1/7. Intoxication by star fruit (Averrhoa carambola) in 32 uraemic patients: treatment and outcome.BACKGROUND: Clinical symptoms and outcomes of uraemic patients ingesting star fruit are quite variable and may progress to death. The purpose of the present report was to discuss the neurotoxic effects of star fruit intoxication in uraemic patients and to present the efficacy of different therapeutic approaches. methods: We studied a total of 32 uraemic patients who had ingested star fruit. Before the intoxication episodes, 20 patients were on regular haemodialysis, eight were on peritoneal dialysis and four were not yet undergoing dialysis. Two patients were analysed retrospectively from their charts, 17 were directly monitored by our clinic and 13 were referred by physicians from many areas throughout the country, allowing us to follow their outcome from a distance. Intoxicated patients were given different therapeutic approaches (haemodialysis, peritoneal dialysis and supportive treatment), and their outcomes were analysed. RESULTS: The most common symptoms were persistent and intractable hiccups in 30 patients (93.75%), vomiting in 22 (68.7%), variable degrees of disturbed consciousness (mental confusion, psychomotor agitation) in 21 (65.6%), decreased muscle power, limb numbness, paresis, insomnia and paresthesias in 13 (40.6%) and seizures in seven (21.8%). patients who were promptly treated with haemodialysis, including those with severe intoxication, recovered without sequelae. patients with severe intoxication who were not treated or treated with peritoneal dialysis did not survive. CONCLUSIONS: Haemodialysis, especially on a daily basis, is the ideal treatment for star fruit intoxication. In severe cases, continuous methods of replacement therapy may provide a superior initial procedure, since rebound effects are a common event. peritoneal dialysis is of no use as a treatment, especially when consciousness disorders ensue.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
2/7. Star fruit intoxication in uraemic patients: case series and review of the literature.Star fruit, belonging to the Oxalidaceae family, species Averrhoa carambola, is a popular fruit among Orientals. There have been reports of hiccup, confusion, and occasional fatal outcomes in uraemic patients after ingestion of star fruit. An excitatory neurotoxin from star fruit has been implicated although the exact nature of this toxic substance has not been identified. A group of seven patients is described from the dialysis centres at Queen Mary and Tung Wah hospitals who developed symptoms including hiccup, confusion, vomiting, impaired consciousness, muscle twitching and hyperkalaemia shortly after ingestion of star fruit. Symptoms of most patients resolved after intensified dialysis or spontaneously, and no mortality was observed. The close temporal relationship of ingestion of star fruit and onset of symptoms strongly suggests the existence of a causal relationship between the two. It is recommended that uraemic patients should totally abstain from star fruit due to these rare but potentially fatal complications. The clinical manifestations of other reported series and current evidence for the possible candidate(s) of the neurotoxin are discussed.- - - - - - - - - - ranking = 0.8keywords = intoxication (Clic here for more details about this article) |
3/7. Decrease of tumor-like calcification in uremia despite aggravation of secondary hyperparathyroidism: a case report.Extraskeletal pseudotumoral calcifications generally develop in uremic patients with a high calcium x phosphorus (Ca x P) product and severe secondary hyperparathyroidism. In the present case report we describe a chronic hemodialysis patient presenting with a massive calcification of the left shoulder region, severe aluminum (Al) intoxication and moderate hyperparathyroidism. Her initial serum Ca x P product was only slightly elevated: 5.01 mmol2/l2. Under deferoxamine treatment during the subsequent 4 months, Al overload decreased. On the other hand, parathyroid overfunction worsened, as reflected by an increase of the serum immunoreactive parathyroid hormone [1-84] level from initially 690 to 1052 pg/ml (normal, 15-60 pg/ml) and an increase of alkaline phosphatase activity, and plasma calcitriol increased from undetectable to a low-normal value. Predialysis serum total Ca levels decreased rapidly from 2.9 to 2.5 mM but serum P concentrations remained elevated: 1.6-2.5 mM. Unexpectedly, the extent of the periarticular calcification diminished considerably during the same time period. The present observation shows that in a subset of uremic patients with Al overload, pseudotumoral calcifications may regress during Al chelation therapy despite progression of hyperparathyroidism. Since Al may predispose collagen to develop dystrophic or metastatic calcification, it is suggested that this process is reversible by correcting Al intoxication.- - - - - - - - - - ranking = 0.4keywords = intoxication (Clic here for more details about this article) |
4/7. sarcoidosis-related hypercalcemia in 3 chronic hemodialysis patients.hypercalcemia is a frequent complication in chronic hemodialysis (CHD) patients. A rare cause of this condition is sarcoidosis, and has only been reported 6 times in CHD. Herein, we report on 3 cases of sarcoidosis-related hypercalcemia in CHD patients: an overt case, a probable case, and a recurrence of pre-dialysis sarcoidosis. hypercalcemia is a frequent complication in chronic hemodialysis patients: it is often related to uncontrollable secondary hyperparathyroidism or to the inappropriate use of calcium phosphate binders, 1alpha-hydroxylated vitamin d metabolites, high dialysate calcium concentrations, or to aluminium-related bone disease [Uach and Bover 1996]. However, other rare causes should also be considered, such as multiple myeloma, non-Hodgkin lymphoma [Uach and Bover 1996], vitamin a intoxication [Fishbane et al. 1995], or granulomatous diseases such as sarcoidosis. The latter has only been described in a total of 6 hemodialysis patient reports [Barbour et al. 1981, Barnard et al. 2002, Herrero et al. 1998, Kalantar-Zadeh et al. 1994, Kuwae et al. 2003, Naito et al. 1999]. In the present paper, we report on 3 cases of sarcoidosis-related hypercalcemia in chronic hemodialysis patients with 3 different patterns, i.e. overt sarcoidosis, probable sarcoidosis, and recurrence of pre-dialysis sarcoidosis.- - - - - - - - - - ranking = 0.2keywords = intoxication (Clic here for more details about this article) |
5/7. Acute pancreatitis in six non-transplanted uraemic children. A co-operative study from the French Society of Paediatric nephrology.Ten clinical episodes of acute pancreatitis (AP) occurred in six patients (mean age 10 years, range 3-15 years) with chronic renal failure (CRF) during a 9-year period (1977-1986). The underlying cause of CRF was vesicoureteral reflux (2); urethral valves (1); ureterohydronephrosis (1); nephronopthisis (1) and a haemolytic uraemic syndrome which occurred 12 years before (1). In all patients a diagnosis of AP was established both on clinical grounds and with a serum amylase level of greater than 600 IU/l. In 3 patients laparotomy was performed because of suspected appendicitis. All patients required exclusive parenteral feeding (mean duration 25 days) and 2 patients had a partial pancreatectomy. No patient developed pancreatic pseudocysts, 2 patients experienced one relapse (3 and 21 months later) and 1 patient had two relapses and died. Mean duration of follow up was 3 years (range 1-10 years). Possible aetiological factors were: choledochal cyst (1); parotitis without a rise in mumps antibodies (1); familial dyslipidaemia but without AP in other family members (1), and aluminium intoxication with hypercalcaemia and convulsive encephalopathy treated with valproic acid in 1 patient. Severe hyperparathyroidism with radiological signs was absent in all patients. transplantation had been performed either before AP in 2 patients (1 and 3 years before AP) or had followed AP in 1 patient (7 years after) without occurrence or relapse of AP.- - - - - - - - - - ranking = 0.2keywords = intoxication (Clic here for more details about this article) |
6/7. Aluminum intoxication from aluminum-containing phosphate binders in children with azotemia not undergoing dialysis.Aluminum intoxication developed in three infants with azotemia who were not undergoing dialysis and who had been treated with aluminum hydroxide from the first month of life. Biopsies of the iliac crest demonstrated the presence of severe osteomalacia and massive deposition of aluminum in the bone. serum aluminum levels were significantly (P less than 0.001) higher in these 3 infants and in 1 other, all of whom received more than 100 mg of elemental aluminum per kilogram of body weight per day (mean /- S.D., 371.0 /- 178.9 ng per milliliter [13.75 /- 6.6 mumol per liter] ) than they were in 8 older children with azotemia who were not undergoing dialysis and who received less than 100 mg of elemental aluminum per kilogram per day (27.0 /- 18.6 ng per milliliter [1.0 /- 0.68 mumol per liter] ), 7 such children who did not receive aluminum hydroxide (20.28 /- 9.2 ng per milliliter [0.75 /- 0.34 mumol per liter] ), and 16 children with normal renal function (21.04 /- 4.9 ng per milliliter [0.78 /- 0.18 mumol per liter] ). In all the children with azotemia who were treated with aluminum hydroxide, there was a positive correlation (r = 0.90; P less than 0.01) between the serum aluminum level and the daily dose of elemental aluminum. These studies indicate that gastrointestinal absorption of aluminum can lead to aluminum intoxication in children with azotemia, and that infants may be particularly susceptible to this complication of therapy.- - - - - - - - - - ranking = 1.2keywords = intoxication (Clic here for more details about this article) |
7/7. Accumulation of aluminum in a nondialyzed uremic child receiving aluminum hydroxide.A child with renal insufficiency was treated with the oral phosphate binder aluminum hydroxide from age 6 to 31 months. The prescribed dose of elemental aluminum varied from 31 to 108 mg/kg/d. Concurrently the patient developed vitamin d-resistant osteomalacia which failed to improve with parathyroidectomy. Encephalopathy with myoclonic seizures, loss of speech, and motor impairment also occurred. serum and bone aluminum levels were elevated at 334 micrograms/L (normal 7 /- 3 micrograms/L) and 156 mg/kg (normal 3.3 /- 2.9 mg/kg), respectively. This case demonstrates that aluminum may accumulate in tissue of children receiving oral aluminum hydroxide. The accumulation of aluminum may have contributed to the vitamin d-resistant osteomalacia and the encephalopathy in this patient. Children receiving aluminum-containing antacids as phosphate binders should be monitored for aluminum accumulation and signs of aluminum intoxication.- - - - - - - - - - ranking = 0.2keywords = intoxication (Clic here for more details about this article) |