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At least 19 recordsLinked to original sources
PubMed1977

Apallic syndrome in chronic mercury poisoning.

This report includes five cases afflicted by chronic mercury poisoning which was observed in Iraq in 1972. All five cases showed the symptomatology of a severe cerebral damage combined with peripheral nerve lesion. The clinical picture reveals an apallic syndrome or a prestage ensuring in the full-blown picture. The combination of CNS lesions with polyneuropathy is typical of mercury poisoning with failure of all brain functions and the appearance of brain stem automatism, combined with severe muscular atrophy. When such conditions are established the remission seems to be impossible. The historical as well as the clinical and morphological facts of the Minamata disease is reviewed. The different stages of chronic mercury poisoning in Iraq are described.

Adolescent↗
PubMed1978

Mental effects of mercury poisoning.

Three dentists suffered symptoms of mercury poisoning from the use of this substance in the production of amalgam for dental fillings. The problem of mercury absorption in dental offices has been well documented in the dental literature. The three cases are presented.

Adult↗
PubMed1975

[Chronic mercury poisoning from cosmetic creams (author's transl)].

Two cases of chronic mercury poisoning are reported. Both patients had used a skin cream containing mercury for years which contained the latter substance in various strengths (3%-50%). The creams are commercially available, usually in 20 g tin as a skin whitener or skin care preparation. According to the regulations in force, preparations containing not more than 5% Hg in the form of white precipitate can be freely obtained without prescription in drug-stores and perhaps also in shops dealing in cosmetics. The limits of tolerance at which the first symptoms of mercury poisoning may appear may perhaps have been already reached by the regular use of freely purchasable preparations.

Adult↗
PubMed1978

Chronic mercury poisoning from a single brief exposure.

For a number of years we have observed six patients whose illness began after inhaling high concentrations of mercury vapor in a single exposure. They all had symptoms of acute mercury poisoning with fever, chills, chest pain, and weakness. Three men had diffuse pulmonary infiltrates on chest x-ray suggesting chemical pneumonitis. Two of the men excreted large amounts of mercury in their urine two days after exposure following BAL therapy. Their chronic symptoms differed somewhat, but many complained of nervousness, irritability, lack of ambition, and loss of sexual desire. Chronic mercury poisoning is generally felt to follow only long periods of exposure. Although thess patients had symptoms which are not pathognomonic of chronic mercury poisoning, we feel the events described strongly suggest their relationship to a single brief exposure and represent a form of chronic mercurialism.

Accidents, Occupational↗
PubMed1992

An acute mercuric mercury poisoning: chemical speciation of hair mercury shows a peak of inorganic mercury value.

A woman ingested a dose of sublimate (approximately 0.9 g) in an attempted suicide. She survived and recovered in response to a combination of therapies including chelate (BAL) therapy, plasma exchange, haemodialysis and peritoneal dialysis. Serum inorganic mercury concentration, urinary inorganic mercury excretion and hair inorganic and organic mercury and selenium concentrations, along the length from the scalp to the distal part, were measured. Longitudinal analysis of hair, revealed a peak in inorganic mercury corresponding to the time of mercury ingestion. Organic mercury and selenium in the hair had different patterns of longitudinal variation from that of inorganic mercury. The biological half-life (23.5 d) of serum inorganic mercury levels was in good agreement with values previously reported in the literature.

Adult↗
PubMed1976

Mercury poisoning in a dentist.

We examined a dentist with chronic elemental mercury poisoning electrophysiologically. Motor conduction in the upper and lower limbs was normal. Sensory nerve action potentials in the ulnar and median nerves were normal, but could not be elicited in the superfical peroneal nerves. Conduction velocity of the sural nerves was normal, but the action potential amplitude was abnormal. Following treatment with penicillamine, sensory conductions in the lower limbs returned to normal.

Dentistry↗
PubMed1978

Biochemical effects of mercury poisoning in rats.

Acute HgCl2 poisoning was shown to decrease significantly the pyruvate dehydrogenase (PyDH) and alpha-ketoglutanic dehydrogenese (alphaKgDH) activity in the kidney and liver but not in the brain. Rats receiving 77% of the 2 hr 50% lethal dose showed 57% of normal renal PyDH activity and 69% of normal renal alphaKgDH activity. Chronic Hg Cl2 poisoning resulted in an unexpected increase in PyDH and alphaKgDH activity in the kidneys where mercury was most concentrated. In acute methyl mercury injection, no significant effect on PyDH or alpha KgDH activities was observed after 2 days. Less mercury was accumulated in the tissues with methyl mercury poisoning than in the other treatments.

Acute Disease↗
PubMed1975

[Nail changes and loss of hair: cardinal signs of mercury poisoning from hair bleaches (author's transl)].

In the German Federal Republic it has recently become known that generalised disorders of chronic mercury poisoning (loss of weight, stomatitis, hearing and sensory loss, emotional disturbances) have accompanied the cardinal signs of nail discolouration and loss of hair. The mercury content of nails in such patients was extremely high (1720 mg/l). The urinary level of mercury after dimercaprol injection was 1.97 mg/l, about 400 times above the upper limit of normal (0.005 mg/l). The poisoning was apparently caused by the use of mercury-containing bleaches (about 5% and 6% Hg) which do not require prescription and are marketed without any statement about composition or possible side-effects. The cases are a warning against uncontrolled use of external application of mercury-containing preparations.

Alopecia↗
PubMed1975

Barbiturate potentiation in mercury poisoning.

Barbiturate potentiation was observed in Japanese quail fed dietary levels of 4, 21, and 24 ppm Hg as methyl mercuric chloride. Gross symptoms of mercury poisoning were not observed until after BP was observed. After the initial increase in BP time was observed in the birds receiving 4 and 12 ppm mercury, there followed a plateau in response until those birds receiving 24 ppm Hg began to show gross symptoms of toxicity and the BP time markedly rose again. Pronounced BP persisted 7 weeks after removal of mercury from the diet reflecting the long biological half-life of mercury as the methyl derivative. Selenium effectively prevented BP after 7 days exposure to toxic levels of methyl mercury chloride. Therefore, results suggest that early toxic effects of mercury can be observed readily by BP and that this environmental contaminant may influence drug activity or increase the sensitivity of the nervous system to sodium pentobarbital.

Animals↗
PubMed1978

[Monoamine metabolites and cyclic nucleotides in the cerebrospinal fluid of patients with bismuth or mercury poisoning].

The central metabolism of dopamine, serotonin, cyclic AMP and cyclic GMP was studied by use of the probenecid test in three patients with bismuth encephalopathy and in one patient with mercury encephalopathy. The accumulation of HVA and of cGMP in the cerebrospinal fluid was depressed during the acute phase of bismuth encephalopathy with severe hyposomnia, while it was increased in a patient with regression of clinical symptoms and normal in a patient with more advanced recovery. The patient with chronic mercury poisoning showing a severe cerebellar ataxia and rigidity had an almost complete suppression of HVA accumulation and an increase of cGMP accumulation. No pronounced differences of 5-HIAA and cAMP behavior were found. It is concluded that the central metabolism of dopamine and of cGMP is severely affected in bismuth and mercury encephalopathies.

Adult↗
PubMed1977

[An unusual case of panarteritis nodosa associated with chronic mercury poisoning (author's transl)].

In a 50-year-old woman, working as a dental assistant for more than ten years, chronic mercury poisoning developed insidiously, apparently from careless handling of mercury-amalgam. The main signs consisted of mental and neurological changes such as erethism, tremor and mercurial psellism. Peripheral arterial circulatory disorders occurred in the course of the disease, as well as abdominal colic and a polyneuropathy, which provided the first clues to panarteritis nodosa subsequently confirmed histologically.

Biopsy↗
PubMed1977

Selected case histories and epidemiologic examples of human mercury poisoning.

To illustrate the various clinical pictures resulting from toxic effects of mercury and its compounds, highlighted literature excerpts have been prepared and arranged in a logical sequence. Particular emphasis is placed upon early diagnosis and prevention of epidemic outbreaks involving intoxication through organomercurials.

Adolescent↗
PubMed1976

Indirect sources of mercury poisoning in the Iraqi epidemic.

Secondary sources of intoxication with methylmercury poisoning other than home-made bread were explored. Mercury levels in various food items were below 0.05 mg/kg.Over 30 000 specimens of meat and internal organs of sheep were analysed because of the strong suspicion that the animals had been fed treated barley. It was found that 6-12% of the specimens analysed contained more than 0.5 mg/kg of mercury. Consumption of meat did not appear to constitute a danger of intoxication during the outbreak.

Animals↗
PubMed1979

[Chronic mercury poisoning following topical application of skin bleachers (author's transl)].

In two female patients chronic mercurialism following topical application of skin bleachers for the treatment of freckles was diagnosed. Over 20 to 25 years 3 to 10% mercurial ointments were applied twice daily. Recurrent attacks of headache, dyspnoea and abdominal colic-like cramps had lead repeatedly to emergency hospitalisations, multiple medical check-ups and surgical exploratory procedures. The diagnosis of mercurialism was made clinically because of a slate-grayish skin hyperpigmentation in the presence of freckles, and the drug-history. Metallic deposits in facial biopsies were demonstrated by electron microscopy. On admission 15.4 microgram% and 5.0 microgram % total Hg respectively were found in the two patients (normal values up to 2.0 microgram %). Following D-penicillamine treatment the mercury excretion via the urine could be elevated up to 25 microgram %. Neither the slate-gray facial discoloration nor the neurasthenic complaints were affected by this therapeutic trial. In one patient, a maculo-papular drug-induced skin rash to D-penicillamine developed. Persistent unsolved neurological complaints and cramp-like abdominal pains should remind that percutaneous mercury intoxication through intact skin following skin bleachers is still possible today.

Adult↗
PubMed1975

[Anuria caused by mercury poisoning (apropos of 15 cases)].

15 cases of acute renal failure following ingestion of bichloride of mercury were studied at Pahlavi medical center, university of Teheran, between 1962 and 1972. All the patients admitted suicide attempts. All had oliguria and uremia except one, in whom oliguria was moderate without azotemia. There were four deaths among the 15 patients, three of them with gastrointestinal hemorrhage; secondery infection and the prolonged acute uremia probably were the cause of death in another one. Early administration of B. A. L. and early frequent hemodialysis helps to support the patient through the period of oliguria and possibly to remove the mercury B.A.L. Complex. Although the mortality of mercury intoxication has decreased, gastrointestinal hemorrhages and secondery infections make its prognosis still unfavorable.

Acute Disease↗