Reaction to iron sorbitol injection in three cases of malabsorption.

Karhunen, Pekka J.; Härtel, Günter; Kivikangas, V.; Reinikainen, M

doi:10.1136/bmj.2.5708.521

Cited by 6 publications

(2 citation statements)

References 2 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is noteworthy, in this respect, that iron toxicity, hyperkalaemia and ECG alterations were also associated in vitamin E-deficient piglets with ironinduced myopathy [3 I], whereas cardiac conduction defects without documentation of the serum potassium and lactate concentration were observed in vitamin E-deficient patients receiving iron-sorbitol therapy [32,331. It is noteworthy, in this respect, that iron toxicity, hyperkalaemia and ECG alterations were also associated in vitamin E-deficient piglets with ironinduced myopathy [3 I], whereas cardiac conduction defects without documentation of the serum potassium and lactate concentration were observed in vitamin E-deficient patients receiving iron-sorbitol therapy [32,331.…”

Section: Discussionmentioning

confidence: 99%

“…In our animals, progressive hyperlactataemia was accompanied by hyperkalaemia and by ECG alterations, suggesting a potassium-related conduction defect. It is noteworthy, in this respect, that iron toxicity, hyperkalaemia and ECG alterations were also associated in vitamin E-deficient piglets with ironinduced myopathy [3 I], whereas cardiac conduction defects without documentation of the serum potassium and lactate concentration were observed in vitamin E-deficient patients receiving iron-sorbitol therapy [32,331. Both observations underscore the oxidative character of iron toxicity in the heart.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Hyperlactataemia, hyperkalaemia and heart block in acute iron overload: the fatal role of the hepatic iron‐incorporation rate in rats on ferric citrate infusions

Rosenmund

Brand

Straub

1988

Eur J Clin Investigation

View full text Add to dashboard Cite

An animal model is presented that provides constant and controllable conditions for approaching gradually, and within reasonable time, different stages of iron overload and, probably, an iron-induced mitochondrial disorder. Thirty-five rats were infused with ferric citrate, sodium citrate and saline at constant rates for 6-24 h. In the 200-3200 micrograms Fe h-1 loading range, the iron-incorporation capacity of the liver was not saturable and the fractional iron uptake by the liver remained at approximately 30% even at a loading rate of 3200 micrograms Fe h-1. Up to a loading rate of 200 micrograms Fe h-1, iron storage was not associated with toxic effects. Beyond this loading rate, however, the liver was no longer able to prevent a massive plasma iron increase on one side and hyperlactataemia on the other. These signs most probably represent hepatocellular decompensation with respect to a critical iron-storage rate. The product of plasma iron x exposition time was significantly correlated with increased plasma lactate levels (r = 0.89, P less than 0.005), whereas increased plasma iron levels per se were not. Hyperlactataemia was associated with hyperkalaemia and progressive cardiac conduction defects leading to cardiac arrest at lactate concentration of 9.1 +/- 4.3 mmol l-1. The hypothesis is discussed that toxicity in acute iron overload may entirely be due to hepatocellular (mitochondrial) damage, and not to multiple organ iron overload.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%