Therapeutic doses of erythromycin esteolate is not cholestatic in rats in vivo.

The effect of erythromycin esteolate (EE) on bile flow and bile acid secretion was studied in male Wistar rats in vivo. Daily oral treatment with a dose of up to 100 mg/kg for 1 week increased the bile flow and the bile acid secretion. Increasing the days of treatment to 4 weeks with a dose of 20 mg/kg did not alter the measured parameters significantly. Acute intravenous injection of erythromycin lactobionate (50 mg/kg) also increased bile flow and biliary bile acid secretion temporarily. The increase in bile flow may partly be due to the osmotic effect of the drug and its metabolites in bile. Since EE failed to produce cholestasis in the range of therapeutic doses, rats do not seem to be a suitable experimental model for studying EE-cholestasis.

[Hypoglycemia in puppies and young dogs, especially in toy breeds]. / Hypoglykämie bei Welpen und Junghunden insbesondere der Zwerghunderassen.

This article deals with diseases producing hypoglycemia in juvenile dogs, especially in toy breeds. This leads to a life-threatening condition, which has to be recognized and treated as quickly as possible to prevent irreversible brain damage. Pathophysiological mechanisms of transient juvenile hypoglycemia and persistent forms of hypoglycemia in young dogs are discussed.

[Lipid storage disease similar to Wolman's disease in humans in the fox terrier]. / Lipidspeicherkrankheit vom Typ der Wolmanschen Erkrankung des Menschen beim Foxterrier.

In three young fox terriers a lipid storage disease is reported. This thesaurosis is almost identical to Wolman's disease in children. Clinically and pathologically hepatosplenomegaly is the most striking feature. Morphologically the disease is characterized by extensive lipid deposition mainly in liver, spleen, lymphnodes, intestinal mucosa, and bone marrow. Circular corneal lipid deposit (Arcus lipoides corneae) is of diagnostic significance. Some of the material has the typical structure of cholesterol crystals. Under polarized light the deposits consist of birefringent and non-birefringent lipids. All three dogs with lipid storage disease have one common ancestor. In addition their pedigrees reveal close relationship amongst the nearer forefathers and the affected animals themselves. From analogy with human Wolman's disease it is concluded, that in the Foxterrier, too, this lipid storage disease is caused by an inheritable deficiency of acid esterase. The mode of inheritance of this inborn lysosomal disease is probably autosomal recessive.