Clinical features of hematological disorders caused by copper deficiency during long-term enteral nutrition.

OBJECTIVE: Copper deficiency has been reported to cause hematological disorders. However, its clinical and hematological characteristics are not fully understood. Therefore, we investigated bedridden patients suffering from copper deficiency and tried to clarify the clinical features of hematological disorders caused by this condition. PATIENTS AND METHODS: Five patients with typical copper deficiency who had been dependent upon enteral nutrition for a long period of time due to various diseases were investigated. We measured hematological parameters and observed the response to copper supplementation therapy and the recovery process of hematological disorders. RESULTS: Their mean age was 82.6+/-10.4 years and the mean duration of enteral nutrition was 16.4+/-5.2 months. Their serum copper concentration was extremely decreased (range, 3 to 8 microg/dl). All five patients had anemia and neutropenia. On the other hand, platelet count remained within the normal range. After copper supplementation therapy, hemoglobin concentration increased from 6.8+/-0.7 g/dl to 9.9+/-0.7 g/dl within a few months (p<0.01). Neutrophil count also increased from 750+/-370/microl to 3,690+/-1,210/microl in a few weeks (p<0.01). Mean corpuscular volume (MCV) decreased from 94.3+/-7.3 fl to 86.0+/-4.8 fl (p<0.05). Elevated serum ferritin and erythropoietin (EPO) levels were normalized after the improvement of anemia. CONCLUSION: Bicytopenia (anemia and neutropenia) with normal platelet count is a feature of hematological disorders caused by copper deficiency. MCV tends to indicate macrocytic anemia. Serum ferritin and EPO levels are elevated. These hematological abnormalities are improved within a few months after copper supplementation therapy.

Halothane modulates NMDA and non-NMDA excitatory synaptic transmission in rat cortical neurons.

PURPOSE: Although general anesthetics may decrease neuronal excitation, their detailed effects on spontaneous excitatory postsynaptic currents (EPSCs) remain controversial. We investigated and compared the effects of halothane on N-methyl-D-asparate (NMDA) and non-NMDA receptor-mediated postsynaptic currents. METHODS: Spontaneous synaptic currents were recorded by the patch clamp technique in cultured rat cortical neurons. They were isolated by specific pharmacological blocking agents and their electrophysiologic properties were examined. RESULTS: The frequency of NMDA EPSCs was preferentially decreased as compared with that of non-NMDA EPSCs at halothane 1.2 mM. The total net charge of EPSCs mediated by NMDA and non-NMDA receptors was depressed to 56% +/- 6% (mean +/- SD) and 71% +/- 7% of control by halothane 0.6 mM, and to 11% +/- 9% and 59% +/- 11% of control by halothane 1.2 mM, respectively. CONCLUSION: These results show that halothane causes decrease of excitatory synaptic activity, with NMDA EPSCs being more sensitive than non-NMDA EPSCs.