Our aim was to evaluate oxygen/haemoglobin relationships in a large . Three- way plots of relationships between SaO2 (y axis), ferritin/iron (x. Under normal conditions, levels of serum ferritin show a close correlation with iron stores in liver biopsy samples , the “gold standard” for. Presently, normal ranges for serum ferritin (SF) vary from lab to lab. I did everything he told me to do and I put my trust and hope on him. . 1) I requested that I get back my ex and our relationship last for the rest of our.
The greatest concentrations of ferritin are in the brain and the liver. One function of ferritin is to serve as the primary iron reservoir from which iron can be mobilized and used in the production of new red blood cells to circulate in hemoglobin.
Another function of ferritin is to contain iron as part of the Iron Withholding Defense System.
Free iron, a powerful oxidant, can severely damage healthy tissues and alter DNA. Functioning in a defensive mode, ferritin keeps iron away from invading cancer and pathogenic microorganisms.
These invaders need iron in order to multiply and grow. For this reason, ferritin rises when inflammation is present even though hemoglobin or serum iron might drop slightly. Were it not for this sequestering function, iron would be free to nourish and increase the growth of cancer cells as well as harmful and opportunistic bacteria. When serum ferritin is elevated along with an elevated gamma-glutamyl transpeptidase GGT the risk of disease and premature death is increased.
Serum ferritin is a good measure of iron stores, especially for someone who is iron-deficient.
SF can also be elevated in conditions where both iron overload and anemia are present, generally seen in patients with red blood cell production abnormalities thalassemia, sickle cell disease, sideroblastic anemia.
Often these individuals require long term red blood cell transfusions to correct anemia and to sustain life. Additionally, ferritin can be elevated in chronic renal kidney insufficiencies, infections, chronic inflammation, some forms of leukemia and cancers.
Elevated SF can also be seen in patients as a response to medication or hormone replacement therapy or in chronic users of nicotine gums or alcohol. Serum ferritin can be highly elevated in conditions not categorized as iron overload: HFCS is a disorder that results in early onset cataracts; SF will be dramatically increased in these individuals.
Phlebotomy is not warranted and could actually do harm if performed therapeutically to lower serum ferritin in a person with HFCS. Tips to discuss with your healthcare provider: If iron supplements are recommended, take them with vitamin C-rich foods or beverages.
If you have elevated body iron, lower your ferritin with these approaches: For others, iron chelation therapy, consuming calcium rich foods, drinking coffee and tea at mealtime, and limiting supplemental vitamin C at mealtime can help.
- International Journal of Chronic Diseases
Lifesaver tip from HealtheIron: Abstract Background Oxygen, haemoglobin and cardiac output are integrated components of oxygen transport: Arterial oxygen content was calculated by SaO2 x haemoglobin x 1. Principal Findings There was wide variation in SaO2 on air Secondary erythrocytosis was achievable with low iron stores, but only if serum iron was high-normal: Low serum iron levels were associated with reduced haemoglobin per erythrocyte, and overall arterial oxygen content was lower in iron deficient patients median A pre-defined athletic group had higher Hb: SaO2 and serum iron: PAVM embolisation increased SaO2, but arterial oxygen content was precisely restored by a subsequent fall in haemoglobin: Significance Haemoglobin and oxygen measurements in isolation do not indicate the more physiologically relevant oxygen content per unit blood volume.
Serum iron concentrations, not ferritin, seem to predict more successful polycythaemic responses.
Iron Disorders Institute:: Iron Deficiency
Introduction The primary function of haemoglobin is to transport oxygen from the alveolar capillaries to the tissues. Blood oxygen content is determined by the haemoglobin concentration, and the partial pressure of oxygen in blood PaO2 which governs the percentage haemoglobin saturation SaO2 . In turn, the overall transport of oxygen to the tissues depends upon the oxygen content of arterial blood, and the volume of blood reaching the tissues in any given period cardiac output .
Profound arterial hypoxaemia can be tolerated if subjects are gradually acclimatised    . Similarly, severe anaemia is tolerated if chronic compensatory mechanisms can be employed: Although this is an integrated system of oxygen delivery, and challenged by multiple different pathological states, the problem is that components are generally discussed in a discipline-restricted manner.
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Synthesis of iron-containing haemoglobin is impaired by iron deficiency which affects more than a billion individuals worldwide but in the iron deficiency literature, anaemia is generally discussed without reference to oxygen transport: HPV is the physiological response to alveolar hypoxia, responsible for ventilation-perfusion matching  .
As HPV leads to local or generalised elevation of pulmonary vascular resistance  this process has the potential to confound physiological and clinical responses in hypoxaemic subjects. PAVMs are abnormal blood vessels that usually develop by teenage years, and provide direct capillary-free communications between the pulmonary and systemic circulations .
Hypoxaemia results from deoxygenated pulmonary arterial blood transiting these right-to-left R-L shunts and bypassing the alveolar capillary sites of gas exchange. There is good agreement between the calculated R—L shunt using measured SaO2, and the anatomic R-L shunt, confirming that the R-L shunt is the predominant cause of the arterial hypoxaemia .
Hypoxaemic PAVM patients are therefore not at risk of hypoxic pulmonary hypertension, and pulmonary vascular resistance at rest is low in patients with severe PAVMs  . Arterial PaO2 and SaO2 are inversely related to the proportion of the cardiac output passing through the R—L shunts            and hypoxaemia may be severe.
Limitations of Serum Ferritin in Diagnosing Iron Deficiency in Inflammatory Conditions
As at altitude, and in patients with other cardiorespiratory cyanotic disease, secondary polycythaemia              and increased cardiac outputs   help to sustain long term oxygen delivery in hypoxaemic PAVM patients.
High proportions of PAVM patients have iron deficiency, due to the presence of underlying hereditary haemorrhagic telangiectasia HHT and inadequate replacement of haemorrhagic iron losses   . Importantly, such iron deficiency generally occurs in the absence of confounding inflammation: The study objectives were achieved.
Here we present data that provide new insights into the regulation of blood oxygen content through polycythaemia, and add to the evidence base from which clinical guidance may be developed. Hammersmith Hospital patients with pulmonary arteriovenous malformations and hereditary haemorrhagic telangiectasia HHT.
Individuals were asked for written consent as part of separate ethics approvals for any research protocol questionnaire, blood test, scan or other study that was not part of standard clinical practice, but no such data are reported in this manuscript.
The study cohort represents the consecutive patients with CT-proven PAVMs first seen between June Septemberand excludes the May May patients whose findings  precipitated the current study. Presentation assessments At initial assessment, SaO2 was measured by pulse oximetry Ohmeda BioxBoulder, Colorado while breathing room air. Measurements were made for 10 minutes in the erect posture, recorded at one minute intervals, with the mean value from minutes 7—10 reported, as utilised in previous clinical studies        and recently validated .