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CLIENT #: LAB #: B DOCTOR: PATIENT: 6DPSOH3DWLHQW ID: 3$7,(176-00006'RFWRU V'DWD,QF SEX: Male ,OOLQRLV$YH AGE: 51 6W&KDUOHV,/ !!"#$%&'&())*+,$-.&(.*/*+,)0&12".*&3.""4 ESSENTIAL AND OTHER ELEMENTS RESULT / UNIT REFERENCE INTERVAL 2.5 Calcium (Ca) 5.5 mg/dL 4.4- 6.0 Magnesium (Mg) 3.4 mg/dL 2.9- 4.3 Copper (Cu) 82 µg/dL 63- 100 Zinc (Zn) 794 µg/dL 500- 820 Manganese (Mn) 11 µg/L 5- 17 Lithium (Li) 0.4 µg/L 0.4- 20 Selenium (Se) 223 µg/L 170- 400 Strontium (Sr) 12 µg/L 9- 36 Molybdenum (Mo) 1.9 µg/L 0.7- 3.0 th 16 PERCENTILE th th 50 84 th 97.5 TOXIC METALS RESULT / UNIT REFERENCE INTERVAL Arsenic (As) 12 µg/L < 9.0 Barium (Ba) 0.2 µg/L < 5.0 Cadmium (Cd) 0.4 µg/L < 3.0 Cobalt (Co) 0.3 µg/L < 1.0 Lead (Pb) 1.7 µg/dL < 3.5 Mercury (Hg) 25 µg/L < 5.0 Nickel (Ni) <3 µg/L < 5 Platinum (Pt) 0.2 µg/L < 2.0 Thallium (Tl) < 0.1 µg/L < 1.0 Tungsten (W) < 0.1 µg/L < 1.0 Uranium (U) < 0.1 µg/L < 1.0 PERCENTILE 95th 99th SPECIMEN DATA Comments: Date Collected: 05/05/2014 Date Received: 05/07/2014 Date Completed: 05/10/2014 Time Collected: 09:15 AM Fasting: Methodology: ICP-MS v8.10 Blood lead levels in the range of 5-9 µg/dL have been associated with adverse health effects in children aged 6 years and younger. ©DOCTOR’S DATA, INC. ! ADDRESS: 3755 Illinois Avenue, St. Charles, IL 60174-2420 ! CLIA ID NO: 14D0646470 ! MEDICARE PROVIDER NO: 148453 0001546 th Lab number: B Patient: 6DPSOH3DWLHQW Comp WB Panel Page: 1 Client: 1 WHOLE BLOOD ELEMENT REPORT INTRODUCTION This analysis of elements in whole blood was performed by ICP Mass Spectroscopy following specimen digestion with nitric acid in a closed container microwave oven system. This procedure measures the total concentration of an element in whole blood, regardless of biochemical form and regardless of partitioning of the element in blood fractions. For units of measurement, mg/L is approximately equivalent to ppm, and mcg/L is approximately equivalent to ppb. Whole blood element analysis is intended to be a diagnostic method that assists in determining imbalance, insufficiency, or excess of certain elements that have essential or beneficial functions. Additional testing of blood fractions or other body tissues may be necessary for differential diagnosis of imbalances. Additional testing also may be necessary to assess specific dysfunctions of assimilation, transport, retention, or excretion of elements. Whole blood element analysis is additionally intended to determine elevated or excessive levels of elevn potentially toxic elements. If an element is sufficiently abnormal per the whole blood measurement, a descriptive text is included with the report. For elements with essential or beneficial functions, a text will print if the measured result is below -1.5 standard deviations from the mean of the reference population, or if the result is above +1.5 standard deviations from the mean of the reference population. For potentially toxic elements, a text prints whenever the measured result exceeds the expected range. Doctor’s Data states the reference range as + 1SD from the mean of the reference population. This is considered to be the nutritionally and physiologically optimal range for elements with essential or beneficial functions. Physiological imbalance corresponds to levels beyond + 1SD but pathological consequences are not expected until the blood level is beyond + 2SD. Element levels beyond + 2SD may only be temporary nutritional problems or they may reflect a failure of homeostasis to control blood quantities. Pathological consequences depend upon cell and tissue functions which are disrupted by such levels. ZINC HIGH The concentration of zinc (Zn) is abnormally high in this blood specimen. Causal conditions related to elevated blood Zn levels include: inappropriate or over-supplementation of Zn salts, parenteral overdose, inhalation of Zn dust or fumes, iron deficiency, copper deficiency, constant diet of unusually high-Zn foods (mussels, oysters, mushrooms and yeast), and ingestion of zinccontaminated food or drink (galvanized metal containers). Excessive dietary Zn can impair intestinal absorption of iron while elevated tissue levels of Zn reduce retention of iron. Liver uptake of iron, and ferritin levels can be decreased with Zn excess. Iron deficiency anemia and sideroblastic anemia are reported in chronic Zn excess. Zinc therapy also is reported to induce subnormal blood copper levels. Symptoms consistent with chronic Zn excess include: fatigue and lethargy, 1999-2011 Doctor’s Data, Inc. Lab number: B Patient: 6DPSOH3DWLHQW Comp WB Panel Page: 2 Client: 1 difficulty writing and with fine motor skills, lightheadedness, and renal failure. Immediate symptoms (within 12 hours) of acute Zn toxicity via ingestion include: nausea, vomiting, diarrhea, exhaustion, headache, dizziness, and myalgia. Other laboratory findings consistent with Zn excess would be: elevated leukocyte count, elevated serum amylase and lipase, and elevated red blood cell Zn levels. Excess of Zn exerts detrimental chronic effects mostly by interfering with iron and copper functions. Mildly or moderately elevated whole blood Zn with normal iron and copper levels and normal enzyme activities and leukocyte levels may be asymptomatic. BIBLIOGRAPHY FOR ZINC, HIGH 1. Falchuk K.H., Chapt 28 in Harrison’s Principles of Internal Medicine, 13th ed, McGraw-Hill, New York, NY, 1994, pp 481-82. 2. Zinc in Human Medicine, Proceedings of a Symposium on the Role of Zinc in Health and Disease, Inst. Child Health (London), TIL PubLtd, Toronto, Canada, 1984. 3. Prasad A.S. et al, ”Hypocupremia Induced by Zinc Therapy in Adults”, JAMA, 240 (20), Nov. 10, 1971 pp. 2166-68. 4. Forman W.B. et al, ”Zinc Abuse - An Unsuspected Cause of Sideroblastic Anemia”, Western J. Med. 150 (2), Feb. 1990, pp 190-92. 5. Lantzsch H-J and H. Schenkel, ”Effects of Specific Nutrient Toxicities in Animals and Man: Zinc” in CRC Handbook Series in Nutrition and Food, Sect. E, vol. I, CRC Press, West Palm Beach, FL1978, pp 291-307. LITHIUM LOW The concentration of lithium (Li) in this blood specimen is lower than expected. Li occurs almost universally in water and in the diet, and Li has essential functions in the body. Intracellularly, Li inhibits the conversion of phosphorylated inositol to free inositol. In the nervous system this moderates neuronal excitability. Li also influences monamine neurotransmitter concentrations at the synapse (this function is increased when Li is used therapeutically for mania or bipolar illness). Recent studies suggest that long-term, low dose Li supplementation is neuroprotective and may help preserve integrity of the central nervous system with aging. Bibliography for Lithium, low 1999-2011 Doctor’s Data, Inc. Lab number: B Patient: 6DPSOH3DWLHQW Comp WB Panel Page: 3 Client: 1 1. Williams RSB , Harwood AJ. ” Lithium therapy and signal transduction”. Trends in Pharmacol. Sci. (2000)21:61-64. 2. Moore Gj et al. ”Lithium-induced increase in human grey matter”. Lancet (2000)356:1241-1242. 3. Chuang DM. ”Lithium exerts robust neuroprotective effects in vitro and in the CNS in vivo : Therapeutic implications”. Neuropsychopharmacol. (2000)23:S39. 4. Chuang DM et al. ”Beta-amyloid peptide-induced death of PC 12 cells and cerebellar granule neurons is inhibited by long-term lithium treatment”. Eur. J. Pharmacol. (2000)392:117-23. ARSENIC HIGH The concentration of arsenic (As) is abnormally high in this blood specimen. Usually, arsenic clears the blood rapidly after a point-in-time exposure. The finding of elevated blood As suggests: (1) recent exposure, (2) chronic or on-going exposure, (3) decreased metabolic capacity to clear As. Arsenic has two oxidation states or valences, As+3 and As+5. As+3 is more reactive and toxic. Both forms of As accumulate primarily in skin and skeletal tissue; also in liver, kidney and spleen. Over one-half of ingested or absorbed As is normally excreted via urine and feces in 2 to 8 days. In blood , As binds primarily to globulin, but generally As seeks out thiols and sulfhydryl binding sites. The vitamin cofactor, lipoic acid, is particularly affected, and this may be the reason for inhibition of alphaketoacid oxidation. Much of the enzymatic inhibition caused by As occurs in cells with mitochondrial structures. Arsine gas, AsH3, does react rapidly with erythrocytes, combining with hemoglobin and causing hemolysis, hemoglobinuria and hematuria. An important detoxification pathway for As involves methylation with methyl groups donated by S-adenosylmethionine; methylated arsenic can produce a garliclike breath odor. Early symptoms of As excess include: fatigue, malaise, eczema or allergiclike dermatitis, and increased salivation. Increased body burden of arsenic can lead to further manifestations: skin hypopigmentation, white striae on fingernails, hair loss, stomatitis, peripheral neuropathy, myocardial damage, hemolysis, and anemia (aplastic with leukopenia). Sources of As include: contaminated foods, water or medications. Industrial sources are: ore smelting/refining/processing plants, galvanizing, etching and plating processes. Tailing from or river bottoms near gold mining areas (past or present) may contain arsenic. Insecticides, rodenticides and fungicides (Na-,Karsenites, arsenates, also oxides are commercially available). Commercial As products include: sodium arsenite, calcium arsenate, lead arsenate and ”Paris 1999-2011 Doctor’s Data, Inc. Lab number: B Patient: 6DPSOH3DWLHQW Comp WB Panel Page: 4 Client: 1 green” which is cupric acetoarsenite, a wood preservative. Net retention of As in the body can be assessed by comparison of pre- and post-provocation urinalysis using DMPS, DMSA or D-penicillamine. BIBLIOGRAPHY FOR ARSENIC 1. Carson B.L. et al. Toxicology and Biological Monitoring of Metals in Humans, Lewis Publishers, Chelsea, MI, 1987 pp 24-33. 2. Tsalev D.L. and Z.K. Zaprianov Atomic Absorption Spectrometry in Occupational and Environmental Health Practice, vol 1, CRC Press, Boca Raton, FL, 1983 pp 8793. 3. Clarkson T.W. et al. eds. Biological Monitoring of Toxic Metals, Plenum Press, New York, NY, 1988 pp 309-15. 4. Harrison’s Principles of Internal Medicine, 11th ed., McGraw Hill, New York, NY, 1987 pp 850. 5. Heyman A. et al. ”Peripheral Neuropathy Caused by Arsenical Intoxication” New Eng. J. Med., 254, no. 9, 1956 pp 401-9. 6. DeKimpe J. et al, ”More Than Tenfold Increase of Arsenic in Serum and Packed Cells of Chronic Hemodialysis Patients” Am. J. Nephrology 13, 1993 pp 429-34. MERCURY HIGH The concentration of mercury (Hg) is abnormally high in this blood specimen. Elevated blood Hg indicates higher than average exposure to the metal, but does not provide information about net bodily retention of Hg. Whole blood constitutes both organic (RBC) and inorganic (serum) Hg. However, blood Hg is not indicative of past exposures if the Hg has cleared the blood and deposited in other tissues. The biological half-lives of inorganic and organic Hg in blood are about 3 days and 60 days, respectively. Blood Hg levels are typically higher than average in ”high-end” fish consumers. The symptomatology of Hg excess can depend on many factors: the chemical form of absorbed Hg and its transport in body tissues, presence of other synergistic toxics (Pb and Cd have such effects), presence of disease that depletes or inactivates lymphocytes or is immunosuppressive, organ levels of xenobiotic chemicals and sulfhydryl-bearing metabolites (e.g. glutathione), and the concentration of protective nutrients, (e.g. zinc, selenium, vitamin E). Early signs of excessive Hg exposure include: decreased senses of touch, hearing, vision and taste, metallic taste in the mouth, fatigue or lack of physical endurance, and increased salivation. Symptoms may progress with moderate or chronic exposure and retention include: anorexia, numbness and paresthesias, headaches, hypertension, irritability and excitability, and immune 1999-2011 Doctor’s Data, Inc. Lab number: B Patient: 6DPSOH3DWLHQW Comp WB Panel Page: 5 Client: 1 suppression, possibly immune dysregulation. Advanced disease processes from Hg toxicity include: tremors and incoordination, anemia, psychoses, manic behaviors, possibly autoimmune disorders, renal dysfunction or failure. Mercury is commonly used in: dental amalgams, explosive detonators, in elemental or liquid form for thermometers, barometers, and laboratory equipment; batteries and electrodes; and in fungicides and pesticides. The use of Hg as a funcicial/pesticide (including that in paints) has declined somewhat due to environmental concerns, but mercury residues persist from past use. Methylmercury, the common, most neurotoxic form, results from methylation of hg in aquatic biota or sediments, both freshwater and ocean sediments. Methylmercury accumulates in aquatic animals and fish and is concentrated up the food chain reaching high concentrations in large fish and predatory birds. Except for fish, the intake of dietary mercury is negligible unless food is contaminated with one of the previously listed forms/sources. Measurement of fecal Hg provides an indication of exposure to inorganic mercury from dental amalgams. Net retention of Hg in the body can be assessed by comparison of pre- and post-provocation urinalysis using DMPS, DMSA or Dpenicillamine. BIBLIOGRAPHY FOR MERCURY 1. Suzuki T. et al eds, Advances in Mercury Toxicology, Plenum Press, New York, NY, 1991. 2. World Health Organization: ”Methylmercury”, Environ. Health Criteria 101 (1990); ”Inorganic Mercury”, Environ. Health Criteria118 (1991), WHO, Geneva, Switzerland. 3. Tsalev D.L. and Z.K. Zaprianov, Atomic Absorption Spectrometryin Occupational and Environmental Health Practice, CRC Press, Boca Raton, FL, 1983, pp 158-69. 4. Birke G. et al ”Studies on Humans Exposed to Methyl Mercury Through Fish Consumption”, Arch Environ Health 25, 1972, pp 77-91. 5. Ishihara N. et al ”Inorganic and Organic Mercury in Blood, Urineand Hair in Low Level Mercury Vapor Exposure” Int. Arch. Occup. Environ. Health 40, 1978, pp 249-53. 6. Werbach M.R. Nutritional Influences on Illness, 2nd ed, Third Line Press, Tarzana CA, 1993, pp 349, 647, 679. 1999-2011 Doctor’s Data, Inc.