Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
Add more filters










Database
Publication year range
1.
Hum Exp Toxicol ; 28(5): 263-72, 2009 May.
Article in English | MEDLINE | ID: mdl-19755458

ABSTRACT

Information on the prognosis and electrophysiological follow-up of severe thallium poisoning is limited. We report two patients (mother and daughter) who were repeatedly exposed to thallium poisoning experienced hair loss, polyneuropathy, and visual impairment. Nerve conduction studies (NCSs), visual evoked potentials (VEP), brainstem auditory evoked potentials (BAEP) changes, and optical neuropathy developed within a few months latency after the first subjective signs. Normal findings of these electrophysiological methods in the first 2 weeks therefore led in one of our patients to exclusion of thallium as the cause of symptoms. Thallium poisoning was, however, later confirmed by toxicological analysis of blood and/or urine and feces in both the patients and in the microscopic hair analysis of the daughter. Both patients were treated with Prussian blue that increased the elimination of thallium in urine and feces. The hair loss was fully reversible. During a 2-year follow-up after the poisoning, polyneuropathy in the lower extremities improved substantially, but residual impairment in both motor and sensory function, NCSs, VEP, and BAEP remained. Additionally, severe asymmetrical vision impairment persists in both women, with central scotomata and impaired color discrimination in both eyes. Substantial improvement of their visual function is unlikely.


Subject(s)
Thallium/poisoning , Adult , Alopecia/chemically induced , Animals , Antidotes/therapeutic use , Crime , Dogs , Electroencephalography , Evoked Potentials, Auditory, Brain Stem/drug effects , Evoked Potentials, Visual/drug effects , Female , Ferrocyanides/therapeutic use , Hair/chemistry , Humans , Neurologic Examination , Optic Nerve Diseases/chemically induced , Pain/chemically induced , Paresthesia/chemically induced , Peripheral Nervous System Diseases/chemically induced , Poisoning/physiopathology , Poisoning/therapy , Sensation Disorders/chemically induced , Thallium/analysis , Vision Disorders/chemically induced , Vision Tests , Visual Acuity , Young Adult
2.
Physiol Res ; 56(1): 113-122, 2007.
Article in English | MEDLINE | ID: mdl-16497089

ABSTRACT

We have found that the determination of thiodiglycolic acid (TDGA) in urine may help to characterize metabolic imbalance of substances participating in methionine synthesis, which leads to hyperhomocystinuria. From the metabolic scheme, based on a proper combination of known facts, we attempted to theoretically explain and to demonstrate the possibilities of TDGA formation via different ways of homocysteine transformation. This scheme was used in evaluating the results obtained by testing urine of a woman suffering from impaired function of methionine synthase reductase (CblE type of homocystinuria). The amount of TDGA excreted in her morning urine was very sensitive to the changes in her treatment based upon a combination of N5-formyl tetrahydrofolate, betaine and vitamin B12. Vitamin B12 given in the evening either alone or together with betaine increased the TDGA excretion in the morning urine up to ten times. On the other hand, in the absence of vitamin B12, betaine in combination with N5-formyl tetrahydrofolate hindered the appearance of TDGA in the morning urine. Generally, the determination of TDGA in urine of an appropriately pretreated patient may indicate the degree of success of the treatment.


Subject(s)
Folic Acid/pharmacology , Sulfhydryl Compounds/metabolism , Thioglycolates/urine , Vitamin B 12/pharmacology , Adult , Betaine/pharmacology , Betaine/therapeutic use , Biomarkers , Homocysteine/blood , Humans , Injections, Intramuscular , Leucovorin/therapeutic use , Male , Vitamin B 12/blood , Vitamin B 12/therapeutic use , Vitamin B 12 Deficiency/urine
3.
Cas Lek Cesk ; 144(4): 282-4, 2005.
Article in Czech | MEDLINE | ID: mdl-15945490

ABSTRACT

The authors describe severe lead intoxication in a male patient who swallowed about 20 lead shots by accident. It caused an acute lead intoxication with highest blood lead reaching about 2.4 fold value of biological exposure limit for blood lead concentration for occupational exposure (0.97 mg/l), coproporphyrines in urine reaching 30 fold increase of biological exposure limit (1000 nmol/mmol creatinine), and 5-aminolevulic acid about 2.7 fold increase of biological limit (35.0 micromol/mmol creatinine). After first dose of chelating antidote (calcium disodium edetate, EDTA) the patient excreted 9.0 mg of lead in urine during 24 hours. Clinical symptoms and results of examinations led to suspicion of gastroduodenal ulcer at first. Diagnosis was defined after detailed examination and completing of the patient's history. Typical symptoms of intoxication developed--normocytic normochromic anemia and saturnine colics. Elimination of shots from digestive tract and treatment with 8 doses of antidote led to crucial change and improvement in the course of one month. The article should serve as an instruction to early recognition of lead intoxication.


Subject(s)
Foreign Bodies/complications , Lead Poisoning/etiology , Abdomen , Accidents , Adult , Deglutition , Humans , Male
SELECTION OF CITATIONS
SEARCH DETAIL
...