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F Laubenthal

Publications and source records attributed to F Laubenthal.

9 recordsLinked to original sources
PubMed1984

Lead poisoning as a toxogenetic disease.

In two non-related patients suffering from acute lead intoxication a persistent decrease in red cell delta-aminolevulinic acid dehydratase (synonym: porphobilinogen synthase) activity of 30%-60% of controls was noted after treatment and normalisation of lead levels and heme precursors in urine and blood. An inherited enzyme deficiency was suggested and confirmed by a subnormal activity in the mothers of both patients. These four persons are considered as heterozygotes with an increased sensitivity to lead exposure.

Adult↗
PubMed1984

Lead poisoning in inherited delta-aminolevulinic acid dehydratase deficiency.

delta-Aminolevulinic acid dehydratase (ALA-D), respectively porphobilinogen synthase, EC 4.2.1.24) activity can be lowered by toxic, metabolic and hereditary factors. A 30-year-old painter was suffering from lead poisoning with an acute abdominal-neurologic syndrome and anemia. Blood lead was measured at 414 micrograms/l. Urinary ALA and coproporphyrin excretion as well as erythrocyte protoporphyrin had increased extremely, whereas ALA-D activity in erythrocytes had decreased extremely to 8% of controls. Excretion parameters, protoporphyrin, hemoglobin and lead returned to normal after treatment, but four years later ALA-D activity still remained diminished (30% of controls). An inherited enzyme deficiency was assumed and found in the mother, analogous to the subnormal ALA-D activity in heterozygotes of four other families. The inherited enzyme deficiency sensitized the patient to lead exposure and intoxication, which is a toxogenetic disease in this case.

Adult↗
PubMed1975

[Fatal vitamin D intoxication].

A 43-year-old man with alopecia maligna was treated for 4 weeks with a total of 130 mg vitamin D3. Two weeks later, after intensive exposure to the sun, he developed a hypercalcaemic crisis and died 5 weeks later of acute cardiac failure. The hypercalcaemia proved treatment-resistant despite good diuresis. Causes other than vitamin D intoxication were excluded clinically and on histopathological investigations. It is suggested that vitamin D should be administered only on the strictest indications and with regular control of the patient.

Adult↗