Calcinosis at the site of leakage from extravasation of calcium disodium edetate intravenous chelator therapy in a child with lead poisoning

Painful calcinosis appeared at the wrist of an eight-year-old girl with lead poisoning. Careful history revealed that calcification occurred at the site of previous extravasation of calcium disodium edetate (EDTA) used in chelation therapy. Light microscopic, ultrastructural, electron activation, and X-ray diffraction studies demonstrated apatites with some suggestion of an admixture of octacalcium phosphate.     

Effects of tolazamide and exogenous insulin on pattern of postprandial carbohydrate metabolism in patients with non-insulin-dependent diabetes mellitus. Results of randomized crossover trial

To determine whether therapy with exogenous insulin or sulfonylureas results in a postprandial pattern of carbohydrate metabolism in patients with non-insulin-dependent diabetes mellitus (NIDDM) that resembles that in nondiabetic individuals, we employed a dual-isotope technique combined with forearm catheterization to examine meal disposition in NIDDM patients, before and after 3 mo of therapy with tolazamide and after 3 mo of therapy with exogenous insulin, with a randomized crossover design. Results were compared with those observed in nondiabetic subjects. Although both forms of therapy improved chronic glycemic control (glycosylated hemoglobin concentration went from 9.6 +/- 0.7 to 7.6 +/- 0.5 and 7.1 +/- 0.2%, respectively, P less than .01), exogenous insulin resulted in a lower postprandial glycemic response than tolazamide (P less than .001). Both agents comparably increased (P less than .01) fasting and integrated postprandial insulin concentrations. However, the initial rate of postprandial increase was greater with exogenous insulin (P less than .05). Tolazamide (P less than .05) but not exogenous insulin increased postprandial C-peptide concentrations. However, tolazamide did not improve the deficient early insulin release. Both agents (P less than .05) lowered postabsorptive hepatic glucose release (from 2.8 +/- 0.3 to 2.3 +/- 0.2 mg . kg-1 . min-1), but not to normal rates (1.8 +/- 0.1 mg . kg-1 . min-1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Greater efficacy of pulsatile insulin in type I diabetics critically depends on plasma glucagon levels

The aim of this study was to investigate the role of plasma glucagon levels on the blood glucose response to intravenous insulin administered continuously or in a pulsatile manner. Six type I diabetic patients proven to have no residual insulin secretion were investigated. Endogenous glucagon secretion was inhibited by a continuous intravenous infusion of somatostatin (100 micrograms/h) and replaced by exogenous infusions of the hormone at three different rates (7.5, 4.5, and 2.5 micrograms/h), resulting in three different plasma glucagon steady-state levels (i.e., approximately equal to 200, approximately equal to 130, and approximately equal to 75 pg/ml, respectively). Each subject, in random order and on different days, was infused intravenously with regular human insulin either continuously (0.17 mU X kg-1 X min-1) or with the same amount of insulin infused in a pulsatile manner (0.85 mU X kg-1 X min-1 during 2 min followed by 8 min during which no insulin was infused). At plasma glucagon levels approximately equal to 200 pg/ml, blood glucose rose from approximately 10 to approximately 13 mM without any difference between the two modalities of insulin infusion. For plasma glucagon levels approximately equal to 130 pg/ml, plasma glucose remained steady throughout the experiments, but during the last 40 min, plasma glucose levels were significantly lower when insulin was administered intermittently. This greater blood glucose-lowering effect of pulsatile insulin occurred earlier and was more pronounced for plasma glucagon levels averaging 75 pg/ml. We conclude that the greater hypoglycemic effect of insulin administered intravenously in a pulsatile manner in type I diabetics critically depends on plasma glucagon circulating levels.     

Full-length ureteric splintage in the management of bilharzial ureteric strictures

Our experience with full-length ureteric splintage is reviewed with a note on the technique and its outcome. It is safe, effective and simple, easy to teach and easy to learn. It is recommended as the operation of choice in bilharzial ureteropathy.     

Management of iron overload in the pediatric patient

Iron overload is a major complication of long-term transfusion therapy. In the absence of treatment, the excessive iron causes diffuse organ damage, usually culminating in death from heart disease. Deferoxamine, an iron-chelating drug, removes tissue iron, prevents iron-induced organ dysfunction, and prolongs life. Proper administration of deferoxamine requires careful attention to dose, route and duration of administration, and compliance. Better chelators are needed but are unlikely to be available soon. Other methods for preventing or reducing iron accumulation involve alterations in the transfusion program or the blood product. Prevention of iron overload should improve the lives of patients with transfusion-dependent anemias and extend the usefulness of transfusion in chronic hematologic disorders.     

Caffeine and the benign encephalopathy of pregnancy

D. W. Barnes, D. A. Sirbasku & G. H. Sato, (eds.): Cell culture methods for molecular and cell biology. P. M. Gootman (ed.): Developmental neurobiology of the autonomic nervous system. M. Sandler, C. Feuerstein, B. Scatton (eds.): Neurotransmitter interactions in the basal ganglia. Harry M. Zimmerman (ed). Progress in neuropathology. M. Yahr & K. J. Bergmann (eds.): Parkinson's disease. G. Bock & M. O'Connor (eds.): Selective neuronal death. H. Julia Hannay (ed.): Experimental techniques in human neuropsychology. D. Papakostopoulos, S. Butler, I. Martin (eds.): Clinical and experimental neuropsychophysiology J. C. Rothwell: Control of human voluntary movement.     

Necrotizing myopathy with paracrystalline inclusion bodies in hypervitaminosis E

Summary A necrotizing, nonprogressive myopathy with unusual paracrystalline inclusion bodies is described in a patient who underwent long-term treatment with megadoses of vitamin E. The clinical course and morphological findings suggest a close relationship to the administration of the vitamin. The theoretical pathogenesis of muscle damage and the possible origin of paracrystalline inclusion bodies are discussed.Presented at the Jahrestagung der österreichischen Gesellschaft für Neuropathologie in Bad Ischl, on April 17, 1986This study was supported by a grant from the Deutsche Forschungsgemeinschaft (Ba 916)     

Golgi study on brain of macular mutant mouse as a model of Menkes kinky hair disease

Summary This study was undertaken to elucidate, using the Golgi method, the neuropathological change in the brain of the macular mutant mouse, whose hemizygote (Ml/y) is considered to be a model of Menkes kinky hair disease (MKHD). The hemizygote mice gradually lost weight after 10 days of age and died with emaciation and seizure around day 15. The normal littermate (+/y) was well developed. In the cerebrum, the arborization of pyramidal neurons in the layer V of the Ml/y was the same as that in the +/y on day 10. However, development of arborization in the Ml/y was delayed in comparison with that in the +/y on days 12 and 14. Purkinje cells with several somal sprouts were observed in the cerebellum in both the Ml/y and +/y on day 7. The somal sprouts in the +/y had regressed gradually by day 12, while they were still in the anterior and middle lobes of the Ml/y on day 14. Additionally, the trunks of Ml/y stem dendrites became thicker and a cactus formation was recognized on the branching portion of the dendrites on day 14. Arborization of these abnormal Purkinje cells was distinctly poor compared with that in the +/y. These results suggest that the growth of the neurons is delayed in the Ml/y and simultaneously their cytoskeletal developments are disturbed, especially in the Purkinje cells. There is a close similarity in many respects to the neuropathological change in MKHD.