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DUH, I am so dumb, CowgirlJane - have you tried calcitriol? That might help. I'm trying to find the one baby pills again, I had problems with the big Calcium pills and could try to find that mini I used to do before I tried the chews and started to choke on them.

Btw, have you been checked for any swallowing disorder or gastroparesis?

"Calcitriol will work only if you get the right amount of calcium from the foods you eat. If you get too much calcium from foods, you may experience serious side effects of calcitriol, and if you do not get enough calcium from foods, calcitriol will not control your condition."

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http://www.jaoa.org/content/109/11/601.full.pdf+html
Nutritional deficiences after gastric bypass surgery

http://www.eje-online.org/content/165/2/171.full.pdf+html
The Endocrine Society’s Clinical Practice Guideline on endocrine and nutritional

management of the post-bariatric surgery patient: Commentary from a European Perspective

http://pen.sagepub.com/content/35/5_suppl/52S.full.pdf+html
Nutrition and Metabolic Complications After Bariatric Surgery and Their Treatment

http://spectrum.diabetesjournals.org/content/25/4/222.full.pdf+html
Standardizing the Evolution of the Postoperative Bariatric Diet

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3432875/
The Neurological Complications of Nutritional Deficiency following Bariatric Surgery

http://www.ncbi.nlm.nih.gov/pubmed/20202584
Postoperative metabolic and nutritional complications of bariatric surgery.
Patients who have undergone bariatric surgery require indefinite, regular follow-up care

by physicians who need to follow laboratory parameters of macronutrient as well as

micronutrient malnutrition. Physicians who care for patients after bariatric surgery need

to be familiar with common postoperative syndromes that result from specific nutrient

deficiencies.

http://www.ncbi.nlm.nih.gov/pubmed/20152742
Medical follow up after bariatric surgery: nutritional and drug issues. General

recommendations for the prevention and treatment of nutritional deficiencies.
The risk of nutritional deficiencies depends on the percentage of weight loss and the type

of surgical procedure performed. Purely restrictive procedures (AGB, SG), for example, can

induce digestive symptoms, food intolerance or maladaptative eating behaviours due to pre-

or postsurgical eating disorders. Iron deficiency is common with the three types of

bariatric surgery, especially in menstruating women. Rare deficiencies can lead to serious

complications such as encephalopathy or protein-energy malnutrition. Long-term problems

such as changes in bone metabolism or neurological complications need to be carefully

monitored. In addition, routine nutritional screening, recommendations for appropriate

supplements and monitoring compliance are imperative, whatever the bariatric procedure.

Key points are: (1) virtually routine mineral and Multivitamin supplementation; and (3)

regular, life-long, follow-up of all patients. The role of the general practitioner has

also to be emphasized: clinical visits and follow-ups should be monitored and coordinated

with the bariatric team, including the surgeon, the obesity specialist, the dietitian and

mental health professionals.

http://www.ncbi.nlm.nih.gov/pubmed/20363593
Micronutrient deficiencies after bariatric surgery.
The literature suggests that bariatric surgery patients are at risk for deficiency of the

following nutrients after surgery: Vitamins B(12), B(1), C, folate, A, D, and K, along

with the trace minerals Iron, selenium, zinc, and copper. Over-the-counter Multivitamin

and mineral supplements do not provide adequate amounts of certain nutrients such as

Vitamin B(12), iron, or fat-soluble Vitamins and patients will require additional doses of

prophylactic supplementation life-long to maintain optimal micronutrient status. In

addition, preconception care for adequate prenatal supplementation is critical for

pregnant women who have undergone bariatric surgery, as iron, Vitamin A, Vitamin B(12),

vitamin K, and folate deficiencies are associated with maternal and fetal complications,

including severe anemia, congenital abnormalities, low birth weight, and failure to

thrive. All bariatric surgery patients would be best served by receiving regular

monitoring of serum nutrient levels starting at 3 mo after surgery and periodically

thereafter.

http://www.ncbi.nlm.nih.gov/pubmed/22525731
Nutritional deficiencies after bariatric surgery.
The major macronutrient deficiency after bariatric surgery is Protein malnutrition.

Deficiencies in micronutrients, which include trace elements, essential minerals, and

water-soluble and fat-soluble vitamins, are common before bariatric surgery and often

persist postoperatively, despite universal recommendations on multivitamin and mineral

supplements. Other disorders, including small intestinal bacterial overgrowth, can promote

micronutrient deficiencies, especially in patients with diabetes mellitus. Recognition of

the clinical presentations of micronutrient deficiencies is important, both to enable

early intervention and to minimize long-term adverse effects. A major clinical concern is

the relationship between Vitamin D deficiency and the development of metabolic bone

diseases, such as osteoporosis or osteomalacia; metabolic bone diseases may explain the

increased risk of hip fracture in patients after RYGB. Further studies are required to

determine the optimal levels of nutrient supplementation and whether postoperative

laboratory monitoring effectively detects nutrient deficiencies. In the absence of such

data, clinicians should inquire about and treat symptoms that suggest nutrient

deficiencies.

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http://www.ncbi.nlm.nih.gov/pubmed/20842487

Prevention and treatment of peripheral neuropathy after bariatric surgery.
As a result, deficiencies in Vitamins, minerals, and trace elements may develop, leading

to a variety of neurologic complications. The peripheral neuropathies best described with

a clear-cut cause are an acute, frequently painful neuropathy or polyradiculoneuropathy

associated with thiamine deficiency, and an isolated neuropathy or myeloneuropathy

associated with deficiencies of either Vitamin B12 or copper. Thiamine deficiency tends to

occur in the first weeks or months after surgery, vitamin B12 deficiency may develop at

any time from a few years to many years after surgery, and copper deficiency tends to be a

fairly late complication, developing several years to many years following surgery.

Patients who have undergone bariatric surgery may also have an increased risk of

developing focal neuropathies, though these are less clearly related to specific

nutritional deficiencies.Ideally, one would like to prevent these neuropathies, but there

is no consensus of opinion as to what vitamins and micronutrients need to be taken

following bariatric surgery. In addition, many patients who take supplements early on fail

to maintain the regimen even though some of the neuropathies can occur fairly late.

Supplements frequently recommended include a multivitamin, Iron, Vitamin D, folic acid,

calcium citrate, and vitamin B12. Although thiamine is typically included in a

multivitamin, the amount is fairly small, so I recommend adding 100 mg daily for at least

the first year. Some have suggested zinc supplementation, but this is potentially

problematic because exogenous zinc may interfere with copper absorption. Obtaining blood

work every 6 months after surgery will help to identify and treat nutritional deficiencies

early.For those patients who have had a bariatric procedure and then develop a neuropathy,

evaluating levels of thiamine, copper, vitamin B12, methylmalonic acid, and homocystine is

indicated. In addition, since one deficiency is frequently associated with others,

obtaining levels of Vitamin A, C, D, K, and E, as well as iron, zinc, selenium, and

magnesium is worthwhile. Checking total Protein, albumin, and cholesterol also gives a

sense of general nutritional status. Occasionally, no clear-cut deficiency of a vitamin,

mineral, or trace element can be identified in patients with various peripheral nervous

system manifestations. Nevertheless, these patients may have at least some recovery with

improving nutritional intake and vitamin supplementation, suggesting that we still do not

fully understand how nutritional status affects the peripheral nervous system.

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http://www.medscape.com/viewarticle/803376

Proton Pump Inhibitors and Risk of Vitamin and Mineral Deficiency
PPIs have been associated with an increased risk of vitamin and mineral deficiencies

impacting vitamin B12, Vitamin C, Calcium, Iron and magnesium metabolism. While these

risks are considered to be relatively low in the general population, they may be notable

in elderly and malnourished patients

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http://www.ncbi.nlm.nih.gov/pubmed/23642197
Annu Rev Nutr. 2013;33:183-203. doi: 10.1146/annurev-nutr-071812-161225.
Epub 2013 Apr 29.
Nutrient deficiencies after gastric bypass surgery.
"Diet and multivitamin use are unlikely to consistently prevent deficiency, thus supplementation with additional specific nutrients is often needed"

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http://www.ncbi.nlm.nih.gov/pubmed/20842487
Prevention and treatment of peripheral neuropathy after bariatric surgery.
As a result, deficiencies in Vitamins, minerals, and trace elements may develop, leading to a variety of neurologic complications. The peripheral neuropathies best described with a clear-cut cause are an acute, frequently painful neuropathy or polyradiculoneuropathy associated with thiamine deficiency, and an isolated neuropathy or myeloneuropathy associated with deficiencies of either Vitamin B12 or copper. Thiamine deficiency tends to occur in the first weeks or months after surgery, vitamin B12 deficiency may develop at any time from a few years to many years after surgery, and copper deficiency tends to be a fairly late complication, developing several years to many years following surgery. Patients who have undergone bariatric surgery may also have an increased risk of developing focal neuropathies, though these are less clearly related to specific nutritional deficiencies.Ideally, one would like to prevent these neuropathies, but there is no consensus of opinion as to what vitamins and micronutrients need to be taken following bariatric surgery. In addition, many patients who take supplements early on fail to maintain the regimen even though some of the neuropathies can occur fairly late. Supplements frequently recommended include a multivitamin, Iron, vitamin D, folic acid, calcium citrate, and vitamin B12. Although thiamine is typically included in a multivitamin, the amount is fairly small, so I recommend adding 100 mg daily for at least the first year. Some have suggested zinc supplementation, but this is potentially problematic because exogenous zinc may interfere with copper absorption. Obtaining blood work every 6 months after surgery will help to identify and treat nutritional deficiencies early.For those patients who have had a bariatric procedure and then develop a neuropathy, evaluating levels of thiamine, copper, vitamin B12, methylmalonic acid, and homocystine is indicated. In addition, since one deficiency is frequently associated with others, obtaining levels of vitamin A, C, D, K, and E, as well as iron, zinc, selenium, and magnesium is worthwhile. Checking total Protein, albumin, and cholesterol also gives a sense of general nutritional status. Occasionally, no clear-cut deficiency of a vitamin, mineral, or trace element can be identified in patients with various peripheral nervous system manifestations. Nevertheless, these patients may have at least some recovery with improving nutritional intake and vitamin supplementation, suggesting that we still do not fully understand how nutritional status affects the peripheral nervous system.

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http://www.ncbi.nlm.nih.gov/pubmed/22525731
Nutritional deficiencies after bariatric surgery.
The major macronutrient deficiency after bariatric surgery is Protein malnutrition. Deficiencies in micronutrients, which include trace elements, essential minerals, and water-soluble and fat-soluble Vitamins, are common before bariatric surgery and often persist postoperatively, despite universal recommendations on multivitamin and mineral supplements. Other disorders, including small intestinal bacterial overgrowth, can promote micronutrient deficiencies, especially in patients with diabetes mellitus. Recognition of the clinical presentations of micronutrient deficiencies is important, both to enable early intervention and to minimize long-term adverse effects. A major clinical concern is the relationship between Vitamin D deficiency and the development of metabolic bone diseases, such as osteoporosis or osteomalacia; metabolic bone diseases may explain the increased risk of hip fracture in patients after RYGB. Further studies are required to determine the optimal levels of nutrient supplementation and whether postoperative laboratory monitoring effectively detects nutrient deficiencies. In the absence of such data, clinicians should inquire about and treat symptoms that suggest nutrient deficiencies.

Share this post


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http://www.ncbi.nlm.nih.gov/pubmed/20202584
Postoperative metabolic and nutritional complications of bariatric surgery.
Patients who have undergone bariatric surgery require indefinite, regular follow-up care by physicians who need to follow laboratory parameters of macronutrient as well as micronutrient malnutrition. Physicians who care for patients after bariatric surgery need to be familiar with common postoperative syndromes that result from specific nutrient deficiencies.

http://www.ncbi.nlm.nih.gov/pubmed/20152742
Medical follow up after bariatric surgery: nutritional and drug issues. General recommendations for the prevention and treatment of nutritional deficiencies.
The risk of nutritional deficiencies depends on the percentage of weight loss and the type of surgical procedure performed. Purely restrictive procedures (AGB, SG), for example, can induce digestive symptoms, food intolerance or maladaptative eating behaviours due to pre- or postsurgical eating disorders. Iron deficiency is common with the three types of bariatric surgery, especially in menstruating women. Rare deficiencies can lead to serious complications such as encephalopathy or protein-energy malnutrition. Long-term problems such as changes in bone metabolism or neurological complications need to be carefully monitored. In addition, routine nutritional screening, recommendations for appropriate supplements and monitoring compliance are imperative, whatever the bariatric procedure. Key points are: (1) virtually routine mineral and multivitamin supplementation; and (3) regular, life-long, follow-up of all patients. The role of the general practitioner has also to be emphasized: clinical visits and follow-ups should be monitored and coordinated with the bariatric team, including the surgeon, the obesity specialist, the dietitian and mental health professionals.

http://www.ncbi.nlm.nih.gov/pubmed/20363593
Micronutrient deficiencies after bariatric surgery.
The literature suggests that bariatric surgery patients are at risk for deficiency of the following nutrients after surgery: Vitamins B(12), B(1), C, folate, A, D, and K, along with the trace minerals Iron, selenium, zinc, and copper. Over-the-counter multivitamin and mineral supplements do not provide adequate amounts of certain nutrients such as Vitamin B(12), iron, or fat-soluble Vitamins and patients will require additional doses of prophylactic supplementation life-long to maintain optimal micronutrient status. In addition, preconception care for adequate prenatal supplementation is critical for pregnant women who have undergone bariatric surgery, as iron, Vitamin A, vitamin B(12), vitamin K, and folate deficiencies are associated with maternal and fetal complications, including severe anemia, congenital abnormalities, low birth weight, and failure to thrive. All bariatric surgery patients would be best served by receiving regular monitoring of serum nutrient levels starting at 3 mo after surgery and periodically thereafter.

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Like liver disease, an elevated Vitamin B12 level cannot adequately provide a diagnosis of leukemia. But it may indicate the need for further testing. Leukemia is a type of cancer in which white blood cells are higher than normal in either your blood or bone marrow. It also causes a reduction in red blood cells and platelets, cells needed for clotting blood.

This basically means that your body will not hold on to the Vitamin unless it is used. The unnecessary vitamin remaining in your body will be excreted in your urine. As stated above, there are instances where a person's kidneys are not filtering properly & may cause an abundance of a multitude of substances. That being stated, the BUN & Creatine levels would have been out of the normal range indicating your kidneys are not functioning properly.

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Do people get their copper checked? Mine went high.

http://www.ncbi.nlm.nih.gov/pubmed/17727313
Clin Chem Lab Med. 2007;45(10):1402-10.
Clinical significance of the laboratory determination of low serum copper in adults.
Kumar N, Butz JA, Burritt MF.
SourceDepartment of Neurology, mayo Clinic, Rochester, MN55905, USA. kumar.neeraj@mayo.edu
In six of the 57 patients with low serum copper, the low copper was due to Wilson disease. In the remaining 51 patients, copper deficiency due to an underlying cause was identified in 38 as a reason for the low serum copper. The most commonly identified neurological manifestation of copper deficiency was myeloneuropathy. Coexisting nutrient deficiencies and hematological manifestations of copper deficiency were often but not invariably present.
CONCLUSIONS: Copper deficiency, Wilson disease (or a carrier state), and aceruloplasminemia are all associated with low serum copper. The presence of coexisting neurological or hematological manifestations that are recognized sequelae of copper deficiency should be considered prior to making a diagnosis of copper deficiency. Gastrointestinal disease or surgery is a common cause of acquired copper deficiency. Even in patients in whom low serum copper is indicative of copper deficiency, the cause of the copper-deficient state may not be evident.

http://www.ncbi.nlm.nih.gov/pubmed/15249607
Neurology. 2004 Jul 13;63(1):33-9.
Copper deficiency myelopathy produces a clinical picture like subacute combined degeneration.
Kumar N, Gross JB Jr, Ahlskog JE.
SourceDepartment of Neurology, Mayo Clinic, Rochester, MN, USA. kumar.neeraj@mayo.edu
RESULTS: Thirteen such patients were found, 11 of them in a 15-month period. All patients presented with prominent gait difficulty, reflecting a sensory ataxia due to dorsal column dysfunction and lower limb spasticity. All patients had polyneuropathy. A high or high-normal serum zinc level was seen in 7 of the 11 patients for whom this information was available. Somatosensory evoked potential studies done in eight patients showed impaired conduction in central proprioceptive pathways. Dorsal column signal change on spine MRI was present in three patients. An initial clue to the diagnosis was a very low ceruloplasmin level; further tests of copper metabolism excluded Wilson disease. The cause remained unexplained in most patients. Oral copper supplementation restored normal or near-normal copper levels in 7 of the 12 patients in whom adequate follow-up data were available; parenteral supplementation restored normal level in 3 further patients. Copper supplementation prevented further neurologic deterioration, but the degree of actual improvement was variable.
CONCLUSIONS: Unrecognized copper deficiency appears to be a common cause of idiopathic myelopathy in adults. The clinical picture bears striking similarities to the syndrome of subacute combined degeneration associated with Vitamin B12 deficiency. Early recognition and copper supplementation may prevent neurologic deterioration.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3432875/
J Obes. 2012; 2012: 608534.
Published online 2012 June 13. doi: 10.1155/2012/608534PMCID: PMC3432875The Neurological Complications of Nutritional Deficiency following Bariatric Surgery

http://www.ncbi.nlm.nih.gov/pubmed/19365170
Am J Med Sci. 2009 Apr;337(4):256-8. doi: 10.1097/MAJ.0b013e31818ad0ff.
Copper deficiency after gastric surgery: a reason for caution.
Prodan CI, Bottomley SS, Vincent AS, Cowan LD, Greenwood-Van Meerveld B, Holland NR, Lind SE.
SourceFrom the Department of Neurology, Veterans Affairs Medical Center and the University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA. calin-prodan@ouhsc.edu
BACKGROUND: : Acquired copper deficiency in adults leads to hematological and neurological manifestations that mimic Vitamin B12 deficiency. A significant number of patients with copper deficiency syndrome have a history of gastric surgery, often remote. We sought to determine whether copper deficiency is present in a population of individuals with longstanding partial gastric resection.
RESULTS: : Hypocupremia and symptoms of copper deficiency were detected in patients with partial gastric resection in contrast to controls (3/20 versus 0/50, P = 0.02). Serum copper and ceruloplasmin levels were significantly lower in individuals with partial gastric resection than in controls (P = 0.04 and P = 0.001, respectively). The mean interval between gastric surgery and testing was 20.7 years.
CONCLUSIONS: : Our results indicate that a significant number of individuals with longstanding history of partial gastric resection have undiagnosed hypocupremia. Screening for copper deficiency after gastric surgery may prevent the development of hematological and neurological complications in these patients.

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http://www.doctorweight.com/bariatricsurgery/narrowingstomach/antirefluxsleevegastroplasty/
At the same time, it is known that 30% of patients complain of heartburn after the procedure, necessitating administration of omeprazole (a drug reducing gastric acid production). This is because the original sleeve gastrectomy procedure destroys the valve mechanism of the junction between the esophagus and the stomach, converting it into a direct tube. If a sleeve gastrectomy is performed as the first stage of gastric bypass, then after the second stage (gastrojejunal bypass) the heartburn disappears. But if a sleeve gastrectomy is planned as a sole operation, then persistent heartburn might be a serious problem for the patient.

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Clinical Biochemistry

Volume 36, Issue 8, November 2003, Pages 585–590

Elevated levels of serum cobalamin may be a sign of a serious, even life-threatening, disease. Hematologic disorders like chronic myelogeneous leukemia, promyelocytic leukemia, polycythemia vera and also the hypereosinophilic syndrome can result in elevated levels of cobalamin. Not surprisingly, a rise of the cobalamin concentration in serum is one of the diagnostic criteria for the latter two diseases. The increase in circulating cobalamin levels is predominantly caused by enhanced production of haptocorrin. Several liver diseases like acute hepatitis, cirrhosis, hepatocellular carcinoma and metastatic liver disease can also be accompanied by an increase in circulating cobalamin. This phenomenon is predominantly caused by cobalamin release during hepatic cytolysis and/or decreased cobalamin clearance by the affected liver. Altogether it can be concluded that an observed elevation of cobalamin in blood merits the a full diagnostic work up to assess the presence of disease.

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