A study of the tissue iron status of patients with alopecia areata

1994 ◽  
Vol 130 (2) ◽  
pp. 261-263 ◽  
Author(s):  
M.I. White ◽  
J. Currie ◽  
M.P. Williams
Keyword(s):  
Alopecia Areata ◽  
Iron Status ◽  
Tissue Iron

scholarly journals Associations of iron overload in Africa with hepatocellular carcinoma and tuberculosis: Strachan's 1929 thesis revisited

Blood ◽  
1996 ◽  
Vol 87 (8) ◽  
pp. 3470-3476 ◽  
Author(s):  
VR Gordeuk ◽  
CE McLaren ◽  
AP MacPhail ◽  
G Deichsel ◽  
TH Bothwell
Keyword(s):  
Hepatocellular Carcinoma ◽  
Risk Factor ◽  
Confidence Interval ◽  
Iron Overload ◽  
Iron Status ◽  
Original Study ◽  
Hepatic Iron ◽  
Common Condition ◽  
Tissue Iron ◽  
Iron Grade

We analyzed data from the first study of iron overload in Africans, conducted between 1925 and 1928, to determine whether this common condition is associated with death from hepatocellular carcinoma and/or tuberculosis. In the original study, necropsies were performed on 714 adult blacks from southern Africa. Hepatic and splenic iron levels were measured semiquantitatively in 604 subjects and one of five iron grades was assigned. We examined death from hepatocellular carcinoma or from tuberculosis and the variables of age, sex, the presence of cirrhosis or other diagnoses that might be influenced by iron status, and tissue iron grades. Nineteen percent of men and 16% of women had the highest grade of hepatic iron. After adjustment for the presence of cirrhosis, hepatic iron grade was the variable most significantly associated with death from hepatocellular carcinoma (P = .021). The odds of death from hepatocellular carcinoma in subjects with the highest grade of hepatic iron was 23.5 (95% confidence interval, 2.1 to 225) times the odds in subjects with the three lowest grades. Splenic iron was the variable most significantly associated with death from tuberculosis (P >.0001). The odds of death from tuberculosis with the highest grade of splenic iron was 16.9 (4.8 to 59.9) times the odds with the two lowest grades. These findings suggest that iron overload in black Africans may be a risk factor for death from hepatocellular carcinoma and for death from tuberculosis.

scholarly journals Iron and Zinc Homeostasis and Interactions: Does Enteric Zinc Excretion Cross-Talk with Intestinal Iron Absorption?

Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1885 ◽  
Author(s):  
Palsa Kondaiah ◽  
Puneeta Singh Yaduvanshi ◽  
Paul A Sharp ◽  
Raghu Pullakhandam
Keyword(s):  
Iron Absorption ◽  
Iron Status ◽  
The Body ◽  
Zinc Homeostasis ◽  
Iron Accumulation ◽  
Intestinal Cell ◽  
Deficiency Anemia ◽  
Intestinal Iron Absorption ◽  
Tissue Iron ◽  
Iron And Zinc

Iron and zinc are essential micronutrients required for growth and health. Deficiencies of these nutrients are highly prevalent among populations, but can be alleviated by supplementation and food fortification. Cross-sectional studies in humans showed positive association of serum zinc levels with hemoglobin and markers of iron status. Dietary restriction of zinc or intestinal specific conditional knock out of ZIP4 (SLC39A4), an intestinal zinc transporter, in experimental animals demonstrated iron deficiency anemia and tissue iron accumulation. Similarly, increased iron accumulation has been observed in cultured cells exposed to zinc deficient media. These results together suggest a potential role of zinc in modulating intestinal iron absorption and mobilization from tissues. Studies in intestinal cell culture models demonstrate that zinc induces iron uptake and transcellular transport via induction of divalent metal iron transporter-1 (DMT1) and ferroportin (FPN1) expression, respectively. It is interesting to note that intestinal cells are exposed to very high levels of zinc through pancreatic secretions, which is a major route of zinc excretion from the body. Therefore, zinc appears to be modulating the iron metabolism possibly via regulating the DMT1 and FPN1 levels. Herein we critically reviewed the available evidence to hypothesize novel mechanism of Zinc-DMT1/FPN1 axis in regulating intestinal iron absorption and tissue iron accumulation to facilitate future research aimed at understanding the yet elusive mechanisms of iron and zinc interactions.

Iron status of patients with alopecia areata

2006 ◽  
Vol 132 (4) ◽  
pp. 662-664 ◽  
Author(s):  
M.J. Boffa ◽  
P. Wood ◽  
C.E.M. Griffiths
Keyword(s):  
Alopecia Areata ◽  
Iron Status

scholarly journals Serum transferrin receptor: a quantitative measure of tissue iron deficiency

Blood ◽  
1990 ◽  
Vol 75 (9) ◽  
pp. 1870-1876 ◽  
Author(s):  
BS Skikne ◽  
CH Flowers ◽  
JD Cook
Keyword(s):  
Iron Deficiency ◽  
Serum Ferritin ◽  
Transferrin Receptor ◽  
Iron Status ◽  
Serum Transferrin ◽  
Mean Cell Volume ◽  
Functional Iron Deficiency ◽  
Iron Stores ◽  
Serum Transferrin Receptor ◽  
Tissue Iron

Abstract This study was undertaken to evaluate the role of serum transferrin receptor measurements in the assessment of iron status. Repeated phlebotomies were performed in 14 normal volunteer subjects to obtain varying degrees of iron deficiency. Serial measurements of serum iron, total iron-binding capacity, mean cell volume (MCV), free erythrocyte protoporphyrin (FEP), red cell mean index, serum ferritin, and serum transferrin receptor were performed throughout the phlebotomy program. There was no change in receptor levels during the phase of storage iron depletion. When the serum ferritin level reached subnormal values there was an increase in serum receptor levels, which continued throughout the phlebotomy program. Functional iron deficiency was defined as a reduction in body iron beyond the point of depleted iron stores. The serum receptor level was a more sensitive and reliable guide to the degree of functional iron deficiency than either the FEP or MCV. Our studies indicate that the serum receptor measurement is of particular value in identifying mild iron deficiency of recent onset. The iron status of a population can be fully assessed by using serum ferritin as a measure of iron stores, serum receptor as a measure of mild tissue iron deficiency, and hemoglobin concentration as a measure of advanced iron deficiency.

scholarly journals The Effect of In Utero Insulin Exposure on Tissue Iron Status in Fetal Rats

1992 ◽  
Vol 31 (1) ◽  
pp. 64-67 ◽  
Author(s):  
Michael K Georgieff ◽  
Richard J Kassner ◽  
William J Radmer ◽  
Dennis J Berard ◽  
Sonal R Doshi ◽  
...  
Keyword(s):  
Iron Status ◽  
In Utero ◽  
Tissue Iron ◽  
Fetal Rats

scholarly journals Dietary-induced gestational iron deficiency inhibits postnatal tissue iron delivery and postpones the cessation of active nephrogenesis in rats

2017 ◽  
Vol 29 (5) ◽  
pp. 855 ◽  
Author(s):  
Mary Y. Sun ◽  
Joseph C. Woolley ◽  
Sharon E. Blohowiak ◽  
Zachary R. Smith ◽  
Ashajyothi M. Siddappa ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Surface Area ◽  
Iron Status ◽  
Weight Ratio ◽  
Planar Surface ◽  
Tissue Iron ◽  
Glomerular Size ◽  
Kidney Maturation ◽  
Iron Delivery ◽  
Nephrogenic Zone

Gestational iron deficiency (ID) can alter developmental programming through impaired nephron endowment, leading to adult hypertension, but nephrogenesis is unstudied. Iron status and renal development during dietary-induced gestational ID (<6 mg Fe kg–1 diet from Gestational Day 2 to Postnatal Day (PND) 7) were compared with control rats (198 mg Fe kg–1 diet). On PND2–PND10, PND15, PND30 and PND45, blood and tissue iron status were assessed. Nephrogenic zone maturation (PND2–PND10), radial glomerular counts (RGCs), glomerular size density and total planar surface area (PND15 and PND30) were also assessed. Blood pressure (BP) was measured in offspring. ID rats were smaller, exhibiting lower erythrocyte and tissue iron than control rats (PND2–PND10), but these parameters returned to control values by PND30–PND45. Relative kidney iron (µg g–1 wet weight) at PND2-PND10 was directly related to transport iron measures. In ID rats, the maturation of the active nephrogenic zone was later than control. RGCs, glomerular size, glomerular density, and glomerular planar surface area were lower than control at PND15, but returned to control by PND30. After weaning, the kidney weight/rat weight ratio (mg g–1) was heavier in ID than control rats. BP readings at PND45 were lower in ID than control rats. Altered kidney maturation and renal adaptations may contribute to glomerular size, early hyperfiltration and long-term renal function.

Cord serum and placental tissue iron status in maternal hypoferremia

1979 ◽  
Vol 32 (7) ◽  
pp. 1462-1465 ◽  
Author(s):  
P N Singla ◽  
S Chand ◽  
K N Agarwal
Keyword(s):  
Iron Status ◽  
Placental Tissue ◽  
Cord Serum ◽  
Tissue Iron

scholarly journals Evaluation of Iron Status by Bone Marrow Iron Stain and its Correlation with Serum Iron Profile in Chronic Kidney Disease (CKD)

1970 ◽  
Vol 25 (3) ◽  
pp. 117-120 ◽  
Author(s):  
Md Mahbubur Rahman ◽  
Pradip Kumar Dutta ◽  
Mahmudul Hoque ◽  
Md Iftikher Hossain Han ◽  
Dhiman Banik ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Bone Marrow ◽  
Kidney Disease ◽  
Serum Ferritin ◽  
Serum Iron ◽  
Iron Status ◽  
Tissue Iron ◽  
Bone Marrow Iron ◽  
The Mean ◽  
Iron Profile

This observational study was done on 52 cases of predialysis chronic kidney disease (CKD) patients with chronic anaemia. The aim of the study was to determine the tissue iron status, comparison of the tissue iron with serum iron profile and justification of giving iron in chronic kidney disease (CKD) patients on the basis of serum iron profile. Bone marrow iron stain was done in each case and compared with the serum iron profile. The mean age of the patients was 46.8 ± 12.6 years and the mean haemoglobin and serum creatinine levels of the study population were 9.36 ± 2.13 gm/dl and 8.0 ± 4.2 mg/dl respectively. Stainable iron deposits were present in 40 (77%) cases. The mean serum ferritin and transferin saturation (TSAT) of the 52 cases were found to be 412.9 ng/ml and 28.3% and that for the 12 iron deficient cases were 101.8 ng/ml and 23.8%. Over all normal (>100ng/ml <500ng/ml), increased (>500ng/ml) or low (>100 ng/ml) serum ferritin was found in 28 and 15 and nine cases respectively. On the other hand, normal (>20% >50%) and low (>20%) TSAT were found in 31 and 12 cases, and high TSAT (>50%) in only nine cases. Out of the 12 cases having no evidence of stainable iron in the marrow low serum ferritin and low TSAT were found in eight (66.6%) and six (50%) cases, and high TSAT and either normal or high serum ferritin in six (50%) & four (33.3%) cases respectively. Low TSAT was also found in six (15%) cases of those having iron deposits in the marrow. It is, therefore, concluded that absence of stainable iron in the bone marrow is a better evidence of iron depletion than the serum iron profile and that serum ferritin and TSAT correlate less well with the bone marrow iron status in patient with chronic kidney disease. (J Bangladesh Coll Phys Surg 2007; 25 : 117-120)

The quantitative assessment of body iron

Blood ◽  
2003 ◽  
Vol 101 (9) ◽  
pp. 3359-3363 ◽  
Author(s):  
James D. Cook ◽  
Carol H. Flowers ◽  
Barry S. Skikne
Keyword(s):  
Iron Deficiency ◽  
Normal Distribution ◽  
Iron Status ◽  
Present Report ◽  
Distribution Analysis ◽  
Body Iron ◽  
Iron Stores ◽  
Tissue Iron ◽  
High Prevalence ◽  
Intervention Trials

Current initiatives to reduce the high prevalence of nutritional iron deficiency have highlighted the need for reliable epidemiologic methods to assess iron status. The present report describes a method for estimating body iron based on the ratio of the serum transferrin receptor to serum ferritin. Analysis showed a single normal distribution of body iron stores in US men aged 20 to 65 years (mean ± 1 SD, 9.82 ± 2.82 mg/kg). A single normal distribution was also observed in pregnant Jamaican women (mean ± 1 SD, 0.09 ± 4.48 mg/kg). Distribution analysis in US women aged 20 to 45 years indicated 2 populations; 93% of women had body iron stores averaging 5.5 ± 3.35 mg/kg (mean ± 1 SD), whereas the remaining 7% of women had a mean tissue iron deficit of 3.87 ± 3.23 mg/kg. Calculations of body iron in trials of iron supplementation in Jamaica and iron fortification in Vietnam demonstrated that the method can be used to calculate absorption of the added iron. Quantitative estimates of body iron greatly enhance the evaluation of iron status and the sensitivity of iron intervention trials in populations in which inflammation is uncommon or has been excluded by laboratory screening. The method is useful clinically for monitoring iron status in those who are highly susceptible to iron deficiency.

Hypoferremia of Fasting in Mice Is Associated with Increased Hepcidin and Decreased Erythroferrone Expression

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4026-4026
Author(s):  
Yihang Li ◽  
Gregory R Booth ◽  
Qi Feng ◽  
Robert E Fleming
Keyword(s):  
Er Stress ◽  
Mrna Expression ◽  
Iron Status ◽  
Dietary Iron ◽  
Rt Pcr ◽  
Hepcidin Expression ◽  
Tissue Iron ◽  
Iron Retention ◽  
Absorptive Enterocytes ◽  
Iron Concentrations

Abstract Background: Protein-calorie restriction in humans is associated with changes in iron metabolism that differ from dietary iron-deficiency. Dietary iron absorption and tissue iron distribution and are regulated by the hepatocellular peptide hormone hepcidin, which mediates a decrease in circulating iron concentrations and increase in cellular iron stores. Hepcidin is upregulated in response to increased serum and tissue iron, upregulated in response to ER-stress via the transcription factor CREB-H, and down-regulated in response to erythroid iron demand via the circulating signaling molecule erythroferrone/myonectin (ERFE). An overnight fast was reported to decrease expression of skeletal muscle ERFE in mice. Objective: The aim of this study was to investigate the regulation of hepcidin in the hypoferremia of fasting. Design/Methods: We analyzed parameters of iron homeostasis in five 5 week old male AKR mice fasted for 18 hours overnight (and allowed access to water) compared with mice with access to chow ad libitum. Serum and tissue iron concentrations were measured. Liver hepcidin mRNA was quantified by real-time RT-PCR and verified by Northern blot analysis. Marrow ERFE and liver CREB-H mRNA expression was quantified by RT-PCR and normalized to beta actin. Results: As anticipated, fasted mice had significantly lower serum iron concentrations (203 vs 321 mcg/dL, P<0.001) and transferrin saturations (64.4 vs 79.6%, P<0.05). Duodenal iron concentrations were increased in fasted mice, 2.3-fold (P<0.01). Histochemical staining demonstrated iron retention in the absorptive enterocytes. Liver (916 vs 735 mcg/g, P=0.1) and splenic (480 vs 414 mcg/g, P=0.001) iron concentrations were modestly higher in the fasted mice. Despite hypoferremia, the fasted mice demonstrated increased liver hepcidin expression (1.9 fold, P < 0.05). Liver CREB-H mRNA expression was increased ~10 fold, P<0.01; however there was no change in liver XBP-1 processing (marker of ER stress). Marrow ERFE expression was downregulated by approximately one third (P<0.01). Conclusions: The fasting state in mice is associated with increased hepcidin expression, iron retention in absorptive enterocytes, and decreased circulating iron. These observations suggest that the hypoferremia of fasting is not consequent to limited iron availability, but rather to hepcidin-mediated retention of iron in the duodenum and storage tissues. They moreover support a role for nutritional state, independent of iron status, as a regulator of hepcidin and mediated by changes in expression of ERFE and CREB-H. Disclosures No relevant conflicts of interest to declare.

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