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Biomedical subjects

L S Valberg

Publications and source records attributed to L S Valberg.

At least 55 records · Page 3Linked to original sources
PubMed1979

Evaluation of the body iron status of native Canadians.

The serum ferritin concentration was measured in 1417 Indians and 310 Inuit aged 1 to 89 years. The subjects were initially selected to produce a representative sample of the entire native population, but the rate of nonresponse was high, and the results reported in this paper are representative only of the people studied.In males the median serum ferritin values increased during early life and tended to plateau after the age of 30 years. In females the median values rose during childhood, tended to plateau during adolescence, increased slightly during the reproductive period, then gradually rose thereafter. Ranges of values were wide in all age groups, reflecting the variations in body iron stores. When compared with the Inuit, the Indians had a significantly higher prevalence of abnormal serum ferritin values.From an analysis of the serum ferritin values in Indians it is probable that iron stores were reduced in approximately 30% of children, 40% of adolescents, 34% of nonpregnant women of reproductive age, 11% of older women and 5% of adult males. The corresponding figures for the Inuit were 15%, 23%, 22%, 6% and 1%. In contrast, iron deficiency anemia was found in only 3% to 4% of native peoples. If "normality" requires more than small amounts of iron stores to meet physiologic needs, the results suggest a high probability of iron deficiency in 20% to 40% of native children, adolescents and nonpregnant women of reproductive age, and in 0% to 10% of other subjects; but if "normality" is defined as adequate iron stores for erythropoiesis the prevalence of iron deficiency was approximately 1% to 2% in children and adolescents, 3% to 5% in women and less than 1% in adult males.

Adolescent↗
PubMed1978

Histocompatibility antigens as markers of abnormal iron metabolism in idiopathic hemochromatosis.

To determine the frequency of HLA histocompatibility antigens in persons with idiopathic hemochromatosis and their usefulness as genetic markers of the disease, HLA typing for the A, B and C loci was carried out. HLA-A3 was found in 61% of 18 unrelated individuals with idiopathic hemochromatosis compared with 25% of 253 randomly chosen control subjects (P less than 0.001), and HLA-B7 was found in 50% and 22% respectively (P less than 0.025). Eighty-six members of seven families with idiopathic hemochromatosis were screened for abnormalities in iron metabolism with tests for serum iron concentration, transferrin saturation, serum ferritin concentration and iron content of the hepatocytes. Of the 14 persons selected for liver biopsy because of abnormalities detected by these tests, 8 had increased amounts of stainable iron in the hepatocytes. Body iron overload was subsequently demonstrated in six of the seven, who had undergone repeated phlebotomy. In sibships having one member with hemochromatosis, only 1 of 22 members had two haplotypes in common with the proband, whereas in sibships having more than 1 member with the disease 4 of 5 affected members had two haplotypes in common. HLA typing in families with hemochromatosis may provide a means of identifying persons at risk of acquiring the disease.

Epitopes↗
PubMed1978

Usefulness of the serum ferritin concentration in the detection of iron deficiency in a general hospital.

The efficacy of measuring the transferrin saturation and the serum ferritin concentration to detect iron deficiency was determined under routine conditions in a general hospital. The tests were performed on 100 adult patients who consecutively underwent bone marrow aspiration for the appraisal of a wide range of clinical conditions. The absence of stainable reticuloendothelial iron in smears of the aspirate was used as the benchmark of iron deficiency. Of the 86 patients who were anemic 19 lacked hemosiderin in the bone marrow. The percentage of patients with iron deficiency who were correctly classified by the tests (i.e., the tests' sensitivity) was 84% for the transferrin saturation and 79% for the serum ferritin concentration, and the percentage of patients free of iron deficiency who were correctly classified by the tests (i.e., the tests' specificity) was 63% and 96% respectively. The predictive value of an abnormal (positive) result for the detection of iron deficiency was 39% for the transferrin saturation and 83% for the serum ferritin concentration, whereas the predictive value of a normal or high (negative) result for the exclusion of iron deficiency was 93% and 94% respectively. Measurement of the serum ferritin concentration was superior to measurement of the transferrin saturation only in its specificity. The former is of particular value in clinical settings where the prevalence of iron deficiency is low and conditions that increase the serum ferritin concentration out of proportion to the size of the body iron stores are infrequent.

Adult↗
PubMed1978

Diagnostic efficacy of tests for the detection of iron overload in chronic liver disease.

The value of tests for the detection of body iron overload was investigated in 8 patients with clinically manifest primary hemochromatosis, 12 patients with cirrhosis and iron overload and 20 patients with liver disease and low or normal iron stores. Iron overload was defined as the presence of stainable iron in more than 50% of hepatocytes in a liver biopsy specimen. The percentages of patients with a true-positive (abnormal) or true-negative (normal) result were: serum iron concentration 65%, transferin saturation 85%, serum ferritin concentration 78%, serum ferritin:serum glutamic oxaloacetic transaminase (SGOT) index 78%, percent iron absorption 58%, percent iron absorption in relation to serum ferritin concentration 80% and percent iron absorption in relation to serum ferritin:SGOT index 93%. The calculated predictive value of a normal test result for the exclusion of iron overload in patients with liver disease, a group with an assumed prevalence of iron overload of 10%, was 98% to 99% for transferrin saturation and serum ferritin concentration used alone and 100% for these measures used together; the predictive value of an abnormal result for the diagnosis of iron overload was less than 50% for all of the above measures used alone or in combination. Hence, in patients with an increased serum ferritin concentration or transferrin saturation, or both, determination of the hepatocellular iron content of a specimen from a percutaneous liver biopsy is required for the diagnosis of iron overload.

Adolescent↗
PubMed1978

Measurement of dietary cadmium absorption in humans.

Total body counting was used to determine cadmium absorption in 14 healthy subjects and in 1 patient with an ileostomy. Breakfast was extrinsically tagged with 115mCdCl2, and a poorly absorbed marker, 51CrCl3, was added to determine the point of complete elimination of unabsorbed radiocadmium from the gastrointestinal tract. The 51Cr was not an ideal marker: fecal excretion of radiocadmium continued beyond the point at which chromium was completely eliminated from the body, Nevertheless, it was helpful in six subjects in identifying the presence of unabsorbed radiocadmium still in transit in the lumen of the gastrointestinal tract 3--5 wk after the test meal. The average body retention of radiocadmium determined between 7 and 14 d after the disappearance of the chromium marker from the body was 4.6 +/- 4.0% (SD), with a range of 0.7--15.6%. The biological half-time of absorbed radiocadmium in one of the subjects was 100 d.

Adult↗
PubMed1978

Zinc, cadmium, and iron interactions during intestinal absorption in iron-deficient mice.

Zinc absorption from a test dose of (65Zn) zinc chloride was increased in mice with a high capacity to absorb iron induced by a low-iron diet. When radiolabelled zinc chloride in concentrations varying from 0.025 to 0.30 mM was perfused through open-ended duodenal loops of mice fed this diet, the proportion of zinc taken up from the lumen and transferred to the body was greater from lower than from higher doses. The addition of iron to the perfusate inhibited zinc uptake and transfer, and zinc had a similar effect on iron absorption. Cadmium, a potent inhibitor of iron uptake in mice fed a low-iron diet, impaired zinc uptake under these dietary conditions. These results suggest that in dietary-induced iron deficiency there are analogous mucosal binding sites for the uptake of iron and zinc. There also appear to be mutually exclusive binding sites for the absorption of these metals: radiolabelled iron absorption from an intragastric test dose was enhanced in mice with a high capacity to absorb iron produced by bleeding, whereas the absorption of zinc was not increased.

Animals↗
PubMed1978

Increased dietary cadmium absorption in mice and human subjects with iron deficiency.

In mice fed a low iron diet, the addition of low levels of cadmium chloride (10 micrometer) to the drinking water impaired growth and accentuated the development of anemia. Cadmium had no effect on mice given a similar diet supplemented with iron. Iron deficiency increased the concentration of cadmium in the duodenal mucosa, the transfer of cadmium to the body from the intestinal tract, and the deposition of absorbed cadmium in the kidneys. In human subjects, the average absorption of 25 microgram of cadmium, labeled with 115mCd, from a test meal was 8.9 +/- 2.0% (mean +/- SE) in 10 people with low body iron stores (serum ferritin less than 20 ng per ml) and 2.3 +/- 0.3% in 12 subjects with normal iron stores (serum ferritin greater than 23 ng per ml). The biological half-time of the radiocadmium in 3 of the subjects ranged from 90 to 202 days. Thus, the intestinal adaptive response to iron deficiency in both experimental animals and human subjects leads to the increased absorption of cadmium, a potentially toxic element.

Anemia, Hypochromic↗
PubMed1977

Cadmium-induced enteropathy: comparative toxicity of cadmium chloride and cadmium-thionein.

In protecting the body against the noxious effects of dietary cadmium ions, cadmium is bound to metallothionein in the proximal intestine, and subsequently excreted into the lumen with desquamation of the epithelium. The purpose of this study was to determine the extent to which cadmium in the form of intestinal cadmium-thionein is absorbed from the intestinal lumen and to appraise the toxicity of cadmium-thionein on the intestinal mucosa. With open-ended duodenal perfusion, equivalent amounts of cadmium administered as CdCl2 or cadmium-thionein entered the mucosa, but significantly less cadmium from the perfusate of cadmium-thionein passed into the body. Exposure of the mucosa to CdCl2 for 1 hr led to minor abnormalities in the form of broadening of villi with pseudostratification of epithelium, and swelling of mitochondria, whereas cadmium-thionein produced extensive necrosis of absorptive cells. The results suggest that cadmium-thionein may play a paradoxical role, providing protection against the cadmium ion in the intracellular milieu, but promoting cadmium toxicity when it is present in sufficient amounts in the lumen of the intestine.

Animals↗
PubMed1977

Mucosal iron-binding proteins in mice with X-linked anaemia.

The mouse with X-linked anaemia [sla] has a defect in iron absorption which can be temporarily reversee by feeding a low iron diet. Duodenal non-haem iron was significantly higher in the sla than in the normal mouse on an iron supplemented diet but non-haem iron was reduced to minute amounts when the mice were fed a low iron diet. Gel chromatography on Sephadex G-200 of th partial-free supernatant of pooled mucosal homogenates revealed the presence of three proteins binding 59Fe. Fraction I [mol wt 450 000] resembled ferritin and was present in both normal and sla mice fed an iron supplemented diet. Fraction II [mol wt 78 ooo] eluted in a similar position to transferrin and was evident in both normal and sla mice fed an iron deficient diet. Fraction III [mol wt less than 15 000] contained equivalent amounts of radioiron in normal and sla mice fed the iron deficient diet, whereas this fraction contained less radioactivity in sla animals in two of three experiments in which the animals were fed an iron supplemented diet. The iron transport defect in sla mice does not appear to reside in the iron-binding proteins in the supernatant fraction of the intestinal mucosa and the cause of the defect in iron absorption remains to be elucidated.

Anemia, Hypochromic↗
PubMed1976

Serum ferritin and the iron status of Canadians.

Serum ferritin concentration was determined in 1105 Canadians aged 1 to 90 years. Geometric mean values (ng/ml) were as follows: children 1 to 4 years old, 12; children 5 to 9 years old, 15; adolescent girls, 17; adolescent boys, 18; women 20 to 39 years, 23; women 65 years and older, 52; men 20 to 39 years, 93; and men 40 and older, 92. Ranges were side in all age groups, reflecting variations in size of body iron stores. From analysis of the ferritin values it is highly probably that iron stores were greatly reduced in approximately 25% of children, 30% of adolescents, 30% of menstruating women, 60% of pregnant women and 3% of men. Iron-deficiency anemia was noted in only 2% of subjects. If "normality" requires more than small amounts of storage iron to meet physiologic demands, the study results suggest a high probability of iron deficiency in 60% of the pregnant women and in 19% of the other subjects; but if normality is defined as maintenance of adequate iron stores for erythropoiesis, the prevalence of iron deficiency was zero in the pregnant women and 2% in the other subjects.

Adolescent↗
PubMed1976

Kinetics of the subcellular distribution of iron and cobalt in the intestinal mucosa of the rat.

A differential centrifugation technique was used to compare the subcellular distribution of labeled iron (Fe) and cobalt (Co) in iron-deficient animals (FeD), in which transport was active, with iron-loaded animals (FeL), in which transport was by diffusion. In FeL the amount of Fe and Co in each subcellular fraction was dependent upon dose; there was a linear relation between the amount of Fe or Co in each fraction and metal absorption. In FeD a curvilinear relation was noted between both Fe dose and absorption, and the amount of Fe in the particulate fractions I and II. In contrast, a linear relation was noted between both dose and absorption, and the smaller amounts of Fe in the other fractions. Most of the Co was in V ("soluble"), and the relation between Co in all the fractions and absorption was linear. The addition of Co to the Fe test dose was associated with a decrease in Fe in I and II. The results suggest that a constituent(s) in the particulate fractions I and II is involved in the enhanced absorption of Fe in FeD. The subcellular fraction responsible for the increased Co absorption in FeD was not identified.

Animals↗
PubMed1976

Gastrointestinal metabolism of cadmium in experimental iron deficiency;.

The average gastrointestinal uptake 4 h after an intragastric dose of 400 nmol of cadmium chloride labeled with 109CdCl2 in iron-deficient mice, 25%, was significantly greater than the result, 16%, in iron-normal animals, and more cadmium entered the body of the former, 3.8%, than the latter, 2% (P less than 0.05). Between 4 and 72 h, gastrointestinal radioactivity declined without further increase in body activity; however, more radiocadmium remained in the duodenum of iron-deficient than iron-normal animals (P less than 0.05). The radiocadmium sequestered in the duodenum was bound to a protein with a molecular weight of about 12,000. After subcutaneous injection of radiocadmium, the rate of excretion of radioactivity from the body was similar in iron-normal and iron-deficient mice; however, a greater proportion of the injected dose accumulated in the duodenum of the iron-deficient animals (P less than 0.05). Thus, the intestinal adapative response to iron deficiency may enhance cadmium toxicity, whereas sequestration and subsequent excretion of cadmium by the intestinal mucosa serves to protect the body against toxic effects. The duodenum, particularly in iron-deficient mice, is especially vulnerable to the toxic effects of cadmium.

Animals↗