1/12. Acute colchicine intoxication--possible role of erythromycin administration.A 29-year-old patient with familial mediterranean fever and amyloidosis involving the kidney, liver, and gastrointestinal tract received longterm colchicine, 1 mg daily. In the last year she developed diarrhea and abdominal pain, that coincided with toxic colchicine blood levels. After 2 weeks of oral erythromycin therapy she was hospitalized for acute, life threatening colchicine toxicity, with fever, diarrhea, abdominal pain, myalgia and lower extremity parasthesias and later convulsions and alopecia. pancytopenia evolved into rebound leukocytosis, disturbed liver function and hypoglycemia. After a long stormy course she improved. colchicine toxicity with combined liver and renal impairment and the role of erythromycin in her colchicine toxicity are discussed.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
2/12. Severe lithium toxicity treated by hemodialysis: a case report.A 51-year-old manic woman who developed acute severe lithium intoxication with neurotoxicity and nephrotoxicity during rapid abatement of manic episode was reported. The underlying causes of the serious toxicity were reviewed. awareness and early detection of the toxic symptoms are emphasized in order to avoid permanent toxic sequelae. It is suggested that hemodialysis is the treatment of choice and should not be delayed, especially in severe toxic states and a daily 10 hours hemodialysis is needed to prevent the rebound effect as lithium in intracellular fluid equilibrates with extracellular fluid.- - - - - - - - - - ranking = 0.25keywords = intoxication (Clic here for more details about this article) |
3/12. The pathology and pathogenesis of chronic lead nephropathy occurring in queensland.Many children who suffered acute lead poisoning in queensland eventually died with contracted kidneys. In most cases the kidneys were granular and showed microscopically fibrosis, hypertensive vascular changes and "alterative glomerulitis". Clinically in these patients, hypertension and chronic renal insufficiency had always preceded death which was usually due to uraemia. In a minority of cases the kidneys showed the changes of benign hypertension but were unusually small; fibrosis and "alterative glomerulitis" were not present. Clinically these patients had had hypertension but minimal renal insufficiency and death was usually due to cerebral haemorrhage. The evidence indicates that lead caused severe damage to the kidney at the time of the lead intoxication by some mechanism other than hypertension. The sequence of events postulated comprises severe renal damage with destruction of glomeruli during childhood lead poisoning, disappearance of the destroyed tissue during childhood and adolescence, onset of hypertension in adolescence or early adult life, gradual onset and progress of chronic uraemia during which fibrosis and granularity developed. In milder cases the sequence is not complete because renal function has remained adequate.- - - - - - - - - - ranking = 0.25keywords = intoxication (Clic here for more details about this article) |
4/12. Acute diquat intoxication. Interest of its repeated determination in urine and the evaluation of renal proximal tubule integrity.A 33-year old farmer ingested approximately 300 ml of a 20% solution of diquat along with about 80 mg flunitrazepam. The patient presented neurological (coma grade I), digestive (oro-pharyngeal erosions, ileus), hepatic (cytolysis), hematological (thrombopenia) and renal (tubular dysfunction) signs. plasma creatinine did not exceed 1.22 mg/dl (upper normal value), but retinol binding protein level in urine (a marker of renal tubular dysfunction) reached a value of 337 mg/d (normal values less than 300 micrograms/d). Its level returned to normal value 18 days after the ingestion. Four hours after the poisoning, diquat level in blood amounted to 10.4 mg/l, but its level was below the detection limit (0.2 mg/l) 6 hours later. In urine, however, diquat was detected until day 13. The following therapy was applied: ventilation (FiO2:0.21), gastro-intestinal lavage, hemoperfusion, anti-oxidants and prolonged forced diuresis. The patient made an uneventful recovery. intestinal washout must be applied with caution since an ileus is a classical complication of diquat poisoning. hemoperfusion was found to be of little value. The interest of prolonged application of forced diuresis is suggested by the detection of diquat in urine for about 2 weeks along with the presence of biological signs of renal tubular dysfunction.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
5/12. Subacute fluorosis: a consequence of abuse of an organofluoride anesthetic.A young woman presented with a novel multisystem disease: painful periostitis, osteosclerosis, hypertension, and renal dysfunction. The similarity of some of this clinical picture to fluoride intoxication led to the discovery of massively elevated fluoride levels in serum, urine, and bone. Although initially an enigma, the source of fluoride was later found to be the illicit use of an anesthetic agent, methoxyflurane. This agents is one of a class of organofluorides that, by virtue of biotransformation, is a known cause of inorganic fluoride exposure. Though the drug is potentially nephrotoxic as generally used, exposure to it is transient and has not previously led to discernible bone disease.- - - - - - - - - - ranking = 0.25keywords = intoxication (Clic here for more details about this article) |
6/12. rhabdomyolysis in paraphenylenediamine intoxication.edema of the upper airways and rhabdomyolysis developed in a young patient as a consequence of paraphenylenediamine poisoning. Treatment with adrenaline, steroids and enforced diuresis prevented tracheostomy and renal failure.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
7/12. Fatal tubular nephropathy following an overdose of theophylline in an infant.A case of fatal acute intoxication in a 4-month and 20-day-old male infant from an overdose of theophylline (Paidomal) drops retard is described. Apart from the usual symptoms caused by theophylline overdose, severe obstructive tubular nephropathy was also observed.- - - - - - - - - - ranking = 0.25keywords = intoxication (Clic here for more details about this article) |
8/12. germanium intoxication with sensory ataxia.Sensory ataxia in inorganic germanium intoxication is rare. A 63-year-old housewife had taken inorganic germanium preparations at a dosage of 36 mg a day for about 6 years (total dose about 80 g). She subsequently developed difficulty in writing and gait disturbance with peripheral neuropathy and renal involvement. germanium, which is not usually detected in the non-germanium user, was accumulated in her hair and nails, permitting a diagnosis of inorganic germanium intoxication. The peripheral neuropathy and renal injury were not reversible after discontinuing the preparation. pneumonia and sepsis then supervened and the patient died. autopsy findings showed degeneration and loss of the dorsal root ganglion cells and degeneration of the dorsal column of the spinal cord. Two previously reported cases presented with ataxia. These patients took germanium for long periods and/or large quantities like our case. It was supposed that sensory ataxia was induced by chronic and dose dependent toxicity of inorganic germanium.- - - - - - - - - - ranking = 1.5keywords = intoxication (Clic here for more details about this article) |
9/12. Acute arsine intoxication as a consequence of metal burnishing operations.The report concerns a 30-year-old factory worker, employed in a small galvanizing plant for over ten years in the burnishing, copper- and nickel-plating of small metal articles for the shoe industry. Acute arsine poisoning was attributed to the use of a dilute solution of CuSO4 (3%), HCl (32%), and As2O3 (2%) for burnishing metal (Fe-Zn) shoelace eyelet holes, in the absence of local exhaust ventilation and with no respiratory protection. Arsine caused severe intravascular hemolysis with a rapid drop in hematocrit and hemoglobin levels. Other body organs were involved as a result of the hypoxic effect of anemia and hemolysis, or as a direct toxic effect of the arsine itself. Our experience confirms that exchange transfusion is capable of rapidly arresting the adverse effects of arsine. The importance of preventive measures and worker information to avoid acute arsine poisoning is emphasized.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
10/12. Spontaneous exfoliation of teeth following severe elemental mercury poisoning: case report and histological investigation for mechanism.BACKGROUND: Although the spontaneous exfoliation of teeth and breakdown of oral tissues from severe mercury intoxication have been noted for over a century, there are no published reports investigating the mechanisms of these phenomena. Severe mercury poisoning is rare in modern times, but it does occur. We present a case report and a histopathologic investigation into the mechanism of the associated tooth loss. methods: An exfoliated tooth and periodontal and gingival tissues were obtained from a 15-month-old patient who had been severely intoxicated with elemental mercury over a period of months and hospitalized for severe neurologic and renal effects. The tissues were examined both by routine hematoxylin and eosin stain and by autometallography specific for mercury. For comparison, control tissue from an age-matched subject was examined with the autometallography technique. RESULTS: Under light microscopy, the gingival tissue showed evidence of moderate to severe acute and chronic inflammation. The tooth pulp tissue showed evidence of moderate vascular dilatation and congestion, and it was infiltrated by many neutrophils. The autometallographic sections showed intense accumulations of mercury in the soft tissues of the mercury-exposed subject, but not in the tissues of the control subject. The deposits were primarily found in fibroblasts, which are essential to maintaining the integrity of the oral tissues. CONCLUSIONS: Histopathologic and autometallographic examination of the affected tissue indicates that the primary mechanism of the spontaneous sloughing of tissue and loss of teeth may be the cytotoxic effects of the accumulation of mercury in fibroblasts. Studies of additional cases would be valuable to confirm this hypothesis.- - - - - - - - - - ranking = 0.25keywords = intoxication (Clic here for more details about this article) |
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