Diphyllobothrium pacificum infection is seldom associated with megaloblastic anemia.

Twenty cases of Dyphillobothrium pacificum (fish tapeworm) infections were prospectively studied to determine whether this tapeworm is associated with megaloblastic anemia, as commonly reported for D. latum infections. The most frequent symptoms were fatigue and mild abdominal pain, which were identified in approximately 66.6% of the 18 patients interviewed. Fourteen patients received treatment with niclosamide and all were cured. The other six patients spontaneously eliminated the tapeworms. One patient, who also had chronic diabetes and gastric atrophy, had low vitamin B12 levels and megaloblastic anemia. In all other patients, including three other patients with anemia, baseline vitamin B12 levels were in the reference range and did not significantly change when re-assessed three months later. Unlike D. latum, infection with D. pacificum is seldom associated with megaloblastic anemia or vitamin B12 deficit.

Some biochemical effects of the growth hormone analogue produced by plerocercoids of the tapeworm Spirometra mansonoides on carbohydrate metabolism of adipose tissue from normal, diabetic, and hypophysectomized rats.

Plerocercoids of Spirometra mansonoides produce a functional analogue of mammalian growth hormone (GH). Plerocercoid growth factor (PGF) mimics the growth-promoting actions of GH, but has not been shown to duplicate all of the actions reported for GH. The purpose of this study was to determine the effects of plerocercoid infection (chronic PGF treatment) on glucose metabolism of adipose tissue and to compare the effects to those elicited by insulin and GH in intact, diabetic, and hypophysectomized male rats. Groups of rats were constantly exposed to PGF (via plerocercoid infection) or injected twice daily with bovine GH, insulin, or saline for 10 days. Basal oxidation rates of [U-14C]glucose to 14CO2 in adipose tissue segments were measured in vitro immediately after tissue removal. Other aliquots of adipose tissue were preincubated in hormone-free medium for 3 hr prior to testing the ability of the tissue to respond to insulin or human GH (hGH) added in vitro. Adipose tissue from PGF-treated intact and hypophysectomized rats had significantly elevated basal glucose oxidation rates, and the tissue was sensitive to further stimulation by insulin or hGH. The results obtained with intact and hypophysectomized rats were essentially the same, indicating that the effects of PGF were not due to suppression of endogenous GH. The basal glucose oxidation rate in adipose tissue from diabetic rats was stimulated (P less than 0.01) by PGF, but the tissue was not sensitive to insulin added in vitro. Furthermore, PGF had no effect on body growth or blood glucose concentrations of diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Disorders of cobalamin metabolism.

Recent developments in our knowledge of the biochemistry and metabolism of cobalamin have given us some insight into clinical disorders. N2O, which easily induces cobalamin deficiency, both in vivo and in vitro, has greatly contributed to the investigation of the cobalamin deficient state, especially in relation to folate and amino acid metabolism. Demonstration of the cobalamin analog in human serum and a new enzyme which requires cobalamin as a coenzyme has led to recent increased interest in this field. The disorders of cobalamin metabolism will be summarized briefly as well as those areas currently of particular interest.

Biochemistry and clinical chemistry of vitamin B12 transport and the related diseases.

This review focusses on research performed by the author and coworkers. The absorption, turnover and excretion of cobalamin and the pathogenesis of cobalamin deficiency states are described and the laboratory tests used to diagnose these states are discussed. Topics dealt with in detail include: overall turnover, daily need, enterohepatic circulation and excretion of cobalamin and other corrins . The soluble proteins mediating cobalamin transport and their cellular receptors are described and their nomenclature, isolation, structure and mode of action, the role of calcium in the membrane transport, the evolution of these systems and the analogies with transport systems for other substrates are discussed together with deficiency states, especially fish tapeworm anemia and familial selective vitamin B12 malabsorption with proteinuria. Folate deficiency is a relatively rare cause of megaloblastic anemia in Scandinavia but common in North America and explanations for this difference are suggested. The methods of assaying cobalamin in serum and plasma and the performance of radiovitamin B12 absorption tests are critically evaluated. The measurement of intrinsic factor in gastric juice, serum, amniotic fluid and urine is described.

Parasites and malabsorption.

In summary, it appears that giardiasis, coccidiosis, cryptosporidiosis, strongyloidiasis, capillariasis and perhaps P. falciparum malaria are the only parasitic diseases which cause malabsorption of many nutrients. D. latum and A. lumbricoides interfere with vitamin B12 and vitamin A absorption, respectively. In view of the increasing use of immunosuppressive therapy, it is likely that malabsorption caused by intestinal parasites may become even more evident in the future.

Castle's test (with vitamin B12 and normal gastric juice) in the ileum in patients with genuine and patients with tapeworm pernicious anaemia.

A mixture of vitamin B12 and normal gastric juice, instilled through an intestinal tube into the ileum, produces haematological remission in patients with tapeworm pernicious anaemia. When a similar mixture is administered by mouth, this effect fails to occur. This observation constitutes evidence in favour of the view that Diphyllobothrium latum, attached to the proximal portion (jejunum) of the intestine, absorbs the vitamin B12 contained in the food, thus preventing vitamin bound to the intrinsic factor of the gastric juice from reaching the receptors in the distal portions of the small intestine of the host. In genuine pernicious anaemia, remission results from the administration of vitamin B12+gastric juice both by mouth and into the ileum.