Posted by Tony from ? (167.88.192.30) on Thursday, October 03, 2002 at 2:29PM :
Gulf War Syndrome FMS/ CFS & ALS:
By George Nadzan
Medical Reporter
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.
Diagnosis
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.
Physical:
· 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.
Frequency:
· 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%.
Lab Studies:
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.
Other Tests:
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.
Normal calcium homeostasis
Hormonal influences
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.
Renal function
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:
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.
Neurological symptoms
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.[2] Abnormal
electroencephalograms are seen in patients with marked hypercalcemia.[1]
Cardiovascular symptoms
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
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.
Renal symptoms
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.
Bone symptoms
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 1˝ 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. That’s 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 don’t 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 don’t 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 God’s vitamins or minerals.
THE PROTOCOL FOR GULF WAR SYNDROME/ALS THAT HAS MOST HELPED ME!
See www.rainbowminerals.net for liquid Ionic minerals.
A.M.
P.M.
(Zn) Zinc – 2 tsp.
(S)Sulfur – 2
tsp.
(Cu) Copper – 1 ounce for one week 1
tsp. thereafter
(Ag) Silver – 2 tsp.
(Mg) Magnesium—4 tsp.
(Mg) Magnesium—4tsp
(Ca) Calcium—2 tsp.
(Ca) Calcium—2 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
˝ 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.
References:
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.
References:
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 radiol
-- Tony
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