Ekkehard W. Reimold

Erythrocyte enzymes in experimental lead poisoning

Intravenous administration of 6 mg per kg lead acetate to rabbits resulted in plumbism with elevated erythrocyte lead levels and marked depression of activity of erythrocyte δ-aminolevulmic acid dehydratase. By comparison other erythrocyte enzymes were insensitive to the effects of lead. Activities of anaerobic glycolysis and of the hexose monophosphate shunt were unaffected by lead administration as were erythrocyte methemoglobin reductase, acid phosphatase, glucose-6-phosphate dehydrogenase, malic dehydrogenase and acetylcholinesterase. The insensitivity of these erythrocyte enzymes to inhibition by lead excludes their usefulness for detection or diagnosis of plumbism.ZusammenfassungKaninchen erhielten eine einmalige intravenöse Injektion von Bleiacetat (6 mg/kg KG) und entwickelten eine typische Bleivergiftung mit erhöhtem Erythrocyten-Bleigehalt und starker Erniedrigung der Erythrocyten δ-Aminolävulmsäure-Dehydratase-Aktivität. Weitere Erythrocyten-Enzyme wurden untersucht und durch Blei nicht beeinträchtigt gefunden. Insbesondere bleiben die anaerobe Glykolyse und der Hexosemonophosphat-Shunt ungestört ebenso wie die Aktivität der Erythrocyten-Methämoglobin-Reduktase, der sauren Phosphatase, der Glucose-6-phosphat-Dehydrogenase, der Maleinsäure-Dehydrogenase und der Acetylcholin-Esterase. Die Erwartung, daß diese Erythrocyten-Enzyme von Nutzen sein können bei der Feststellung oder Diagnose der Bleivergiftung, hat sich nicht erfüllt.

Trisomy 18 with biliary atresia

El-trisomy (group 16-18) syndrome, Pediatrics 33: 258, 1964. 3. Oikawa, K., Kochen, J. A., Schoor, J. B., and Hirschhorn, K.: Trisomy-17 syndrome with phocomelia due to complete and partial chromosomal trisomy. Abstract Thirty-third Meeting Society for Pediatric Research, J. PEDIAT. 63: 715, 1963. 4. Voorhess, M. L., Aspillaga, M. J., and Gardner, L. I.: Trisomy 18 syndrome with absent radius, varus deformity of hand, and rudimentary thumb, J. PEDIAT. 65: 130, 1964. 5. Moorhead, P. S., Nowell, P. C., Mellman, W. J., Battips, D. M., and Hungerford, I. A.: Chromosome preparations of leukocytes cultured from human peripheral blood, Exper. Cell Res. 20: 613, 1960. 6. Edwards, J. H., Harnden, D. G., Cameron, A. H., Crosse, V. M., and Wolff, O. H.: A new trisomy syndrome, Lancet 1: 787, 1960. 7. Kohler, H. G.: Congenital transverse defects of limbs and digits, Arch. Dis. Childhood 37: 263, 1962.

Hypovolemic shock complicating the nephrotic syndrome in children

Summary Two patients with apparent hypovolemic shock and the nephrotic syndrome are reported. Both had severe abdominal pain and vomiting, lowered serum albumin concentrations, and an elevated hematocrit during the acute episode. One patient had hyponatremia. Both had remarkable symptomatic improvement following the intravenous administration of albumin.

The Effect of Furosemide on Hypercalcemia Due to Dihydrotachysterol

Abstract In an attempt to study the effect of saluretic agents on hypercalcemia, rats were given dihydrotachysterol and treated at the same time with furosemide. The elevated serum calcium level of dihydrotachysterol was lowered by simultaneous furosemide administration. A normocalcemic blood level was temporarily depressed by furosemide administered alone. The reduction of hypercalcemic blood levels by furosemide is best explained by an increase in calcium excretion. A uniform drop in serum sodium was observed. Sodium and fluid losses were continuously replaced to prevent contraction of the extracellular volume and to sustain increased calcium excretion. The phosphorus blood level was temporarily increased; the level of magnesium and potassium remained unchanged. Clinical reports are confirmed in which hypercalcemia was effectively treated with furosemide.

ACUTE SUDDEN HYPERTENSION IN THE NEWBORN PERIOD

After an initial normotensive period the blood pressure rose in 3 infants at the age of 6 days, 8 days and 4 weeks to 180-230 mmHg. In each case an umbilical artery catheter had been inserted because of respiratory distress on the first day of life to the level of T-10, L-3 and L-6 and remained in place for 3, 4½ and 11 days. Cardiac, intestinal, hematologic and metabolic complications were observed in addition to congestive heart failure, abdominal mass, hepatomegaly, vomiting, irritability, weight loss. The IVP was unremarkable in 1 case but visualized poorly one or both kidneys in the other 2 cases. Abdominal angiography showed thrombosis of the renal artery with partial occlusion of the lumen and extensive irregularities and narrowing of the abdominal aorta. Peripheral or renal vein renin were 11.8, 9.4 and 13 ng/ml/hr.In all 3 infants the hypertension was controlled by medical antihypertensive treatment. They are now normotensive at the age of 12-18 months and only 1 infant still requires antihypertensive treatment. A reevaluation shows one nonfunctioning kidney in 1 case, persistent irregularities of abdominal arteries with normal IVP in the third case.These findings suggest development of renovascular hypertension caused by thrombosis of the renal artery or its branches. The thrombosis most likely was induced by placement of the umbilical catheter.

1097 ZINC EXCRETION AND PLASMA ZINC LEVEL IN CHILDREN WITH NEPHROTIC SYNDROME

According to earlier reports albuminuria is accompanied by an increased excretion of zinc and corticosteroid treatment causes a precipitous fall in serum zinc level. These questions were examined in 92 children with nephrotic syndrome and in 33 controls in whom zinc studies were performed at time of initial diagnosis during Prednisone treatment and after treatment was terminated. The plasma zinc content was low in all children with active nephrosis, mean 51.7 μg/100 ml, with values as low as 22 μg/100ml. A slow increase was observed with improvement of the disease. It remained low, however, even in cases of complete and long-lasting remission (69 μg/100 ml).For all groups the quantitative zinc excretion was not significantly different from the controls except for patients undergoing massive diuresis and those in long-lasting remission. During the polyuric phase our patients excreted up to 2500 μg zinc/24 hrs (mean 1770 μg/24 hrs). The zinc excretion of patients in remission was twice the control value (mean 860 μg/24 hrs). The correlation between plasma and urinary zinc and total protein, albumin and α2-globulin concentrations was studied also. The hair zinc level was low in all cases of nephrotic syndrome.A significant urinary zinc loss is not observed in nephrotic syndrome. The low plasma zinc level is not caused by either zinc excretion or corticosteroid administration and can not be explained by changes in serum protein or its fractions. Additional factors will have to be investigated.

IMPROVED PROGNOSIS OF POLYARTERITIS COMPLICATED BY RENAL FAILURE IN CHILDREN THROUGH CYCLOPHOSPHAMIDE TREATMENT

The prognosis of polyarteritis in children is poor, particularly if complicated by early renal failure. Three girls, 9 to 10 years of age, have been treated with a combination of corticosteroids and cyclophosphamide. A complete remission of the disease ensued in all three cases.An early diagnosis has been made by biopsies of the kidney or skin. All three patients initially were severely ill presenting with high fever, skin and joint manifestations, hypertension, and seizures. Additional complications included renal failure in two girls, primary pulmonary infiltrates in one, hallucinations in one. All three patients were started on Prednisone treatment (1.5-2 mg/kg) and after two to four weeks cyclophosphamide treatment (2 mg/kg) was added. After an initially stormy course all clinical symptoms gradually subsided and the renal function improved. Cyclophosphamide treatment was continued for up to 12 months. All three patients are now off medication for periods of 15 to 24 months with no or minimal residual symptoms. The creatinine clearance has returned to normal in two girls, proteinuria is still present in two patients. The additional administration of cyclophosphamide seems to effectively influence the disease process of polyarteritis leading to a resolution of infiltrates and necrosis which have not been accessible to therapy previously.