (Forth and Henning 1979). Brain areas densely populated with neurons have been found to accumulate thallium more readily than other brain regions thallium is also accumulated in the testes, and this may lead to reduced sperm motility (Manzo and Sab-bioni 1988). 

Tsai, Y.T., Huang, C.C., Kuo, H.C., et al, 2006. Central nervous system effects in acute thallium poisoning. Neurotoxicology 27, 291-295. 

The usual symptoms in human thaHotoxicosis resulting from acute, subacute, or chronic intoxication are generaHy the same. Common symptoms include nausea, vomiting, abdominal coHc, pain in legs, nervousness and irtitabHity, chest pain, gingivitis or stomatitis, and anorexia. Alopecia (hair loss) does not always occur, especiaHy in cases of mass intake of thallium and low resistance where the patient may die before the occurrence of hair loss. 

During World War II (1939 to 1945), as a result of acute domestic shortages of common rodenticides, such as thallium, strychnine, and red squill, a testing program was initiated for... 

Exercise tolerance (stress) testing (ETT) is recommended for patients with an intermediate probability of CAD. Results correlate well with the likelihood of progressing to angina, occurrence of acute MI, and cardiovascular death. Ischemic ST-segment depression during ETT is an independent risk factor for cardiovascular events and mortality. Thallium myocardial perfusion scintigraphy may be used in conjunction with ETT to detect reversible and irreversible defects in blood flow to the myocardium. 

Thallium and its compounds (particularly soluble salts) can cause serious or fatal poisoning from accidental ingestion or external application. Acute symptoms are nausea, vomiting, diarrhea, weakness, pain in extremities, convulsions, and coma. Chronic effects are weakness, pain in extremities, and rapid loss of hair. Thallium and its compounds are listed under Federal toxics regulations. It is listed hy the US EPA as a priority pollutant metal in the environment. 

Thallium chloride is highly toxic. Acute toxic effects are those of thallium poisoning. 

Dobert N, Britten M, Assmus B, Berner U, Menzel C, Lehmann R et al. Transplantation of progenitor cells after reperfused acute myocardial infarction evaluation of perfusion and myocardial viabiUty with FDG-PET and thallium SPECT. Eur J Nucl Med Mol Imaging 2004 31 1146-1151... 

Cs) and urinary thallium concentrations can guide the recommended duration of therapy. Adjunctive supportive care for possible acute radiation illness (137Cs) or systemic thallium toxicity should be instituted as needed. 

A 34-year-old woman with acute promyelocytic leukemia was given arsenic trioxide solution 0.1%, 10 ml/day for 7 days. A generalized skin rash appeared, and her serum transaminases rose. An electrocardiogram was normal. A second course of arsenic trioxide was used about 3 months later. She felt palpitation and mUd dyspnea and had complete atrioventricular block. Echocardiography showed a normal left ventricle. A thallium myocardial perfusion scan did not show a perfusion defect. Arsenic trioxide was withheld. Sinus rhythm returned 3 days later. Complete atrioventricular block recurred later when arsenic trioxide was re-administered, albeit in a lower dosage for a shorter period of time. 

For acute exposure, ipecac should be administered and lavage performed. The use of single- or multiple-dose activated charcoal is supported by in vitro binding experiments and some animal data, and charcoal hemoperfusion may be a useful adjunct. Forced potassium diuresis appears to be harmful. Flemodial-ysis is also recommended with potassium administration. Since calcium metabolism is disturbed, supplementary calcium is indicated. The use of traditional metal chelators such as dimercaprol (British antilewisite) and penicillamine is not supported by the available evidence. In fact, the use of penicillamine may lead to redistribution of thallium into the central nervous system. Multiple animal studies have found evidence of enhanced elimination and improved survival with Prussian blue however, despite the fact that many humans have been treated with Prussian blue, the data presented are insufficient to judge its true efficacy. Despite this, one publication notes that... 

The principle of dipyridamole and adenosine thallium imaging is related to their coronary arteriolar vasodilator properties. Dipyridamole inhibits adenosine cellnlar renptake, resulting in increased concentrations of adenosine in the blood and tissues. Adenosine is a potent coronary artery vasodilator and can increase perfusion four to five times over baseline. Areas distal to a coronary artery obstruction will show a relative hypoperfnsion compared with normal coronary arteries because there is reduced perfusion pressure owing to preferential perfusion of normal segments over stenotic segments. Acutely, these areas will appear as cold spots, but on the redistribution scans, the defects will fill, indicating viable bnt jeopardized myocardium. 

Mutch E, Blain PG, Williams FM Interindividual variations in enzymes controlling organophosphate toxicity in man. Hum Exp Toxicol 11 109-116, 1992 Noyes H Internet telemedicine saves woman s life (news). The Mercury (U.S. Army Medical Department, Houston, TX) 24 6,1996 Prick JJG, Smitt WGS, Muller L Thallium Poisoning. Amsterdam, Elsevier, 1955 Reed D, Crawley J, Faro SN, et al Thallotoxicosis acute manifestations and sequelae. JAMA 183 516-522,1963... 

The ecotoxicological importance of thallium is derived from its high acute toxicity on living organisms, comparable to that of lead and mercury. Risk assessment is only possible in limited areas of thallium pollution. Global data are missing. 

The competitive replacement Tl /K creates an interesting toxicokinetic factor in terms of thallium elimination, namely direct active excretion into the intestinal lumen. In contrast to other toxic heavy metals, fecal elimination of thallium is the predominant route of excretion. In addition to thallium possibly binding in the gastrointestinal tract in cases of acute intoxication (cf. Section 22.6.2), reabsorption may occur by the enterohepatic and enterosystemic circulations, thereby prolonging the biological half-life. In fact, half-lives of between 3 and... 

Pickard J, Yang R, Dungan B, McDevitt CA and Eickhoff C (2001) Acute and Sublethal Toxicity of Thallium to Aquatic Organisms. Bull Environ Contam Toxicol 66 94-101. 

B. Other useful laboratory studies include CBC, electrolytes, glucose, BUN, creatinine, and hepatic transaminases. Since thallium is radiopaque, plain abdominal x-rays may be useful after acute ingestion. 

In order to determine the distribution of thallium with time in an organism we administered orally 160 mg of thallium per kg body weight to mice. After fixed periods of time the acutely poisoned mice were killed and the thallium concentrations in the heart, liver, kidney and brain were determined by FDMS (Fig. 19). 

Detailed accounts of the clinical progression of thallium toxicity have been published [20-26]. With acute exposure one of the main symptoms is constipation without response to laxatives, presumably due to iliad paralysis. A neuropathic pain develops in the lower extremities and soles of the feet. Extreme abdominal and retrosternal pains develop, along with sleeplessness and excessive thirst. Other symptoms and findings include paresthesia in the extremities, ptosis, fever, conjunctivitis, anhydrosis, and stomatitis. 

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