Gulf War Syndrome FMS/ CFS & ALS:
By George Nadzan
Hypomagnesemia with secondary hypocalcemia.
Pathophysiology infectious diarrhea, steatorrhea, inflammatory bowel disease, and GI neoplasms may cause hypomagnesemia.... Ionic magnesium and Calcium serum loss.
This is a sample of my blood under a dark field microscope the little spikes sticking out of my cells are Calcium produced by a severe intracellular magnesium depletion.
In recent studies Dr. Garth Nicholson's laboratory findings reported that, there were notable deficiencies of magnesium chromium and zinc in blood serum samples of veterans testing positive for Mycoplasma Fermentans. Is it more the just possible but more likely that some or most of the neurological symptoms experienced by Gulf War Veterans are due to a severe Magnesium and Calcium loss from infectious diarrhea, mucous lining damage of the small and large bowel, and mal-absorption of magnesium/calcium?
Patients with CFS, FMS or GWI usually have nutritional and vitamin deficiencies that must be corrected. For example, these patients are often depleted in vitamins A, B, C, D and E and certain minerals Unfortunately, patients with these chronic illnesses often have poor absorption. Therefore, high doses of some vitamins must be used, and others, such as vitamin B complex, cannot be easily absorbed by the gut, so sublingual natural B-complex vitamins in small capsules or liquids is preferred. General vitamins plus extra C, E, CoQ-10, beta-carotene, folic acid, bioflavoids and biotin are essential. L- cysteine, L-tyrosine, L-carnitine and malic acid can also be useful. Certain minerals are also often depleted in GWI/CFS/FMS patients, such as zinc, magnesium, chromium and selenium. Use of antibiotics that deplete normal gut bacteria can result in over-growth of less desirable flora, so Lactobacillus acidophillus supplementation is recommended.
Hypomagnesaemia: Is defined as an abnormally low serum magnesium level.
Hypocalcemia: Is defined as an abnormally low concentration of calcium in the blood. A low blood calcium level, occurs when the concentration of free calcium ions in the blood falls below 4.0 mg/dL (dL=one tenth of a liter). The normal concentration of free calcium ions in the blood serum is 4.0?6.0 mg/dL.
Hypercalcemia: Is defined as an abnormally high concentration of calcium in the blood.
Hypocalcemia can be caused by hypoparathyroidism , by failure to produce 1,25-dihydroxyvitamin D, by low levels of plasma magnesium, or by failure to get adequate amounts of calcium or vitamin D in the diet. Hypoparathyroidism involves the failure of the parathyroid gland to make parathyroid hormone. Parathyroid hormone controls and maintains plasma calcium levels. The hormone exerts its effect on the kidneys, where it triggers the synthesis of 1,25-dihydroxyvitamin D. Thus, hypocalcemia can be independently caused by damage to the parathyroid gland or to the kidneys. 1,25-Dihydroxyvitamin D stimulates the uptake of calcium from the diet and the mobilization of calcium from the bone. Bone mobilization means the natural process by which the body dissolves part of the bone in the skeleton in order to maintain or raise the levels of plasma calcium ions.
Low plasma magnesium levels (hypomagnesia) can result in hypocalcemia. Hypomagnesemia can occur with alcoholism or with diseases characterized by an inability to properly absorb fat. Magnesium is required for parathyroid hormone to play its part in maintaining plasma calcium levels. For this reason, any disease that results in lowered plasma magnesium levels may also cause hypocalcemia.
Hypocalcimia may also result from the consumption of toxic levels of phosphate. Phosphate is a constituent of certain enema formulas. An enema is a solution that is used to cleanse the intestines via a hose inserted into the rectum. Cases of hypocalcemia have been documented where people swallowed enema formulas, or where an enema has been administered to an infant.
Symptoms of severe hypocalcemia include numbness or tingling around the mouth or in the feet and hands, as well as in muscle spasms in the face, feet, and hands. Hypocalcemia can also result in depression, memory loss, or hallucinations. Severe hypocalcemia occurs when serum free calcium is under 3 mg/dL. Chronic and moderate hypocalcemia can result in cataracts (damage to the eyes). In this case, the term "chronic" means lasting one year or longer.
Hypocalcemia is diagnosed by acquiring a sample of blood serum and measuring the concentration of free calcium using a calcium-sensitive electrode. Hypocalcemia has several causes, and hence a full diagnosis requires assessment of health of the parathyroid gland, kidneys, and of plasma magnesium concentration
Hypomagnesaemia: Is defined as an abnormally low serum magnesium level
Magnesium depletion occurring with intestinal malabsorption or dietary deficiency can cause hypocalcemia. Relative PTH deficiency and end-organ resistance to its action occur with magnesium depletion, resulting in plasma concentrations of < 1.0 mEq/L (< 0.5 mmol/L); repletion of magnesium improves PTH levels and renal Ca conservation.
Symptomatic hypomagnesemia may manifest clinically as CNS and neuromuscular hyperexcitability. Early manifestations may include painful muscle cramps, nausea, vomiting, and lethargy
Pathophysiology: Hypomagnesemia is widespread among hospitalized patients. Hypomagnesemia has been reported in as many as 60% of ICU patients. Prolonged administration of magnesium-free parenteral fluids may be a contributing factor. Prolonged nasogastric suction, infectious diarrhea, steatorrhea, inflammatory bowel disease, and GI neoplasms may cause hypomagnesemia. A congenital defect in GI magnesium absorption also has been described.
· At serum magnesium levels less than 1.0 mEq/L, patients with hypomagnesemia may have tremor, hyperactive deep-tendon reflexes, hyperreactivity to sensory stimuli, muscular fibrillations, positive Chvostek and Trousseau signs, and carpopedal spasms progressing to tetany.
· Mental status changes may become evident and include irritability, disorientation, depression, and psychosis.
· Reversible respiratory muscle failure may occur in severe hypomagnesemia.
Background: Magnesium (Mg) is the second-most abundant intracellular cation and, overall, the fourth-most abundant cation. Almost all enzymatic processes using phosphorus as an energy source require magnesium for activation. Magnesium is involved in nearly every aspect of biochemical metabolism (eg, deoxyribonucleic acid [DNA] and protein synthesis, glycolysis, oxidative phosphorylation). Almost all enzymes involved in phosphorus reactions (eg, adenosine triphosphatase [ATPase]) require magnesium for activation. Magnesium serves as a molecular stabilizer of ribonucleic acid (RNA), DNA, and ribosomes. Because magnesium is bound to ATP inside the cell, shifts in intracellular magnesium concentration may help regulate cellular bioenergetics such as mitochondrial respiration.
Extracellularly, magnesium ions block neurosynaptic transmission by interfering with the release of acetylcholine. Magnesium ions also may interfere with the release of catecholamines from the adrenal medulla. Magnesium has been proposed as an endogenous endocrine modulator of the catecholamine component of the physiologic stress response.
Approximately 60% of total body magnesium is located in bone, and the remainder is in the soft tissues. This soft tissue intracellular compartment comprises about 38% of total body magnesium; relatively higher concentrations.
· Magnesium depletion occurring with intestinal malabsorption or dietary deficiency can cause hypocalcemia. Relative PTH deficiency and end-organ resistance to its action occur with magnesium depletion, resulting in plasma concentrations of < 1.0 mEq/L (< 0.5 mmol/L); repletion of magnesium improves PTH levels and renal Ca conservation.
· Acute pancreatitis causes hypocalcemia when Ca is chelated by lipolytic products released from the inflamed pancreas.
· Hypoproteinemia of any cause can reduce the protein-bound fraction of plasma Ca. Hypocalcemia due to diminished protein binding is asymptomatic. Since the ionized Ca fraction is unaltered, this entity has been termed factitious hypocalcemia.
· Enhanced bone formation with inadequate Ca intake can cause hypocalcemia. This situation occurs particularly after surgical correction of hyperparathyroidism in patients with severe osteitis fibrosa cystica and has been termed the hungry bone syndrome.
· Septic shock may be associated with hypocalcemia due to suppression of PTH release and conversion of 25(OH)D3 to 1,25(OH)2D3.
· Hyperphosphatemia also causes hypocalcemia by one or a variety of poorly understood mechanisms. Patients with renal failure and subsequent phosphate retention are particularly prone to this form of hypocalcemia.
· Drugs associated with hypocalcemia include those generally used to treat hypercalcemia (see Hypercalcemia, below); anticonvulsants (phenytoin, phenobarbital) and rifampin, which alter vitamin D metabolism; transfusion with blood products treated with citrate as well as radiocontrast agents containing the divalent ion chelating agent ethylenediaminetetraacetate.
Although excessive secretion of calcitonin might be expected to cause hypocalcemia, low plasma Ca levels rarely occur in patients with large amounts of circulating calcitonin from medullary carcinoma of the thyroid
Incidence of hypomagnesemia among people with alcohol dependence is approximately 25% and mainly is due to magnesium diuresis caused by alcohol.
Several drugs can cause increased urinary loss of magnesium. Magnesium deficiency is especially common in patients receiving furosemide diuretics. A congenital defect in tubular reabsorption of magnesium also has been described.
Severe hypomagnesemia may occur during the recovery phase of diabetic ketoacidosis. Patients with diabetes who have chronically poor glycemic control may have a total body magnesium deficit, possibly caused by ineffective insulin-mediated cellular uptake of magnesium.
· In the US: Although the incidence of hypomagnesemia in the general population has been estimated at less than 2%, hospitalized patients are more prone to develop hypomagnesemia. Exact inpatient incidence is unknown. Recent studies of ICU patients have estimated frequencies in that setting as high as 60%.
o Laboratory analysis by atomic absorption spectrophotometry (AAS) is the most specific technique available to measure total serum magnesium. Ion-selective electrodes for measurement of free magnesium have been developed; however, their use has not been rigorously tested, and they currently are not readily available for clinical use.
o Hypomagnesemia may be associated with nonspecific ECG changes, including ST-segment depression, altered T waves, or loss of voltage. Severe magnesium deficiency may cause PR prolongation or widened QRS complexes.
Sarcoidosis is associated with hypercalcemia in up to 20% of patients and hypercalciuria in up to 40% of patients. Hypercalcemia and hypercalciuria have also been described in other granulomatous diseases, such as TB, leprosy, berylliosis, histoplasmosis, and coccidioidomycosis. In sarcoidosis, the hypercalcemia and hypercalciuria appear to be due to unregulated conversion of 25(OH)D3 to 1,25(OH)2D3, presumably due to expression of the 1- -hydroxylase enzyme in mononuclear cells within the sarcoid granulomas. Similarly, elevated plasma levels of 1,25(OH)2D3 have been reported in hypercalcemic patients with TB, silicosis, and lymphoma. Other mechanisms must account for hypercalcemia in some instances, since depressed 1,25(OH)2D3 levels have been described in some patients with hypercalcemia in association with leprosy, T-cell lymphoma, or leukemia.
Calcium homeostasis is maintained by two hormones, parathormone (parathyroid hormone or PTH) and calcitriol (1,25-dihydroxy vitamin D). Minute-to-minute regulation of serum ionized calcium is regulated by PTH. PTH secretion is stimulated when ambient serum ionized calcium is decreased. PTH acts on peripheral target cell receptors, increasing the efficiency of renal tubular calcium reabsorption. In addition, PTH enhances calcium resorption from mineralized bone and stimulates conversion of vitamin D to its active form, calcitriol, which subsequently increases intestinal absorption of calcium and phosphorus. Pharmacologic doses of calcitonin act as an antagonist to PTH, lowering serum calcium and phosphorus, and inhibiting bone reabsorption.
Normal, healthy kidneys are capable of filtering large amounts of calcium that is subsequently reclaimed by tubular reabsorption. The kidneys are capable of increasing calcium excretion nearly fivefold to maintain homeostatic serum calcium concentrations. However, hypercalcemia may occur when the concentration of calcium present in the extracellular fluid overwhelms the kidneys' compensatory mechanisms.
Hypercalcemia: Is defined as an abnormally high concentration of calcium in the blood.
Serum Calcium Concentration
Symptoms <3.5 mmol/L >/= 3.5 mmol/L
CNS symptoms 41% 80% constipation 21% 25% malaise-fatigue 65% 50% anorexia 47% 59% nausea and/or vomiting 22% 30% polyuria and/or polydipsia 34% 35% pain 51% 35%
Clinical manifestations can be categorized according to body systems and functions.
Calcium ions have a major role in neurotransmission. Increased calcium levels decrease neuromuscular excitability, which leads to hypotonicity in smooth and striated muscle. Symptom severity correlates directly with the magnitude of serum ionized calcium concentrations and inversely with their rate of change. Neuromuscular symptoms include weakness and diminished deep tendon reflexes. Muscle strength is impaired, and respiratory muscular capacity may be decreased. Central nervous system impairment may manifest as delirium with prominent symptoms of personality change, cognitive dysfunction, disorientation, incoherent speech, and psychotic symptoms such as hallucinations and delusions. Obtundation is progressive as serum calcium concentrations increase and may progress to stupor or coma.[1,2] Local neurologic signs are not common, but hypercalcemia has been documented to increase cerebrospinal fluid protein, which may be associated with headache. Headache can be exacerbated by vomiting and dehydration. Abnormal electroencephalograms are seen in patients with marked hypercalcemia.
Hypercalcemia is associated with increased myocardial contractility and irritability. Electrocardiographic changes are characterized by slowed conduction, including prolonged P-R interval, widened QRS complex, shortened Q-T interval, S-T segments may be shortened or absent, and the proximal limb of T waves may slope abruptly and peak early. Hypercalcemia enhances patients' sensitivity to the pharmacologic effects of digitalis glycosides (e.g., digoxin). When serum calcium concentrations exceed 16 mg/dL (>8.0 mEq/L or 3.99 mmol/L), T waves widen, secondarily increasing the Q-T interval. As calcium concentrations increase, bradyarrhythmias and bundle branch block may develop. Incomplete or complete AV block may develop at serum concentrations around 18 mg/dL (9.0 mEq/L or 4.49 mmol/L) and may progress to complete heart block, asystole, and cardiac arrest.[1,2]
Gastrointestinal symptoms are probably related to the depressive action of hypercalcemia on the autonomic nervous system and resulting smooth muscle hypotonicity. Increased gastric acid secretion often accompanies hypercalcemia and may intensify gastrointestinal manifestations. Anorexia, nausea, and vomiting are intensified by increased gastric residual volume. Constipation is aggravated by dehydration that accompanies hypercalcemia. Abdominal pain may progress to obstipation and can be confused with acute abdominal obstruction.
Hypercalcemia causes a reversible tubular defect in the kidney resulting in the loss of urinary concentrating ability and polyuria. Decreased fluid intake and polyuria lead to symptoms associated with dehydration, including thirst, dry mucosa, diminished or absent sweating, poor skin turgor, and concentrated urine. Decreased proximal reabsorption of sodium, magnesium, and potassium occur as a result of salt and water depletion that is caused by cellular dehydration and hypotension. Renal insufficiency may occur as a result of diminished glomerular filtration, a complication observed most often in patients with myeloma.
Although nephrolithiasis and nephrocalcinosis are usually not associated with hypercalcemia of malignancy, calcium phosphate crystals can precipitate within renal tubules to form renal calculi as a consequence of long-standing hypercalciuria. When they occur, coexisting primary hyperparathyroidism should be considered.
Hypercalcemia of malignancy can result from osteolytic metastases or humerally-mediated bone resorption with secondary fractures, skeletal deformities, and pain.
DR. CARL REICH was a medical maverick. He earned the title quack because he was treating his patients with supplements of 700 mg. calcium and about 5,000 units of vitamin D. Immediately, the children under puberty within about four days were totally cured, asthma gone, allergies gone, complaints gone, Attention Deficit Disorder gone. He wrote a paper, but no one in Canada would publish it. He continued his work with adults and started seeing dramatic successes. Terminal cancer patients and other patients with no other hope poured through his door. He gave them nutrients: the cancer patients were cured, and the diabetic patients within six to twelve months were off their insulin. Heart patients were cured within about 1½ years. He documented his cases meticulously and when he tried to present them at conferences, he was told Calcium is too simple. However, in 1962, the Max Planck Institute, the most prestigious institute in Germany, invited him to present his paper. A man named Otto Warburg was there, a two time Nobel Prize winner for proving that cancer was anaerobic (which means that lack of oxygen induces cancer, and infusion of oxygen kills cancer). So in 1932 we knew what caused cancer, we knew how to prevent it and we sure as heck knew how to cure it, but the trouble was there was too much money in cancer. They were making practically a billion dollars a year. So they put Otto in a corner and told him to be quiet. In any case, Otto Warburg told Carl Reich that he was right and. that the key factor was the calcium factor, and they became colleagues. Unfortunately Otto Warburg died less than three months into their project, so Carl had to look for a calcium chemist, and eventually he found me. He presented me with stacks of records of terminal cancer patients whose autopsies showed absolutely no cancer. I went to the medical library to find more information about calcium and found a book called Biological Calcium written by 227 Ph.D.s, in which they had taken an ugly cancer tumour, cut it in half and put it in two beakers in body fluids at 98 degrees. They put a pinch of calcium salts in one of the beakers. Four days later the tumour with the calcium is a quarter of the size and the one without is four times larger. Thats a 16-fold difference in four days. So, we agreed to go around the world and investigate further, looking for localities with naturally high calcium consumption to document the cancer rate.
CALCIUM IN TRADITIONAL CULTURES Around the world, there are many cultures who never get cancer. They live 30 years longer and they dont grow old. A hundred-year old man looks like a 50-year-old. What is the common denominator? All these people exceed the RDA of vitamins 100 fold. They have 100 times the calcium, 100 times the magnesium, 100 times the vitamin D, every vitamin. We went to visit the Eskimos. They never got heart disease or diabetes until we started feeding them our food. Their diet was 100% meat, no vegetables and the meat was 78% blubber, fat. But there was no cancer. We visited the Indians, the Azerbaijans, high in the mountains, the Hunzas of northern Pakistan, the Georgians, the Tibetans, the Chinese, the Titicaca Indians of Peru, the Vilcabamba Indians in Equador. We found at least one common denominator: high in the mountains and we knew that calcium was a factor. High in the mountains, water comes from the glaciers, and the glacier water contains ground up rock; it looks very turbid and white. The Indians refer to it as the milk of the mountains. Every liter contains 8,000 mg. of undissolved calcium. They drink three to five liters a day. Their vegetables are also loaded with calcium. We calculated they ate 150,000 mg. of calcium a day. It was astounding. Doctors say more than 1,200 mg. could be toxic. Yet these people never get sick. The only consequence is that they have no diseases, they live long and dont grow old. When we looked at their other nutrients, we found they consume 100 times the RDA of everything. RDA stands for recommended death allowance because if you take it, you are going to die prematurely. There is no such thing as overdosing on vitamins and minerals. That is a medical myth designed to prevent you from consuming them. There has never been a case of anybody dying from Gods vitamins or minerals.
THE PROTOCOL FOR GULF WAR SYNDROME/ALS THAT HAS MOST HELPED ME!
See www.rainbowminerals.net for liquid Ionic minerals.
(Zn) Zinc 2 tsp.
(S)Sulfur 2 tsp.
(Cu) Copper 1 ounce for one week 1 tsp. thereafter
(Ag) Silver 2 tsp.
(Mg) Magnesium4 tsp.
(Ca) Calcium2 tsp.
(Ca) Calcium2 tsp.
(Ag) Silver 2 tsp.
(Cr) Chromium 2 tsp.
(S) Sulfur 2 tsp.
(Se) Selenium 2 tsp.
1 capsule Licorice root
Liquid blue green algae from Upper Klamath Lake IN OREGON see below
Other Supplements: Vitamin D 400 Higher concentrations may be need depending on intestinal absorption. Vitamin B-Complex - 1 TBL Vitamin C 1 ½ TBL daily Probiotics as directed
Silver and Zinc are for combating the bacterial infection caused from the parasitic infection.
IMPORTANT NOTE: Food allergies, a removal of all wheat and gluten related products and all Milk, Cheese and related products and all products containing chocolate, for a minimum of 3to 6 months may be necessary to allow for the gut to heal and the gut flora and E3live to do its job. I personally have gone almost completely meat free other than occasionally deep-water fish. The reason why GW Vets and Fibro patients crave chocolate is because chocolate has a high magnesium content. What they are actually craving is magnesium. However patients with intestinal permeability tend to be extremely allergic to chocolate. Milk and wheat gluten proteins closely assimilate our own proteins and when an immune response is triggered to go after allergens, histamines and mast cells are released and can attack our own central nerves system. I found immediate relief from a lot of my intestinal symptoms with the use of E3Live algae and good gut flora; however some people may even be allergic to gut flora if the intestinal damage is severe. Benedryl may be of some use in stopping the release of histamines, mast cells and some of the sever allergic reactions. Dr. D'Adamo's book might be a good start for learning about your diet. If on vegan diet an increase in calcium should be added.
THE SECOND PRODUCT THAT HAS MOST HELPED ME FOR MY INTESTINAL SYMPTOMS:
IS A LIQUID PRODUCT THAT COMES FROZEN IS: ORGANIC E3LIVE AND ENIVA'S LIVING HEALTH FRIENDLY FLORA. CLICK LINKS BELOW.
Eniva's Living Health pro-biotics,
Click here for Eniva's Complete line of Liquid Ionic Minerals and supplements:
E3 Earth's Essential Elements Liquid blue green algae from Upper Klamath Lake in Oregon. (Click Here)
*The information on this site is for educational purposes only. If you are ill, see a health care professional. However, it is your God-given right and your constitutional right under the right of privacy of the Ninth Amendment of the United States Constitution (See Griswold vs. Connecticut 381 US 479, June 7, 1965) to prescribe treatment for yourself, but this can involve risk. If you choose to use the information on this web site without theapproval of a health professional, you must assume the risk.
1. Bajorunas DR: Clinical manifestations of cancer-related hypercalcemia. Seminars in Oncology 17(2, Suppl 5): 16-25, 1990.
2. Mahon SM: Signs and symptoms associated with malignancy-induced hypercalcemia. Cancer Nursing 12(3): 153-160, 1989.
3. Ralston SH, Gallacher SJ, Patel U., et al.: Cancer-associated hypercalcemia: morbidity and mortality. Clinical experience in 126 treated patients. Annals of Internal Medicine 112(7): 499-504, 1990.
1. Warrell RP Jr: Metabolic emergencies. In: DeVita VT Jr, Hellman S, Rosenberg SA, eds.: Cancer: Principles and Practice of Oncology. Philadelphia, Pa: Lippincott-Raven Publishers, 5th ed., 1997, pp 2486-2493.
2. Bilezikian JP: Management of acute hypercalcemia. New England Journal of Medicine 326(18): 1196-1203, 1992.
3. Theriault RL: Hypercalcemia of malignancy: pathophysiology and implications for treatment. Oncology (Huntington NY) 7(1): 47-50, 1993.
4. Mundy GR: Pathophysiology of cancer-associated hypercalcemia. Seminars in Oncology 17(2, Suppl 5): 10-15, 1990.
5. Ralston SH, Gallacher SJ, Patel U., et al.: Cancer-associated hypercalcemia: morbidity and mortality. Clinical experience in 126 treated patients. Annals of Internal Medicine 112(7): 499-504, 1990.
6. Ritch PS: Treatment of cancer-related hypercalcemia. Seminars in Oncology 17(2, Suppl 5): 26-33, 1990.
7. Suki WN, Yium JJ, Von Minden M, et al.: Acute treatment of hypercalcemia with furosemide. New England Journal of Medicine 283(16): 836-840, 1970.
8. Ignoffo RJ, Tseng A: Focus on pamidronate: a biphosphonate compound for the treatment of hypercalcemia of malignancy. Hospital Formulary 26(10): 774-786, 1991.
9. Warrell RP: Etiology and current management of cancer-related hypercalcemia. Oncology (Huntington NY) 6(10): 37-43, 1992.
10. Coleman RE: Bisphosphonate treatment of bone metastases and hypercalcemia of malignancy. Oncology (Huntington NY) 5(8): 55-60, 1991.
11. McCloskey EV, Yates AJ, Beneton MN, et al.: Comparative effects of intravenous diphosphonates on calcium and skeletal metabolism in man. Bone 8(Suppl 1): S35-S41, 1987.
12. Flora L, Hassing GS, Cloyd GG, et al.: The long-term skeletal effects of EHDP in dogs. Metabolic Bone Disease and Related Research 3(4-5): 289-300, 1981.
13. Mautalen C, Gonzalez D, Blumenfeld EL, et al.: Spontaneous fractures of uninvolved bones in patients with Paget's disease during unduly prolonged treatment with disodium etidronate (EHDP). Clinical Orthopaedics and Related Research 207: 150-155, 1986.
14. Fleisch H: Bisphosphonates: pharmacology and use in the treatment of tumour-induced hypercalcaemic and metastatic bone disease. Drugs 42(6): 919-944, 1991.
15. Fenton AJ, Gutteridge DH, Kent GN, et al.: Intravenous aminobisphosphonate in Paget's disease: clinical, biochemical, histomorphometric and radiological responses. Clinical Endocrinology (Oxford) 34(3): 197-204, 1991.
16. Adamson BB, Gallacher SJ, Byars J, et al.: Mineralisation defects with pamidronate therapy for Paget's disease. Lancet 342(8885): 1459-1460, 1993.
17. Boyce BF, Adamson BB, Gallacher SJ, et al.: Mineralisation defects after pamidronate for Paget's disease. Lancet 343(8907): 1231-1232, 1994.
18. Gulcalp R, Ritch P, Wiernik PH, et al.: Comparative study of pamidronate disodium and etidronate disodium in the treatment of cancer-related hypercalcemia. Journal of Clinical Oncology 10(1): 134-142, 1992.
19. Novartis Pharmaceuticals Corporation: Aredia: package insert. May 1998.
20. Elomaa I, Blomqvist C, Porkka L, et al.: Diphosphonates for osteolytic metastases. Lancet I(8438): 1155-1156, 1985.
21. Nussbaum SR, Younger J, Vandepol CJ, et al.: Single-dose intravenous therapy with pamidronate for the treatment of hypercalcemia of malignancy: comparison of 30-, 60-, and 90-mg dosages. American Journal of Medicine 95(3): 297-304, 1993.
22. Burckhardt P, Thiebaud D, Perey L, et al.: Treatment of tumor-induced osteolysis by APD. Recent Results in Cancer Research 116: 54-66, 1989.
23. Bounameaux HM, Schifferli J, Montani JP, et al.: Renal failure associated with intravenous diphosphonates. Lancet 1(8322): 471, 1983.
24. Walker P, Watanabe S, Lawlor P, et al.: Subcutaneous clodronate. Lancet 348(9023): 345-346, 1996.
25. Walker P, Watanabe S, Lawlor P, et al.: Subcutaneous clodronate: a study evaluating efficacy in hypercalcemia of malignancy and local toxicity. Annals of Oncology 8(9): 915-916, 1997.
26. Ostenstad B, Andersen OK: Disodium pamidronate versus mithramycin in the management of tumour-associated hypercalcemia. Acta Oncologica 31(8): 861-864, 1992.
27. Ralston SH, Gardner MD, Dryburgh FJ, et al.: Comparison of aminohydroxypropylidene diphosphonate, mithramycin, and corticosteroids/calcitonin in the treatment of cancer-associated hypercalcaemia. Lancet 2(8461): 907-910, 1985.
28. Thiebaud D, Jacquet AF, Burckhardt P: Fast and effective treatment of malignant hypercalcemia: combination of suppositories of calcitonin and a single infusion of 3-amino 1-hydroxypropylidene-1-bisphosphonate. Annals of Internal Medicine 150(10): 2125-2128, 1990.
29. Ralston SH, Gallacher SJ, Dryburgh FJ, et al.: Treatment of severe hypercalcaemia with mithramycin and aminohydroxypropylidene bisphosphonate. Lancet 2(8605): 277, 1988.
30. Parsons V, Baum M, Self M: Effect of mithramycin on calcium and hydroxyproline metabolism in patients with malignant disease. British Medical Journal 1(538): 474-477, 1967.
31. Kennedy BJ: Metabolic and toxic effects of mithramycin during tumor therapy. American Journal of Medicine 49(4): 494-503, 1970.
32. Perlia CP, Gubisch NJ, Wolter J, et al.: Mithramycin treatment of hypercalcemia. Cancer 25(2): 389-394, 1970.
33. Ashby MA, Lazarchick J: Acquired dysfibrinogenemia secondary to mithramycin toxicity. American Journal of the Medical Sciences 292(1): 53-55, 1986.
34. Benedetti RG, Heilman KJ, Gabow PA: Nephrotoxicity following single dose mithramycin therapy. American Journal of Nephrology 3(5): 277-278, 1983.
35. Fillastre JP, Maitrot J, Canonne MA, et al.: Renal function and alterations in plasma electrolyte levels in normocalcaemic and hypercalaemic patients with malignant diseases, given an intravenous infusion of mithramycin. Chemotherapy 20(5): 280-295, 1974.
36. Purpora D, Ahern MJ, Silverman N: Toxic epidermal necrolysis after mithramycin. New England Journal of Medicine 299(25): 1412, 1978.
37. Bashir Y, Tomson CR: Cardiac arrest associated with hypokalaemia in a patient receiving mithramycin. Postgraduate Medical Journal 64(749): 228-229, 1988.
38. Ahr DJ, Scialla SJ, Kimball DB: Acquired platelet dysfunction following mithramycin therapy. Cancer 41(2): 448-454, 1978.
39. Margileth DA, Smith FE, Lane M: Sudden arterial occlusion associated with mithramycin therapy. Cancer 31(3): 708-712, 1973.
40. Warrell RP Jr, Murphy WK, Schulman P, et al.: A randomized double-blind study of gallium nitrate compared with etidronate for acute control of cancer-related hypercalcemia. Journal of Clinical Oncology 9(8): 1467-1475, 1991.
41. Warrell RP, Lovett D, Dilmanian FA, et al.: Low-dose gallium nitrate for prevention of osteolysis in myeloma: results of a pilot randomized study. Journal of Clinical Oncology 11(12): 2443-2450, 1993.
42. Tashjian AH, Voelkel EF, Levine L: Effects of hydrocortisone on the hypercalcemia and plasma levels of 13,14-dihydro-15-keto-prostaglandin E2 in mice bearing the HSDM1 fibrosarcoma. Biochemical and Biophysical Research Communications 74(1): 199-207, 1977.
43. Mundy GR, Rick ME, Turcotte R, et al.: Pathogenesis of hypercalcemia in lymphosarcoma cell leukemia: role of an osteoclast activating factor-like substance and a mechanism of action for glucocorticoid therapy. American Journal of Medicine 65(4): 600-606, 1978.
44. Ralston SH, Fogelman I, Gardiner MD, et al.: Relative contribution of humoral and metastatic factors to the pathogenesis of hypercalcemia in malignancy. British Medical Journal Clinical Research Edition 288(6428): 1405-1408, 1984.
45. Potts JT: Diseases of the parathyroid gland and other hyper- and hypocalcemic disorders. In: Isselbacher KJ, Braunwald E, Wilson JD, et al. Eds.: Principles of Internal Medicine. New York: McGraw-Hill, 1994, pp 2151-2171.
46. Massry SG, Mueller E, Silverman AG, et al.: Inorganic phosphate treatment of hypercalcemia. Archives of Internal Medicine 121(4): 307-312, 1968.
47. Hebert LA, Lemann J, Petersen JR, et al.: Studies of the mechanism by which phosphate infusion lowers serum calcium concentration. Journal of Clinical Investigation 45(12): 1886-1894, 1966.
48. Shackney S, Hasson J: Precipitous fall in serum calcium, hypotension, and acute renal failure after intravenous phosphate therapy for hypercalcemia: report of two cases. Annals of Internal Medicine 66(5): 906-916, 1967.
49. Goldsmith RS, Ingbar SH: Inorganic phosphate treatment of hypercalcemia of diverse etiologies. New England Journal of Medicine 274(1): 1-7, 1966.
50. Nolph KD, Stoltz M, Maher JF: Calcium free peritoneal dialysis: treatment of vitamin D intoxication. Archives of Internal Medicine 128(5): 809-814, 1971.
51. Cardella CJ, Birkin BL, Rapoport A: Role of dialysis in the treatment of severe hypercalcemia: report of two cases successfully treated with hemodialysis and review of the literature. Clinical Nephrology 12(6): 285-290, 1979.
52. Schreiner GE, Teehan BP: Dialysis of poisons and drugs - annual review. Transactions - American Society for Artificial Internal Organs 18(0): 563-599, 1972.
53. Stoltz ML, Nolph KD, Maher JF: Factors affecting calcium removal with calcium-free peritoneal dialysis 78(3): 389-398, 1971.
54. Seyberth HW, Segre GV, Morgan JL, et al.: Prostaglandins as mediators of hypercalcemia associated with certain types of cancer. New England Journal of Medicine 293(25): 1278-1283, 1975.
55. Seyberth HW, Segre GV, Hamet P, et al.: Characterization of the group of patients with the hypercalcemia of cancer who respond to treatment with prostaglandin synthesis inhibitors. Transactions - American Society for Artificial Internal Organs 89: 92-104, 1976.
56. Coombes RC, Neville AM, Bondy PK, et al.: Failure of indomethacin to reduce hydroxyproline excretion or hypercalcemia in patients with breast cancer. Prostaglandins 12(6): 1027-1035, 1976.
57. Brenner DE, Harvey HA, Lipton A, et al.: A study of prostaglandin E2, parathormone, and response to indomethacin in patients with hypercalcemia of malignancy. Cancer 49(3): 556-561, 1982.
58. Lad TE, Mishoulam HM, Shevrin DH, et al.: Treatment of cancer-associated hypercalcemia with cisplatin. Archives of Internal Medicine 147(2): 329-332, 1987.
59. List A.: Malignant hypercalcemia: the choice of therapy. Archives of Internal Medicine 151(3): 437-438, 1991.
60. Warrell RP, Israel R, Frisone M, et al.: Gallium nitrate for acute treatment of cancer-related hypercalcemia: a randomized, double-blind comparison to calcitonin. Annals of Internal Medicine 108(5): 669-674, 1988.
61. Blomqvist CP: Malignant hypercalcemia -- a hospital survey. Acta Medica Scandinavica 220(5): 455-463, 1986.
62. Mundy GR, Martin TJ.: The hypercalcemia of malignancy: pathogenesis and management. Metabolism 31(12): 1247-1277, 1982.
63. Fisken RA, Heath DA, Bold AM: Hypercalcaemia -- a hospital survey 49(196): 405-418, 1980.
· Knochel JP: Disorders of Magnesium Metabolism. Harrison's Principles of Internal 1994; 2: 2187-2189.
· Nadler JL, Rude RK: Disorders of Magnesium Metabolism. Clinical Disorders of Fluid and Electrolyte Metabolism 1995; 24: 623-637.
· Reinhart RA: Magnesium metabolism. Archives of Internal Medicine 1988; 148: 2415-2420[Medline].
· Rude RK, Singer FR: Magnesium deficiency and excess. Ann Rev Med 1981; 32: 245-259[Medline].
Genesis 9:15-17 And I will remember my covenant, which is between me and you and every living creature of all flesh: and the waters shall no more become a flood to destroy all flesh. 16 And the bow shall be in the cloud; and I will look upon it, that I may remember the everlasting covenant between God and every living creature of all flesh that is upon the earth. 17 And God said unto Noah, This is the token of the covenant, which I have established between me and all flesh that is upon the earth.
Gulf War Vets Home Page