Biologic Turnover Rate of Cyanocobalamin (Vitamin B12) in Human Liver

Schloesser, Lee L.

doi:10.1001/archinte.1958.00260140138020

Cited by 35 publications

(6 citation statements)

References 8 publications

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“…The biological half-life of cobalamin in humans is about 1 year, and signs of co-balamin deficiency do not arise for several years after the onset of cobalamin malabsorption. 38 The rapidity of cobalamin turnover in cats is consistent with absence of the haptocorrin in cat and dog plasma 16 and suggests that after absorption of the cobalamin-intrinsic factor complex in the ileum, cobalamin in cats, as in dogs, is bound to transcobalamin 2 and partially excreted in bile. 17 The presence of substantial amounts of intrinsic factor in the pancreas, but not the stomach, of the cat (and dog) would be advantageous in this situation and would facilitate optimal transfer of cobalamin to intrinsic factor.…”

Section: Discussionmentioning

confidence: 65%

Subnormal Concentrations of Serum Cobalamin (Vitamin B12) in Cats with Gastrointestinal Disease

Simpson¹,

Fyfe²,

Cornetta³

et al. 2001

J Vet Int Med

153

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The present study sought to determine the spectrum of diseases associated with subnormal concentrations of serum cobalamin in cats undergoing investigation of suspected gastrointestinal problems. The solid-phase boil radioassay (RA) for cobalamin employed in the present study was immunologically specific, precise, and accurate, with a sensitivity of 15 pg/mL. The RA yielded results that strongly correlated with those obtained by bioassay (Spearmann rho = .805; P < .0001), although the absolute values were lower for the RA. Forty-nine of 80 serum samples submitted during the period of January 1996-January 1998 had cobalamin concentrations below the reference range for healthy cats (range 900-2,800 pg/mL; mean +/- SD, 1,775 +/- 535 pg/mL; n = 33). Cats with subnormal cobalamin concentrations (mean +/- SD; 384 +/- 272 pg/mL, range 3-883 pg/mL) were middle-aged or older and were presented for weight loss. diarrhea, vomiting, anorexia, and thickened intestines. Definitive diagnoses in 22 cats included inflammatory bowel disease (IBD), intestinal lymphoma, cholangiohepatitis or cholangits, and pancreatic inflammation. Serum concentrations of cobalamin were particularly low in cats with intestinal lymphoma, three-fifths of whom also had subnormal serum concentrations of folate (< 9 ng/mL). The simultaneous presence of disease in the intestines, pancreas, or hepatobiliary system in many cats made it difficult to determine the cause of subnormal cobalamin concentrations. The circulating half-life of parenteral cyanocobalamin was shorter in 2 cats with IBD (5 days) than in 4 healthy cats (12.75 days). The presence of subnormal serum concentrations of cobalamin in 49 of 80 cats evaluated suggests that the measurement of serum cobalamin may be a useful indirect indicator of enteric or pancreatic disease in cats. The rapid depletion of circulating cobalamin in cats suggests that cats may be highly susceptible to cobalamin deficiency. However, the relationship of subnormal serum cobalamin concentrations to cobalamin deficiency and the effect of cobalamin deficiency on cats remain to be determined.

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Section: Discussionmentioning

confidence: 65%

Subnormal Concentrations of Serum Cobalamin (Vitamin B12) in Cats with Gastrointestinal Disease

Simpson¹,

Fyfe²,

Cornetta³

et al. 2001

J Vet Int Med

153

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“…The observation that fecal excretion of small amounts of orally administered [57Co]CN-Cbl lasted significantly longer in control dogs than in affected dogs suggests that enterohepatic recirculation of Cbl occurring in normal dogs was interrupted in the affected dogs. The reported biologic tl12 of placentally derived (25) and parenterally administered (26) Cbl in dogs is 6-16 wk, much shorter than the tl12 of 11-14 mo reported for humans (27). Thus, in contrast to humans, onset of clinical and laboratory signs of Cbl deficiency in the 2nd and 3rd mo of life and rapid relapse after treatment are compatible with congenital Cbl malabsorption in dogs.…”

Section: Discussionmentioning

confidence: 79%

Inherited Selective Intestinal Cobalamin Malabsorption and Cobalamin Deficiency in Dogs

et al. 1991

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ABSTRACT. Inherited selective intestinal malabsorption of cobalamin (Cbl) was observed in a family of giant schnauzer dogs. Family studies and breeding experiments demonstrated simple autosomal recessive inheritance of this disease. Affected puppies exhibited chronic inappetence and failure to thrive beginning between 6 and 12 wk of age. Neutropenia with hypersegmentation, anemia with anisocytosis and poikilocytosis, and megaloblastic changes of the bone marrow were present. Serum Cbl concentrations were low, and methylmalonic aciduria and homocysteinemia were present. Parenteral, but not oral, cyanocobalamin administration rapidly eliminated all signs of Cbl deficiency except for low serum Cbl concentrations. Cbl malabsorption in affected dogs was documented by oral administration of [57Co]cyanocobalamin with or without simultaneous oral administration of intrinsic factor or normal dog gastric juice. Quantitation and function studies of intrinsic factor and transcobalamin-I1 from affected dogs revealed no abnormality. Other gastrointestinal functions and ileal morphology were normal, indicating a selective defect of Cbl absorption at the level of the ileal enterocyte. Immunoelectron microscopy of ileal biopsies showed that the receptor for intrinsic factor-Cbl complex was absent from the apical brush border microvillus pits of affected dogs. This canine disorder resembles inherited selective intestinal Cbl malabsorption (Imerslund-Grasbeck syndrome)

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“…gastrojejunostomy. These two findings are not incompatible, since the body's normal stores of vitamin B12 are sufficient to cope with a considerable period of total deprivation (Schloesser et al, 1958). The degree of reduced absorption in the vagotomized patients was relatively small and most would be expected to replenish their stores at a rate sufficient to meet normal requirements.…”

Section: Rangementioning

confidence: 97%

Aspects of Nutrition after Vagotomy and Gastrojejunostomy

Cox¹,

Bond²,

Podmore³

et al. 1964

BMJ

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The choice of operation in the surgical treatment of chronic duodenal ulcer remains a controversial subject. Partial gastrectomy is now performed less frequently, as surgeons are increasingly attracted to the advantages of vagotomy, which effects a substantial reduction of gastric-acid secretion in most cases. Recurrent ulceration appears to be more common after vagotomy than after partial gastrectomy, but this disadvantage of vagotomy is balanced and possibly outweighed by the higher post-operative mortality rate after partial gastrectomy. The major criticism of partial gastrectomy is that it leads to an unacceptably high incidence of late complications, which include alimentary symptoms such as postprandial abdominal discomfort, dumping, and vomiting, and also impaired nutrition manifested by loss of weight, anaemia, and more rarely osteomalacia. Although agreement is not complete, many publications support the contention that untoward alimentary symptoms are comparatively infrequent after vagotomy. However, there is remarkably little information in the literature to substantiate the view that impaired nutrition is rare after vagotomy. In order to provide data relevant to this latter problem, this paper reports the results of a study of patients after vagotomy and gastrojejunostomy for chronic duodenal ulcer.Vagotomy has been extensively used in Sheffield since 1958, and the interval between operation and the present review varied between 37 and 57 months in the patients studied; we have therefore considered the results as representing a post-operative investigation at approximately four years. A gastric drainage procedure must be performed simultaneously with vagotomy, which by itself causes a high proportion of symptoms due to delayed gastric emptying. Gastrojejunostomy was combined with vagotomy in the present series, and the patients having pyloroplasty in the period under consideration have not been included as they were too few to merit detailed investigation. The study was designed to give as much information as possible without requiring more co-operation than could reasonably be expected from our patients. The tests were therefore restricted to peripheral blood examination, estimation of serum-iron and serum-vitamin-B12 levels, and measurement of vitamin-B1, absorption and faecal fat excretion. In addition, the patients were asked about alimentary symptoms and weight changes before and after operation. Insulin tests to confirm completeness of vagotomy were not performed in all patients, but a recent study from this department suggests that vagal-nerve section was achieved in approximately 90% of patients (Ross and Kay, 1964 Clinical MaterialFrom a consecutive series of 120 patients with chronic duodenal ulcer treated by vagotomy and posterior gastrojejunostomy approximately four years previously, 25 were excluded because of death (5), reoperation (7), failure to attend (7), and distance from Sheffield (6). The 95 patients remaining for detailed investigation were 75 males and 20 females. Some were un...

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Biologic Turnover Rate of Cyanocobalamin (Vitamin B12) in Human Liver

Abstract: The availability of \g=g\-emitting radioactive cyanocobalamin (vitamin

Cited by 35 publications

References 8 publications

Subnormal Concentrations of Serum Cobalamin (Vitamin B12) in Cats with Gastrointestinal Disease

Subnormal Concentrations of Serum Cobalamin (Vitamin B12) in Cats with Gastrointestinal Disease

Inherited Selective Intestinal Cobalamin Malabsorption and Cobalamin Deficiency in Dogs

Aspects of Nutrition after Vagotomy and Gastrojejunostomy

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