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hematocrit, low MCV, low WBC, low RBC, low MCHC. Routine chemistry panels might reveal (or not, due to compensatory and adaptive responses14


stress or liver stress. Routine iron studies might reveal, individually or in combination, reduced serum iron, transferrin (% iron saturation), ferritin and elevated TIBC and/or UIBC. (Ferritin, TIBC, and UIBC values are clues as to the nature of the disorder, based on iron binding, free- form iron availability, and storage activity). Routine urine microscopy tests are also useful in revealing emerging kidney pathology. Contrary to the assertions of many clinicians, authors and papers that ferritin is a sufcient marker for establishing iron deciency or overload, serum ferritin is inaccurate and over-relied upon in the absence of additional markers.20


Clinically, I have encountered many cases of anemia and overload with ferritin well within normal ranges, with the accessory markers re-vealing the dysfunction. Even an established clinical anemia can easily be overlooked by attending only to the most basic of routine tests and by excluding a routine iron study.


exotic tests are very useful in these scenarios. Cystatin-C, zinc protoporphyrin, urine creatinine clearance testing, ASO antibody titers, anti-DNAase antibody titers, microsomal antibodies, urine microalbumin, urine cul- tures for crystals and bacterial burdens, for example, are useful in uncovering suspected renal impairment. For hepatic impairment, when routine chemistries are equivocal, microsomal antibodies, viral load and antibody tests, and additional enzyme tests, to name a few, are useful.


Genetic testing for uncovering SNP’s and variants related to channelopathies and specic disorders are also useful when more routine clinical testing is not revealing. Organic acid testing and micronutrient testing are available and quite useful for more in-depth, real- time diagnostics, as are toxic metals, porphyrins, and environmental chemicals tests. Ideally, however, a more convenient and accurate methodology of quantifying and monitoring therapeutic progress using ferritin is the “Point Strip ferritin-3000” test, which can be done in- ofce as a baseline score (in concert with other markers), and as a follow-up on its own. Testing at a range of 300-3,000 ng/dL, it is more accurate than the standard reagents that measure ferritin at 10-500 ng/mL, which is not sensitive enough to capture functional, emerging, and well-adapted iron overload conditions.22


ferritin and hepcidin also act as acute-phase inammatory responders, C-reactive protein and brinogen are recom- mended to identify inammatory events as a source of paradoxical iron utilization.1


an established, but not yet routine screening test is the serum Hepcidin, which seems to have the most useful diagnostic applications. Adding serum Hepcidin as a routine diagnostic test is becoming a coveted target for iron uncovering utilization challenges.1,2,23


Since serum However, Non-routine and more ) evidence of renal


and utilization. Identifying and removing immunological loads and correcting resultant immune activity if either insufcient or chronically persistent. Identifying and correcting kidney and liver pathologies. Identifying and correcting metabolic conditions, such as diabetes. Identifying and correcting micronutrient imbalances, both supplemental and dietary. If chronic, and refractory to what is prioritized symptomatically and clinically for hepatic, renal, immune, dietary, xenobiotic interventions, identifying the most probable genetic variants that may be responsible for disrupting iron metabolism and determining if they are modiable for treatment options. Examples of other genetic variants that tend to confound a clinical iron utilization disorder are the AAT (alpha-1- antitrypsin deciency) and Wilson’s disease.8,9


Treatment plans depend on the prioritization of the individual’s set of conditions leading to the disorder. The challenge lies in the accurate identication of the individual priority in a clinical setting and the strategic management of the condition’s priority, given the symptomatic and clinical variables that are superimposed. Selecting and de-selecting testing and treatment direction is dependent on the accuracy of evaluation. Some gen- etic variants have no known modiable treatment. Relevant and specic dietary modications, supplemental micronutrient additions or deletions, botanical medicines, pharmaceutical chelation strategies and therapeutic venipuncture to reduce circulating iron loads are a key to resolving an immunological dis-regulation or a chronic pathogen burden. When applicable, non-pharmaceutical interventions for iron overload would circumvent the possible adverse consequences of medications.20


avoidance of, or reduction in, foods that contain a high concentration of phytic acids, soy protein, tannins, oxalic acids, phosvitins, divalent cation supplements (Ca, n, MN), and polyphenolic compounds.1,2


based on the condition priority and may be applied as either additions or subtractions, or strategic combining of foods to avoid or enhance inhibiting/enhancing qualities of micronutrient attributes.1,2


Clinical intervention strategies should include: Iden- tifying and therapeutically reducing or eliminating intake of foods that may challenge iron absorption and binding. Identifying and removing xenobiotic substances and exposures that may challenge iron binding, transport,


30


for its role in kidney health and mineral utilization properties, in the form of cholecalciferol, or vitamin D3. Vitamin C


(at least 100-300 mg/day) to (Continued on next page)


THE ORIGINAL INTERNIST MARCH 2017


iron-competing properties, preferably in the forms of zinc acetate, gluconate, picolinate, and sulfate.2 CKD anemia17


Vitamin D for conditions involving ACD from CKD5,10


journal or dietary inventory during the intervention period would be maintained. Iron supplementation is best avoided if not absolutely necessary. It would be indicated only if/when there is no evidence of a utilization problem, overload, anemia from blood loss or absolute deciency, or signicant chronic or acute inammatory events. Heme sources of supplemental iron are preferable, however, iron in the forms of ferrous sulfate heptahydrate or monohydrate, ferrous gluconate or fumarate.2


inc supplementation for to exploit its


(Table 1) Ideally, a food


Dietary modications with respect to sources of heme- iron from meats red meats, sh, poultry) versus non-heme sources of iron (plant sources, dairy, meats, and foods fortied with iron salts). Also, non-heme iron absorption is known to be enhanced by the actions of sugars such as fructose and sorbitol, acids (ascorbic acid, citric acid, lactic acid, tartaric acid), mucin, and meats such as red meats, poultry, and sh.1,2


(Table 1) Modications are (Table 1) Dietary


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