Plasmapheresis reverses all side-effects of a cisplatin overdose – a case report and treatment recommendation

BACKGROUND: Cisplatin is widely used as an antineoplastic agent since it is effective against a broad spectrum of different tumours. Nevertheless, it has several potential side effects affecting different organ systems and an overdose may lead to life-threatening complications and even death. CASE PRESENTATION: We report on a 46-year old woman with non-small cell lung cancer who accidentally received 225 mg/m(2 )of cisplatin, which was threefold the dose as scheduled, within a 3-day period. Two days later, the patient presented with hearing loss, severe nausea and vomiting, acute renal failure as well as elevated liver enzymes. In addition, she developed a severe myelodepression. After plasmapheresis on two consecutive days and vigorous supportive treatment, the toxicity-related symptoms improved and the patient recovered without any sequelae. CONCLUSION: To date, no general accepted guidelines for the treatment of cisplatin overdoses are available. Along with the experience from other published cases, our report shows that plasmapheresis is capable of lowering cisplatin plasma and serum levels efficiently. Therefore, plasma exchange performed as soon as possible can ameliorate all side effects of a cisplatin overdose and be a potential tool for clinicians for treatment. However, additional intensive supportive treatment-modalities are necessary to control all occurring side effects

Pyruvate: immunonutritional effects on neutrophil intracellular amino or alpha-keto acid profiles and reactive oxygen species production

For the first time the immunonutritional role of pyruvate on neutrophils (PMN), free α-keto and amino acid profiles, important reactive oxygen species (ROS) produced [superoxide anion (O2−), hydrogen peroxide (H2O2)] as well as released myeloperoxidase (MPO) acitivity has been investigated. Exogenous pyruvate significantly increased PMN pyruvate, α-ketoglutarate, asparagine, glutamine, aspartate, glutamate, arginine, citrulline, alanine, glycine and serine in a dose as well as duration of exposure dependent manner. Moreover, increases in O2− formation, H2O2-generation and MPO acitivity in parallel with intracellular pyruvate changes have also been detected. Regarding the interesting findings presented here we believe, that pyruvate fulfils considerably the criteria for a potent immunonutritional molecule in the regulation of the PMN dynamic α-keto and amino acid pools. Moreover it also plays an important role in parallel modulation of the granulocyte-dependent innate immune regulation. Although further research is necessary to clarify pyruvate’s sole therapeutical role in critically ill patients’ immunonutrition, the first scientific successes seem to be very promising

Hypothermia, a pertinent clinical prognostic factor in severe systemic inflammatory response syndrome.

peer reviewe

A patient with lethal cardiomyopathy and a carnitine-acylcarnitine translocase deficiency

In the last few years, increasing attention has been paid to the diagnosis of defects in mitochondrial fatty acid beta-oxidation in man (Stanley 1987). Clinical diagnosis of these disorders is difficult, because affected patients are often free of symptoms between metabolic crises (Hale and Bennett 1992). A total of 13 inherited beta-oxidation defects have been described (Coates and Tanaka 1992). Among those 13 disorders there are four that affect the transport into mitochondria of long-chain fatty acids that are activated to their CoA esters. Defects have been described for the plasma-membrane carnitine transporter and carnitine palmitoyltransferase types 1 and 2 (CPT I and II). Recently three patients have been described with a carnitine- acylcarnitine translocase deficiency, a defect in the transfer of fatty acylcarnitines across the inner mitochondrial membrane in exchange for free carnitine (Pande et al 1993; Stanley et al 1992; Brivet et al 1994). In this short communication we describe what is to our knowledge the fourth case of a carnitine-acylcarnitine translocase deficiency