Biomedical subjects
Publications and source records attributed to H T Lund.
Primary intestinal lymphangiectasia (PIL), first described in 1961, is a rare disease of childhood. Oedema, hypoproteinaemia and diarrhoea are characteristic symptoms. Bioptic demonstration of dilated lymphatic capillary vessels in intestinal villi and increased intestinal protein loss are diagnostic. Two patients successfully treated with a low fat diet, containing medium chain triglycerides (MCT) are reported.
Growth hormone deficiency (GHD) associated with and secondary to asphyxiating perinatal events is a well-established disorder of childhood. However, hypoglycaemic fits due to GHD in children with cerebral palsy simulating symptomatic epilepsy do not seem well-recognized in literature. Within one year we have encountered two boys with cerebral palsy, one aged three and the other six years, who exhibited growth retardation and hypoglycaemic episodes. Both had suffered perinatal asphyxiation. Both had seizures which did not respond properly to antiepileptic drugs. Provocative tests (sleep and clonidine) disclosed GHD. Following growth hormone therapy, fits and hypoglycaemic episodes disappeared, and the children resumed normal growth.
A 12-year retrospective study to elucidate the incidence of "fifth day fits" including 127 infants with neonatal convulsions was carried out in the Randers area of Denmark. The incidence of neonatal convulsions was 8.3/1,000 live-born infants. The etiology in 74 cases of latent and 53 cases of convulsive seizures was asphyxia (38%), intracranial hemorrhage (17%), hypoglycaemia (9%), hypocalcaemia (4%), infections (6%) and developmental defects (4%). In 28 cases (22%) the etiology was unknown. In only two of these cases, the seizures started on day 4-6, and no peak incidence was found.
The Ellsworth Howard test employing human parathyroid hormone has not previously been employed in Denmark. The method is described. The differential diagnosis of hypoparathyroid conditions is illustrated by three case histories: hypoparathyroidism, pseudohypoparathyroidism and pseudopseudohypoparathyroidism. All three patients are children.
The children were admitted over a 14-year period (1975-1988) from an admission area of average Danish population distribution. The incidence was 15.5/100,000 children per year. The area had endemics of meningococcal disease in the years 1983-1984. The etiology was meningococcal in 43%, Hemophilus influenzae in 33% and pneumococci in 9% of the patients. Regardless of etiology, the antibiotic schedule was ampicillin 400 mg/kg body weight/day. Resistance to ampicillin was not found in any of the bacterial cultures. Within two weeks before admission 59% of the children had experienced a febrile illness. The diagnosis of meningitis was missed before admission in 24% of the cases. On admission, 93% had typical clinical signs of meningitis. 87% were lethargic or comatose. 31% had convulsion and in 13% the peripheral circulation was compromised. Recrudescence was suspected in one patient. Sequelae were most commonly found in children with meningococcal meningitis and were persistent in 23% of all the children. Severe or less severe neurological handicaps were seen in 29% (psychomotor retardation, epilepsy, cerebral palsy and hearing loss). One patient with Waterhouse-Friederichsens syndrome died. Thus the overall mortality was 1.2%, which is low compared to treatment results reported by others.
Eighty-seven infants and children aged 1 month to 15 years admitted to the Pediatric Department, Randers Central Hospital 1975-1988 with bacterial meningitis were evaluated with special interest in the course of fever and its relation to sequelae. The children were treated with ampicillin (400 mg/kg/day). We found that 94% were afebrile after six days. 10% had persisting fever, 1% prolonged fever and 38% were found to develop secondary fever. Significantly more children infected with H. Influenzae had secondary fever. In most cases, no reason for secondary fever was found (46%). 18% had drug fever and only one case of relapse was found. 23% had severe sequelae. No significant relationships between persistent, prolonged or secondary fever and sequelae were found.
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In order to evaluate the demand of blood glucose measurements (BG) in the neonatal period, a retrospective study of BG in 177 newborn babies was undertaken. Babies with birth weight less than 2,500 grams, gestational age (GA) less than 37 weeks, and/or a low birth weight in relation til gestational age were included in the study. Accordingly, the babies were grouped as appropriate for GA (AGA), small for gestational age (SGA), or large for GA (LGA). Neonatal hypoglycemia (NH), BG less than or equal to 1.4 mmol/l, was found in 33 babies. In 31 babies, NH occurred before 12 hours of age while six babies had recurrent NH. Correlation was seen between total number of clinical symptoms and NH, which was, as anticipated, commonest among preterm SGA-babies. The risk of subsequent NH in early fed low birth weight newborn seems to be very low, if NH has not appeared within the first 12 hours of life. After this time, serial blood glucose measurements only seem justified, if concomitant perinatal disease is present.
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The Prader-Willi syndrome is among other features characterized by obesity and a high prevalence of glucose intolerance. The fasting plasma insulin concentration and the insulin response to glucose are often increased, indicating some insulin resistance in this disease. To investigate whether this could be due to an insulin receptor defect 7 patients with Prader-Willi syndrome, 10 normal weight subjects and 8 obese subjects were tested for the binding of [125I]insulin to monocytes. Monocytes from patients with Prader-Willi syndrome bound significantly less insulin than cells from normal subjects (P less than 0.01). However, no difference was found between Prader-Willi patients and the obese controls (P greater than 0.1). It is concluded that the insulin resistance found in Prader-Willi patients, similar to that found in obese subjects, in part, may be explained by an insulin receptor defect on target cells for insulin action.
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In a 2 1/2-year-old girl with persistent watery diarrhea a retroperitoneal tumour and lymph node composed of benign ganglioneuroma cells were found. The histological picture was compatible with an original metastasizing neuroblastoma which has passed through a stage of late maturation. Electron microscopy of the ganglioneuroma showed cytological evidence of increased secretory activity. The tumour contained large amounts of vasoactive intestinal polypeptide (VIP) and preoperative plasma concentration of this peptide was increased. Postoperatively the VIP concentration was normalized, and the diarrhea ceased. Analysis of catecholamine metabolites in urine was normal. The findings suggest that the watery diarrhea was due to the benign VIP-producing neural crest tumour.
A boy with pseudohypoaldosteronism was followed from birth to the age of 7 years. Failure to thrive, vomiting, dehydration, hyponatraemia and urinary sodium loss were prominent findings. Urinary excretion of corticosteroid metabolites was normal. Before treatment, excessively high plasma renin concentration was found, associated with a marked activation of aldosterone secretion. A renal biopsy showed pronounced hypertrophy of the juxtaglomerular apparatus. Persisting metabolic acidosis and an insufficient urinary acidifying capacity suggested the presence of distal renal tubular acidosis. Treatment with sodium bicarbonate and sodium chloride from 19 to 31 months of age resulted in normal growth and normal physical and mental development. The plasma electrolytes were normalized but a pronounced activation of the renin-aldosterone system persisted after therapy, and on sodium restriction this system responded with a considerable further activation.