Plasma Iron

Ramsay, W. N. M.

doi:10.1016/s0065-2423(08)60354-6

Cited by 74 publications

(25 citation statements)

References 106 publications

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“…Serum iron was measured according to Peters et al [15], For estimation of TIBC the method of R amsay [17] was used. 5-ALAD activity was as sayed by the method of G ibson et al [5] as described by Batttstini et al [1] slight ly modified [11], The PBG produced after 1 h incubation is expressed in units of optical density (OD) at 553 nm.…”

Section: Methodsmentioning

confidence: 99%

Erythrocyte <i>δ</i>-Aminolaevulinic Acid Dehydratase, Urinary Porphyrins and Porphyrin Precursors in Iron Deficiency Anaemia

Chalevelakis¹,

Lyberatos²,

Manopoulos³

et al. 1977

Acta Haematol

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In 20 iron deficient patients and 21 normal controls the activity of the enzyme δ-ALA dehydratase of erythrocytes was assayed. In addition the urine porphyrins and porphyrin precursor excretions were measured. It was found that in sideropenic patients the erythrocyte δ-ALA dehydratase activity was almost constantly higher than in normals; the difference of the mean values being statistically significant (p < 0.005). A significant diminution of δ-ALA (p < 0.0025) urine excretion was observed, whereas the urine excretion of PBG, CP and UP was found within the normal limits. The results are compared to those reported by other authors.

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Section: Methodsmentioning

confidence: 99%

Erythrocyte <i>δ</i>-Aminolaevulinic Acid Dehydratase, Urinary Porphyrins and Porphyrin Precursors in Iron Deficiency Anaemia

Chalevelakis¹,

Lyberatos²,

Manopoulos³

et al. 1977

Acta Haematol

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“…Serum: sodium, potassium, carbon dioxide, chloride, urea nitrogen, antirachitic activity [46,54], albumin, globulin, bilirubin, serum glutamic oxaloacetic transaminase/serum glutamic pyruvic transaminase, cholesterol, triglycerides, lipoproteins, oral glucose tolerance test, oral iron tolerance test [38], and concentration of vitamin B ia .…”

Section: Routine Testsmentioning

confidence: 99%

Vitamin D-Dependent Rickets: Actions of Parathyroid Hormone and 25-Hydroxycholecalciferol

Rosen

Finberg

1972

Pediatr Res

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ExtractDuring active rickets, the increase in 3',5'-adenosine monophosphate (3',5'-AMP) excretion after infusion of parathyroid hormone (PTH) can be claimed as a demonstration of PTH responsiveness, at least as far as the kidney is concerned (Table II). In patients with vitamin D-dependent rickets, following 25-HGC therapy, the basal excretion ratios of nanomoles 3',5'-AMP/milligrams creatinine fall within the normal range, and, although the basal ratios of milligrams phosphate/milligrams creatinine excretion decrease to normal (Tables III, IV, and V), a phosphaturic response to PTH is still not evident. The high basal ratios of nanomoles 3',5'-AMP/ milligrams creatinine and milligrams phosphate/milligrams creatinine suggest underlying hyperparathyroidism during a phase of this syndrome marked by hypocalcemia and hyperaminoaciduria. During 2-day PTH challenges, while rickets was active, the peak increases in serum calcium above base line were 1.92, 1.80, and 1.86 mg/100 ml. After treatment with 25-hydroxycholecalciferol (25-HCG), no further significant increases in serum calcium above base line could be elicited (Tables VI, VII, VIII). It would seem, therefore, that, while these patients were untreated, small but sufficient amounts of 25-HCC or another metabolite of vitamin D were available to permit the calcium-mobilizing action of PTH on bone. The observed hypocalcemia in vitamin D-dependent rickets, then, is most likely secondary to a defect in gastrointestinal absorption. Mineral balance studies during active rickets revealed an absorptive defect for calcium, phosphorus, and magnesium-a defect completely reversible after 25-HCC treatment. Speculation

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“…A fall in total iron binding capacity has been reported in, elderly hospital patients (Powell and Thomas, 1969). Hamilton et al (1950), Fowler andBarer (1952), Ramsay (1958) and Bowie et al (1963) showed a diurnal variation in serum iron levels with lowest values being found in the evening. Sinniah et al (1969) found that serum iron levels were highest in the morning in subjects who work by day and sleep by night, but in 7 healthy nurses who were on duty at night and slept by day, the highest serum levels were at 8 p.m. and the lowest levels at 8. a.m. Schwartz and Bachner (1968) found no diurnal variation in serum levels in infants, but in older children highest levels were recorded in the morning and lowest levels in the late evening.…”

Section: Rosenbergmentioning

confidence: 97%

Temporal Variation of Serum Levels of Vitamin B12 Folate, Iron and Total Iron-Binding Capacity

Pathy¹,

Newcombe²

1980

Gerontology

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The influence of food ingestion and time of day on the serum levels of B₁₂, folate, iron and total iron-binding values was studied. Food intake had no influence on serum B₁₂, serum iron and total iron-binding capacity (TIBC) levels, but serum folate rose rapidly. Serum B₁₂ showed no change with time of day. Serum iron and TIBC fell significantly from 8 a.m. to 8 p.m. Folate initially rose significantly over 5 h then fell at 12 h, but this fall did not reach statistical significance. Over a period of 1 year serum iron fell, but TIBC showed no significant change. Subjects without pernicious anaemia but with low B₁₂ levels showed no significant change in serum B₁₂ over 4 years.

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Plasma Iron

Cited by 74 publications

References 106 publications

Erythrocyte <i>δ</i>-Aminolaevulinic Acid Dehydratase, Urinary Porphyrins and Porphyrin Precursors in Iron Deficiency Anaemia

Erythrocyte <i>δ</i>-Aminolaevulinic Acid Dehydratase, Urinary Porphyrins and Porphyrin Precursors in Iron Deficiency Anaemia

Vitamin D-Dependent Rickets: Actions of Parathyroid Hormone and 25-Hydroxycholecalciferol

Temporal Variation of Serum Levels of Vitamin B12 Folate, Iron and Total Iron-Binding Capacity

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