Exposure to inorganic mercury (Hg) is a serious problem presenting with a combination of neurological and psychiatric symptoms along with weight loss, pruritus, erythema, arterial hypertension, tachycardia, and renal tubular dysfunction. We report a 4-year-old girl with chronic intoxication of inorganic mercury secondary to the accidental use of an Hg₂Cl₂- and HgCl₂-containing skin whitening cream (urine level of Hg, 41.1 μg/l; reference level, < 25 μg/l). Under treatment with dimercapto-1-propansulficacid, Hg level in the urine raised to 1,175.5 μg/l, neurological deterioration occurred, and brain magnetic resonance imaging (MRI) showed on fluid attenuated inversion recovery sequences new hyperintense lesions in the subcortical white matter. After 4 months, clinical signs and symptoms and brain MRI findings resolved. This is a first case of inorganic mercury poisoning showing hyperintense lesions in brain MRI and confirms earlier cases showing transient deterioration during chelation therapy. Although urinary excretion could be enhanced during chelation therapy, signs and symptoms of intoxication could be worsened.

ABSTRACT. To assess the effect of patent ductus arteriosus (PDA) on left ventricular output (LVO) we studied stroke volume (SV), LVO, and heart rate (HR) in 21 very low birth wt preterm neonates with clinically symptomatic PDA before and after surgical ligation. Six additional infants were also studied before PDA with left-to-right shunt was detectable by the pulsed Doppler technique. Gestational age (median and range) was 28 (24-32) wk. SV was measured by duplex Doppler and M-mode echocardiography, and LVO was calculated as product of SV and HR. LVO was 419 (305-562) mL/min/kg during symptomatic PDA. It decreased to 246 (191-292) mL/min/ kg after ligation (n = 21, p < 0.001). SV was 2.69 (1.98-4.10) mL/kg during symptomatic PDA decreasing to 1.63(1.22-1.98) mL/kg after ductal closure (n = 21,p < 0.001).HR did not change after ductal closure. In the six infants with three examinations, LVO and SV were normal before detectable ductal left-to-right shunt and after ligation, but LVO was increased by 59.5 2 23% (mean + SD) ( p < 0.05), and SV by 60 + 32% (p < 0.05) during symptomatic PDA. In conclusion, preterm neonates with RDS, requiring mechanical ventilation, increased LVO during symptomatic PDA by increasing their SV, and not by changing their HR. (Pediatr Res 27: 278-281, 1990) Abbreviations AoBFV, aortic blood flow velocity (cm/s) HR, heart rate (bpm) LVO, left ventricular output (mL/min. kg) L-R, left-to-right mBP, mean systemic blood pressure PDA, patent ductus arteriosus RDS, respiratory distress syndrome GA, gestational age SV, stroke vol (mL/kg) LVO is determined by SV and HR. It is well known that neonates can regulate LVO by changing their HR. It has also been stated that newborn infants, because of their low contractile reserve, can increase LVO only by increasing their HR (1, 2). Inasmuch as noninvasive assessment of LVO in neonates by Doppler echocardiography became an established method (3), several reports on LVO in neonates have been published (4-6), but only little information is available on intraindividual changes of SV in preterm neonates (7). PDA, a common problem in Received February 10, 1989; accepted October 19, 1989 preterm neonates with RDS, should be associated with an increased LVO, if PDA is hemodynamically significant. We therefore studied the intraindividual changes of SV, HR, LVO, and mBP in preterm infants with RDS and symptomatic PDA. MATERIALS AND METHODSWe studied 21 preterm neonates with a symptomatic PDA before and after surgical ligation. Four of these infants were transferred to our unit from other hospitals for ductal ligation at the age of 21 (15-22) d. Six additional patients were studied before a ductal L-R shunt was detectable, during symptomatic PDA, and after ligation. The time between ductal closure and LVO measurement (mean * SD) was 2 + 1.9 d. In infants with clinical signs such as systolic murmur, precordial pulsations, and bounding pulses, the PDA was verified by pulsed Doppler examination of the blood flow in the main pulmonary artery. The PDA was considere...

ABSTRACT. An age-related dependence of plasma ANP levels was studied in 163 healthy children (94 boys, 69 girls) between the ages of day 1 and 16 yr. In neonates during the first 2-4 days of life, significantly higher plasma ANP plasma levels (range 129-356 pg/ml, mean 227) were found compared with older infants and children ( p < 0.001).Beyond the neonatal period through adolescence no significant difference in ANP concentrations could be found between the various age groups. Plasma ANP levels ranged between 2 and 109 pg/ml (mean 47) for all age groups after the newborn period. ANP levels were also determined in 15 adult volunteers and in arterial and venous cord blood of 16 healthy newborns, and concentrations were similar to those found in children. In addition, plasma ANP levels were measured in 40 children with variolas cardiac diseases; 22 of 40 patients exhibited ANP levels above the upper normal range seen in control children. Of these 22 patients all except two children revealed clinical signs of heart failure. In contrast 15 of 17 children without heart failure showed plasma ANP levels within the range of control children. ANP plasma levels ranged between 93 and 967 pg/ml (mean 284) in patients with heart failure and between 15 and 118 pg/ml (mean 57) in patients without heart failure, respectively. Increased ANP levels in neonates and cardiac patients may result from increased atrial distention and reflect a compensatory mechanism to improve cardiac function by reducing pre-and afterload. (Pediatr Res 20: 1328-1331,1986) Abbreviation ANP, atrial natriuretic peptide Increasing evidence is available that the recently discovered peptide hormone, ANP, is involved in the regulation of water and electrolyte balance in humans (1).The human bioactive peptide (a-ANP) is derived from higher molecular weight precursors (6,000 and 14,000 molecular weight,

Hypertrophic cardiomyopathy (HCM) is a genetically and clinically heterogeneous myocardial disease that is in most cases familial and transmitted in a dominant fashion. The most frequently affected gene codes for the cardiac (ventricular) beta-myosin heavy chain. We have investigated the genetic cause of an isolated case of HCM, which was marked by an extremely severe phenotype and a very early age of onset. HCM is normally not a disease of small children. The proband was a boy who had suffered cardiac arrest at the age of 6.5 years (resuscitation by cardioconversion). Upon screening of the beta-myosin heavy chain gene as a candidate, two missense mutations, one in exon 19 (Arg719Trp) and a second in exon 12 (Met349Thr), were identified. The Arg719Trp mutation was de novo, as it was not found in the parents. In contrast, the Met349Thr mutation was inherited through the maternal grandmother. Six family members were carriers of this mutation but only the proband was clinically affected. Segregation and molecular analysis allowed us to assign the Met349Thr mutation to the maternal and the Arg719Trp de novo mutation to the paternal beta-myosin allele. Thus, the patient has no normal myosin. We interpret these findings in terms of compound heterozygosity of a dominant (Arg719Trp) and a recessive (Met349Thr) mutation. Whereas a single mutated Arg719Trp allele would be sufficient to cause HCM, the concurrent Met349Thr mutation alone does not apparently induce the disease. Nevertheless, it conceivably contributes to the particularly severe phenotype.