1/18. Chronic intoxication by doxycycline use for more than 12 years.We report the clinical case of a 12-years' intoxication by doxycycline. A patient with a depersonalization and derealization syndrome took 1 g doxycycline per day. In addition to hepatocellular necrosis with cholestasis, nephrotoxicity, leukopenia, anaemia and skin hyperpigmentation he suffered from hitherto unreported adverse cardiac events as intermittent supraventricular tachycardia and sporadic Wenckebach heart block. Despite a long period of self-medication these side-effects were reversible.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
2/18. Liver granulomatosis is not an exceptional cause of hypercalcemia with hypoparathyroidism in dialysis patients.In 4 of our patients on chronic dialysis, we were intrigued by the association of hypercalcemia /- hyperphosphatemia and normal intact PTH, with anicteric cholestasis without cytolysis. This picture occurred in 2 patients after they resumed dialysis because of a transplant rejection and in a third one after discontinuation of corticosteroids, prescribed for an idiopathic thrombocytopenia. No patient was under calcitriol, CaCO3 therapy, and their hypercalcemia persisted on a low calcium dialyzate (1.25 mmol/l). Obvious etiologies of hypercalcemia were not found: vitamin d or A intoxication, hyperparathyroidism, aluminum intoxication, hemopathy, hiv infection. The hypothesis of a granulomatous disease was made and a liver biopsy was performed showing granulomas with giant epitheloid cells. In one case foreign material (silicon ?) was present in the macrophages. Extensive investigations for sarcoidosis, tuberculosis and mycosis were negative. In 2 cases the so-called "dialysis" granulomatosis actually occurred in transplanted patients, suggesting the role of a transplantation related factor (toxic or virus). In the last case HCV seroconversion was present. In the 4 cases, corticotherapy led to the disappearance of hypercalcemia and to an increase of PTH. Our patients had the biological pattern of low bone turnover disease (hypercalcemia and normal intact PTH) and bone biopsy performed in 2 showed osteomalacia or ABD without aluminum. The association of this pattern with cholestasis should evoke liver granulomatosis, which should be confirmed by a liver biopsy and lead to a treatment by corticosteroids. The masking effect of previous corticoid therapy for transplantation should be pointed out. In 2 cases serial monitoring of plasma calcitriol showed a relation between decreasing high normal calcitriol with prednisone and normalization of calcemia, suggesting the role of inappropriate synthesis of calcitriol by the granuloma. In conclusion, liver granulomatosis should be looked for in dialysis patients on the association of unexplained hypercalcemia and normal PTH with anicteric cholestasis, and confirmed by a liver biopsy. Although still of unknown etiology, its evolution is favourable under corticotherapy.- - - - - - - - - - ranking = 0.4keywords = intoxication (Clic here for more details about this article) |
3/18. Hepatic hydrothorax associated with vitamin a toxicity.We report the first case of an adult presenting with respiratory symptoms caused by hepatic hydrothorax secondary to vitamin a intoxication. The patient was a 52-year-old woman who presented to the hospital with progressive dyspnea. Evaluation demonstrated mild elevation of her liver function tests, ascites, and a right pleural effusion. The patient consumed a variety of vitamins, including vitamin a. Her estimated vitamin a intake was at least 162,300,000 international units (IU) during 18 years. She dramatically escalated her dose the year before admission for a total acute dose of 98,550,000 IU, with a daily intake of 270,000 IU. The recommended daily allowance is 4,000 IU. A transjugular liver biopsy revealed histopathologic changes consistent with vitamin a toxicity: hypertrophy and hyperplasia of hepatic stellate cells, focal pericellular fibrosis, mild perivenular fibrosis, and minimal, predominantly microvesicular steatosis. Despite the absence of cirrhosis, pressure readings demonstrated portal hypertension. During her hospitalization, the patient's symptoms and biochemical profile improved. As the large and generally unregulated united states dietary supplement industry continues to grow, it is increasingly likely that individuals will present with the signs and symptoms of vitamin excess rather than vitamin deficiency. physicians need to remain alert to the varied presentations and toxic manifestations of excessive vitamin use.- - - - - - - - - - ranking = 0.2keywords = intoxication (Clic here for more details about this article) |
4/18. Acute encephalopathy in siblings. reye syndrome vs salicylate intoxication.siblings, aged 9 and 7 years, had simultaneous onset of vomiting, disorientation, ataxia, and coma. Both children had prodromal symptoms of upper respiratory tract infections, and had been treated with large doses of aspirin. Laboratory data showed evidence of hepatocellular dysfunction, with an elevated serum ammonia level in one patient; salicylate levels were 50 and 44 mg/100 ml. The child who died had autopsy evidence of cerebral edema and fatty liver. The difficulty in clinically differentiating reye syndrome from salicylate intoxication is discussed.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
5/18. Severe manifestations of coricidin intoxication.CoricidinHBP (Schering-Plough health Care Products, Inc, Memphis, TN) is a popular over-the-counter product abused by teenagers for its potent euphoric properties. Clinically significant signs and symptoms after ingestion are usually short-lived and commonly include tachycardia, hypertension, somnolence, and agitation. We report 2 cases of severe toxicity from CoricidinHBP in adolescents that required prolonged hospitalization. The first case demonstrates prolonged anticholinergic complications from a suicidal attempt with CoricidinHBP. The second case demonstrates significant acetaminophen-induced hepatotoxicty from recreational use of CoricidinHBP Maximum Strength Flu. adolescent abuse of these products is encouraged because of the easily accessible medium of the internet. The significant morbidity seen in our cases clearly demonstrates the need for vigilance by health care professionals regarding the abuse of over-the-counter products.- - - - - - - - - - ranking = 0.8keywords = intoxication (Clic here for more details about this article) |
6/18. 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 = 0.8keywords = intoxication (Clic here for more details about this article) |
7/18. Poisoning due to amatoxin-containing Lepiota species.Twenty-seven consecutive mushroom poisoning cases were followed up over a period of 14 days. Fourteen out of 27 died of liver failure. There were no deaths from renal failure. The mushrooms were identified as the amatoxin-containing Lepiota species. Therapeutic measures included nasogastric lavage, charcoal, vitamin C, vitamin B, penicillin g, corticosteroids, oral streptomycin and, in the case of a few patients, limited amounts of thioctic acid. Of the ten haemodialysed, nine died. Unfortunately charcoal haemoperfusion was not available. It appeared that therapeutic measures were ineffective and it also seemed that the amount of mushroom ingested was the determining factor for the prognosis. An important point to make is that renal failure does not occur and liver failure is always delayed (group II). For this reason all suspected cases of mushroom poisoning, regardless of absence of clinical signs and symptoms, must be hospitalised for a period of at least one week. The poisonous properties of wild mushrooms have been recognized since ancient times. However, despite awareness of their inherent dangers, serious poisoning continues to occur. Fatal intoxications can be attributed almost entirely to the amtoxin-containing species. amanita phalloides have been blamed for over 90% of poisoning deaths in north america. There are reports of intoxications of other amatoxin-containing species in europe, but fatalities due to Lepiota species are reported only rarely. It was previously acknowledged that the interval between ingestion of mushrooms and the onset of symptoms is longer than expected in serious poisonings.(ABSTRACT TRUNCATED AT 250 WORDS)- - - - - - - - - - ranking = 0.4keywords = intoxication (Clic here for more details about this article) |
8/18. The occurrence of intramitochondrial Ca2 granules in valproate-induced liver injury.Two epileptic patients treated with anticonvulsants of valproic acid, phenobarbital, nitrazepam, and diphenylhydantoin developed anorexia, convulsions, and unconsciousness. The liver biopsy samples showed degenerated hepatocytes containing enlarged mitochondria with a distorted matrix. The matrix granules in the mitochondria were enlarged in size as compared with those of chronic hepatitis (Po = 0.0009). X-ray microanalysis has revealed the presence of calcium in large mitochondrial matrix granules. Both patients were thought to have valproic acid intoxication because they recovered quickly after the withdrawal of valproic acid.- - - - - - - - - - ranking = 0.2keywords = intoxication (Clic here for more details about this article) |
9/18. iron poisoning.iron poisoning continues to be a major toxicologic problem, with major impact on the gastrointestinal and circulatory systems. Failure to recognize the severity of iron intoxication may result in an inappropriate level of intervention. By using estimates of the total body burden of iron, clinical symptoms, and the serum iron concentration, an appropriate decision can be made to initiate aggressive chelation therapy with deferoxamine. In severe intoxication, the use of intravenous deferoxamine is indicated, along with supportive care, with particular attention to maintaining the intravascular volume. Other important measures include correction of acidosis and disorders of coagulation and replacement of blood components when there is evidence of gastrointestinal hemorrhage. Under rare circumstances in which large numbers of iron tablets are present in the gastrointestinal tract, surgical removal may be indicated. In addition, measures such as hemodialysis and exchange transfusion should be reserved for those unusual poisonings in which more conservative therapy is unsuccessful. In rare cases of iron intoxication, late sequelae such as hepatic necrosis and gastrointestinal scarring with obstruction may occur. The prompt recognition and initiation of management of children with acute iron poisoning is the single most critical element in decreasing the morbidity and mortality associated with these products.- - - - - - - - - - ranking = 0.6keywords = intoxication (Clic here for more details about this article) |
10/18. copper storage disease of the liver and chronic dietary copper intoxication in two further German infants mimicking Indian childhood cirrhosis.A severe copper storage disease of the liver with micronodular cirrhosis resembling Indian childhood cirrhosis (ICC) was found in two siblings of a German family leading to death in one infant at the age of 13 months. The fatal outcome correlated with severe ballooning of hepatocytes and excessive formation of mallory bodies. The copper content of the liver was 698 micrograms per gramme wet weight (control 5 micrograms) in the living patient and 2154 micrograms per gramme dry weight (controls 39, 54 micrograms) in the dead infant. In both cases copper was stored not only in hepatocytes but also to a high degree in mesenchymal cells. Chronic contamination of drinking water supplied from a well via copper pipes could be verified as the cause of copper intoxication, lending further support to ICC as an environmental, acquired disorder. Accumulation of exogenic copper already very early in infancy appears most important for the development of the disease, as both the parents and one child not exposed to copper intoxication during the first 9 months of its life are clinically healthy.- - - - - - - - - - ranking = 1.2keywords = intoxication (Clic here for more details about this article) |
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