Calciphylaxis, molecular mimicry and egg white albumin; an experiment, n = 1

Calciphylaxis is a rare type of wound that is associated with hyperparathyroidism and is most commonly seen in patients who are receiving kidney dialysis due to end stage renal disease. The condition is also associated with an eight times increased risk of morbidity (death) compared to patients who don’t have calciphylaxis.

The term calciphylaxis came to my attention this year when I found out that I had an elevated parathyroid hormone level. See the following posts for more information about calciphylaxis and about other symptoms associated with elevated parathyroid hormone:

  1. Secondary hyperparathyroidism, calcium deficiency and irritability
  2. Elevated parathyroid hormone (PTH) and 1-25-D, calcium deficiency and calciphylaxis‘Calciphylaxis is more of a risk with end stage renal disease but it has also been found in people who had normal vitamin D levels and normal kidney health. And “high dose vitamin D administration is capable of inducing STC (soft tissue calcification) and calciphylaxis in murine models. [56, 57] In an attempt to reestablish normal calcium-phosphate homeostasis, ESRD patients receive vitamin D analogs that could theoretically increase their risk of calciphylaxis if hyperphosphatemia and hypercalcemia ensued. [58, 59]” [3]

    “Experimental sensitizing events and agents included nephrectomy and exposure to parathyroid hormone (PTH) and vitamin D. Substances used as challengers included egg albumin and metallic salts. Calciphylaxis was the end result.4  – from a 1962 study, abstract is free. [4.5]’

  3. Secondary hyperparathyroidism and calciphylaxis symptoms; an update with lab values
  4. Calciphylaxis may be caused by several different nutrient issues

Antibodies against chemicals that are a normal part of the human body can develop in autoimmune disease. The term molecular mimicry refers to the autoimmune antibodies that may be manufactured by overactive white blood cells in response to a large foreign protein allergens that may have made it through ‘leaky’ intestinal walls into the blood stream.  See: Robert S. Fujinami, et. al., Molecular Mimicry, Bystander Activation, or Viral Persistence: Infections and Autoimmune Disease, Clin Microbiol Rev. 2006 Jan; 19(1): 80–94.

To skip to the point, egg white albumin is very similar to the albumin found in human blood. It is an essential protein within plasma and it helps maintain fluid balance between the blood plasma and extracellular fluid (too much extracellular fluid would be noticeable as edema – puffy ankles from excess fluid collecting outside of the cells and blood vessels.

After finding the research about egg white albumin on September 24, I eliminated egg white from my diet. My symptoms did get better fairly rapidly but I had tried a few strategies at the same time so it wasn’t clear whether stopping egg white had been necessary for the symptoms to improve or whether the other strategies I had tried may have been adequate on their own — so after feeling better for a couple weeks I decided to retry egg white to see if eliminating them had been an unnecessary strategy. Sadly I found that the day after trying egg white albumin again (in the form of baked chocolate chip cookies) my skin sores returned. I stopped eating egg white again. The sores aren’t as bad as they had been in September but calciphylaxis sores are termed necrotic wounds and necrosis means death and dead tissue in wounds can lead to gangrene and septic bloodsteam infections.

Open sores with oozing plasma that sticks to fabric is unpleasant and painful as well as being associated with an eight times increased risk of morbidity (which means death of the patient).

So I don’t have proof that my body set up autoimmune antibodies to albumin but I would rather stop eating egg white than continue having oozing sores – that is my choice, it is my body and I should have a right to take care of it to the best of my own ability rather than having to follow mainstream medical advice about a condition that is not well understood but is associated with an increased risk of death.

For more information about albumin antibodies and autoimmune disease see:

  • Rodríguez-Juan C, et. al., Increased levels of bovine serum albumin antibodies in patients with type 1 diabetes and celiac disease-related antibodies., J Pediatr Gastroenterol Nutr. 2003 Aug;37(2):132-5.
  • Excerpt from Abstract: “Although 46% of patients with autoimmune thyroiditis had positive results, the level detected (22.1 +/- 8.7 AU) was significantly lower than that recorded in patients with type 1 diabetes who had celiac disease antibodies (P = 0.04) and celiac patients (P = 0.04). Healthy volunteers showed no antibodies against bovine serum albumin.”  “Thirty-one percent of patients with diabetes yielded a positive result…” End stage renal disease is actually a significant risk for people with autoimmune Type 1 Diabetes because diabetes can cause an increased load on the kidneys from excess blood sugar and increased leaking of protein into the urine. Thirty-one percent of them might benefit from avoiding beef (bovine) or egg white albumin – but more research would probably be necessary before an ‘evidence-based’ recommendation could be made – except Rodriquez- Juan C, et al, did get a nice start on the project.

 

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

Calciphylaxis may be caused by several different nutrient issues

Calciphylaxis usually includes an imbalance of calcium and phosphate and a deficiency of protein C may also be involved. Protein C deficiency may be caused by genetic or acquired reasons. Protein C is involved in blood clotting. Vascular and soft tissue calcification frequently is also present in patients with calciphylaxis symptoms. The mineral content of the calciphylaxis sores has been found to resemble the mineral balance of bone.

Imbalance in vitamin D and hormone D metabolism might affect magnesium levels in some unusual cases and may promote intestinal malabsorption of magnesium. However elevated magnesium is more typically found in patients who have calciphylaxis as a side effect of dialysis in end stage renal disease. The kidney disease causes an abnormal lack of hormone D because the kidneys in normal health are the only place where vitamin D is activated into the hormone D form.

These are copies of links that I was reading and Tweeted last night:

  1. Mineral substance of bone tissue and of experimental cutaneous calcinosis in rats: chemical analysis and ESR study.
  2. Calciphylaxis assoc w cholangiocarcinoma… /heparin & vit K didn’t help/ Thrombosis & protein C deficiency involved/
  3. Retrospective analysis of tissue plasminogen activator as an adjuvant treatment for calciphylaxis. /Ca P homeostasis/
  4. Calciphylaxis… “the reported median survival time is 2.6 months after diagnosis,”
  5. Aggressive calciphylaxis in end-stage renal disease… /assoc w vascular & soft tissue calcification/
  6. Calciphylaxis is a cutaneous process without involvement of internal organs… /assoc w vascular calcification/
  7. Net-like pattern of calcification on plain soft-tissue radiographs in patients with calciphylaxis. – PubMed – NCBI
  8. Is calciphylaxis best treated surgically or medically? – PubMed – NCBI
  9. Calciphylaxis in a morbidly obese woman w RA presenting w severe weight loss & vit D def. /pamidronate & D tx worked/
  10. Calciphylaxis in the absence of end-stage renal disease. – PubMed – NCBI /low vit D but tx surgery/
  11. The surgical management of renal hyperparathyroidism. – PubMed – NCBI
  12. Secondary hyperparathyroidism in children with chronic renal failure: pathogenesis and treatment. – PubMed – NCBI
  13. Vitamin D, parathyroid hormone, and acroosteolysis in systemic sclerosis. /low 25D w 2ndary hyperPTH in sunny climate

  14. Bone metabolism in celiac disease. – /following gluten free diet for 6 mo normalized 25D, calcium & PTH levels/

  15. Hypomagnesemia. Suppression of secondary hyperparathyroidism in chronic renal failure. – PubMed – NCBI

  16. Magnesium deficiency: possible role in osteoporosis associated with gluten-sensitive enteropathy. – PubMed – NCBI
  17. Recent data on magnesium & osteoporosis. “Mg def in post-menopausal osteoporosis, prob caused by Mg malabsorption.”
  18. [The significance of magnesium in medicine. (II) Disturbances of Mg metabolism & their treatment (author’s transl)].
  19. Metabolic disorders of cattle. /pellagra discussed, zinc, B6 Cu Mg def, malabsorption, iron overload can deplete B3/

Why do I care? because even though my symptoms are unusual I feel that I still deserve individualized health care. As a dietitian I was taught to look up information about any unusual diagnoses that patients might have and to provide individualized guidance if available or provide background information to help patients be able to make more informed choices about their treatment plan.

I also care because I think women deserve individualized healthcare even if we may get emotional or moody. Physical and mental illness symptoms can be related to underlying issues and simply medicating a symptom not only fails to address the underlying issue but it also fails to look for an underlying issue which can be life threatening if care is delayed in acute situations:

Whether male or female in a for-profit health industry being your own patient advocate or hiring a professional patient advocate may be life saving when navigating the increasingly complex health care system.

See the previous post for my own patient struggles with symptoms of hyperparathyroidism and calciphylaxis like sores: Secondary hyperparathyroidism and calciphylaxis symptoms; an update with lab values

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

Secondary hyperparathyroidism and calciphylaxis symptoms; an update with lab values

Last month I described some health difficulties that I had been experiencing for quite awhile. Lab tests that had been drawn earlier in the summer suggested that the problem might be secondary hyperparathyroidism and I also had been having a number of odd symptoms including calciphylaxis that can be associated with secondary hyperparathyroidism but is a more common in end stage renal disease (ESRD) particularly for patients on dialysis who were also receiving calcium supplements (and calciphylaxis is associated with eight times increased morbidity in ESRD). In the second post I reported that I was already feeling much better on the treatment plan that I had developed for myself.

I started taking 300-500 mg calcium per day based on the theory that the symptoms were related to calcium deficiency secondary hyperparathyroidism. I also increased my protein intake except for eliminating egg white and tree nuts from my diet – as a precaution in case I had developed autoimmune sensitivity to those protein sources which I had been eating more regularly than other foods during a time when I wasn’t eating enough overall. A steroid skin cream containing Triamcinolon 0.5% applied twice a day helped the calciphylaxis like skin sores heal. And I started taking 40 mg Benicar/olmesartan per day in an attempt to modify the low vitamin 25 D and vitamin 1, 25 D > 42 pg/mL. Levels of vitamin 1, 25 D above 42 pg/mL signals the bones to release calcium and phosphorus and can increase risks of osteoporosis and soft tissue calcification. [1, 2: MPKB- Science behind olmesartan (Benicar).]

  1. Secondary hyperparathyroidism, calcium deficiency and irritability, 
  2. Elevated parathyroid hormone (PTH) and 1-25-D, calcium deficiency and calciphylaxis, 

The 6/15/15 lab values:

  • Parathyroid hormone level – PTH Intact – 154.1 pg/mL — normal range: [15.0-75.0]
  • Calcium – 8.8 mg/dL — normal range: [8.4-10.2]
  • Phosphorus was not ordered but would probably be good to check.
  • Vitamin D, 25 – 10.9 ng/mL — normal is considered: [30.0-100.0]
  • Vitamin D 1, 25 – 55 pg/mL — normal is considered: [18-72] (the active hormone D)

The 10/12/2015 lab values:

  • Parathyroid hormone level — PTH Intact — 66.1 pg/mL — normal range: [15.0-75.0]
  • Calcium — 9.3 mg/dL — normal range: [8.4-10.2]
  • Serum Phosporus — 3.6 mg/dL — normal range: [2.5-4.5]
  • Vitamin D, 25 — 18.4 ng/mL — normal range: [30.0-100.0]
  • Vitamin D 1, 25 — 36  pg/mL — normal range: [18-72] (the active hormone D)

So I started taking calcium supplements and 40 mg of Benicar on September 23 and on October 12 my parathyroid hormone level is back within the normal range. My active 1, 25 D is below the osteoporosis inducing level of 42 pg/mL and my inactive vitamin 25 D level increased from 10.9 to 18.4 ng/mL — even though I am not taking vitamin D supplements but I do get more than fifteen minutes of sunshine most days of the week. My calcium level is still within the normal range but it went up from near the low end of the range to closer to the middle, from 8.8 to 9.3 mg/dL.

During the last couple days the calcium supplements have been causing me to have increased muscle cramps and irritable mood and I found that soaking in Epsom salt tub or footbath helped reduce the muscle cramps and bad mood. So the balance between magnesium and calcium intake is important and intestinal malabsorption of magnesium may be part of the underlying problem.

Overall I’m feeling much better than I was in early September before I started taking the calcium supplements. I had been having a racing heartbeat on very little exertion (like tachycardia) and for a long time I had been having an internal jittery-ness that felt like a bottled up pressure that needed a release valve or pinprick to pop the overfull bubble. The painful skin sores had been a fairly new and very unpleasant development. So yippee I have skin again! And I can walk downstairs without having to pause to let my heart rate slowdown.

I still have autoimmune thyroid antibodies but my thyroid hormone and thyroid stimulating hormone levels are within normal range — 10/12/2015 lab values:

  • Serum Thyroglobulin AB — 41 IU/mL — normal range: [0-40]
  • Serum Thyroid Peroxidase AB — 301 IU/mL — normal range: [0-34]
  • T3 Free Serum — 4.09 pg/mL — normal range: [2.77-5.27]
  • T4 Free Serum — 1.14 ng/dL — normal range: [0.65-1.86]
  • Serum Thyroid Stimulating Hormone — 1.20 mIU/L — normal range: [0.46-4.68]

To prevent autoimmune hyperthyroid symptoms I have been avoiding foods containing gluten and iodine sources since receiving the diagnosis in 2013. The gluten protein molecule contains a section called gliadin that is chemically similar to the thyroid hormone. The chemical similarity between gliadin and the thyroid hormone may allow autoimmune thyroid antibodies to develop in susceptible individuals, so avoiding gluten in the diet may be helping reduce or prevent the production of the autoimmune thyroid antibodies.

–The bad news – my endocrinologist still wants me to take a vitamin D supplement for my low vitamin D. [previous post: Whether to be compliant or to be healthy seems like an easy question to answer

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

 

Elevated parathyroid hormone (PTH) and 1-25-D, calcium deficiency and calciphylaxis

I’m feeling so much better after only two days of calcium supplements that I feel like throwing a party. Fatigue is tiring. Replenishing supplies of a trace nutrient deficiency can help resolve symptoms so quickly that it feels like a miracle. I’ve experienced rapid resolution of symptoms in the past when I had a problem with low B1 intake [2] that was due to a low intake of everything – I had an anorexic appetite at the time which I later found may have been due to an underlying zinc deficiency.

The anorexic appetite symptom resolved when I added zinc and B6 supplements after reading about pyroluria. Pyroluria is not yet treated or accepted by most main stream health practitioners but it is believed to be due to a genetic defect affecting an enzyme that helps break down old hemoglobin for reuse and recycling. Molecules of B6 and zinc are involved in the process and in normal health would be recycled but if the person has the genetic modification than the B6 and zinc is released in urine rather than being retained for reuse. [1]

Calciphylaxis is a symptom that is not well understood but is associated with severe hyperparathyroidism. It is a rare symptom in the general population but is seen more frequently in people with end stage renal disease. When the kidneys are no longer able to make normal amounts of 1, 25 dihydroxy D the plasma calcium levels can drop. And to try to maintain normal calcium levels the body responds by having the parathyroid glands increase production of parathyroid hormone which in normal health would tell the kidneys to activate more 1, 25 dihydroxy D which would then tell the intestines to absorb more calcium and would tell the bones to release more calcium from storage. [3] But in end stage renal disease there aren’t functional kidneys and the elevated levels of parathyroid hormone can cause other symptoms like irregular or rapid heart rate or in severe cases calciphylaxis may occur.

Calciphylaxis “is a poorly understood and highly morbid syndrome of vascular calcification and skin necrosis.” [4] The word calciphylaxis may refer to the syndrome or to the patches of necrotic (decaying) tissue which may occur internally on the surface of bones or externally in patches on the surface of the skin. The decaying areas occur more commonly on the lower legs. The areas can first appear as reddish or purplish bruised areas that may feel like they have small hardened nodules under the skin. The skin surface may be itchy and eventually may break down to be an open wound that doesn’t heal easily. There is a risk of skin infections developing in the open wound which can become severe enough to cause sepsis and death as the patches of decaying skin or bone areas do not heal well.

Calciphylaxis is more of a risk with end stage renal disease but it has also been found in people who had normal vitamin D levels and normal kidney health. And “high dose vitamin D administration is capable of inducing STC (soft tissue calcification) and calciphylaxis in murine models. [56, 57] In an attempt to reestablish normal calcium-phosphate homeostasis, ESRD patients receive vitamin D analogs that could theoretically increase their risk of calciphylaxis if hyperphosphatemia and hypercalcemia ensued. [58, 59]” [3]

“Experimental sensitizing events and agents included nephrectomy and exposure to parathyroid hormone (PTH) and vitamin D. Substances used as challengers included egg albumin and metallic salts. Calciphylaxis was the end result.4  – from a 1962 study, abstract is free. [4.5]

Eczema is something I’ve had to cope with since infancy along with severe congestion problems. The images of calciphylaxis do not look quite like the itchy patches that I’ve been dealing with for a few months but they resemble the images of calciphylaxis more than they look like the patches of eczema that I’ve had off and on since infancy.

The fun thing about autoimmune disease is all the nifty weird symptoms that you get to experience – and which are so rare that many physicians don’t want to see you or the symptoms in their office –  because those unusual symptoms must be covered by some other specialist’s field. This quote said it well:  Calciphylaxis “is a poorly understood and highly morbid syndrome”. [4]  Maybe I wouldn’t want that syndrome to be my professional responsibility either, and maybe it is just too bad for me that it might be my personal responsibility whether I like it or not. However maybe I’m lucky that my professional and personal experiences have left me more informed about odd symptoms than other health professionals, and therefore I may possibly be better equipped to cope with the odd symptoms.

Thankfully just two days of calcium supplements (while continuing to avoid excess vitamin D and sunshine) have left me feeling less itchy and my open wound areas are beginning to form scabs instead of remaining open wounds with seeping plasma.

In normal physiology the activated hormone form, 1, 25 dihydroxy D, is typically found in elevated amounts only in areas of rapid growth or membrane breakdown, such as in scab formation by white blood cells, [6], and within the placenta during pregnancy. [5] – Maybe elevated 1, 25 dihydroxy D can also be an underlying problem causing calciphylaxis rather than it being due only to deficiency of the inactive vitamin 25-D or the active hormone 1, 25-D.

Yes, my vitamin 25-D level was low at 10.9 ng/mL and anything below 20-30 is considered deficient and I was recommended by my endocrinologist to take vitamin D and calcium. However my hormone 1, 25-D level was 55 pg/mL which is considered within the normal range by mainstream medicine (range: 18-72 pg/mL). Specialists in vitamin D/hormone D metabolism would consider levels of 1, 25-D above 42 pg/mL to be elevated enough to be an osteoporosis risk because above that level the bone cells start releasing calcium, phosphorus, and magnesium into the blood supply instead of absorbing the minerals from circulating plasma and storing them for increased bone strength or for later use. [7]

Calcium and magnesium are so important as electrically active ions that the body has a variety of ways to maintain the blood levels of the two minerals within a narrow range. Blood tests for calcium and magnesium levels may be normal even though there is inadequate dietary intake because the bones can act like a savings account at the bank. In normal health if the blood plasma dips a little low for calcium or magnesium, more minerals are released from the bone, and if levels are getting too elevated than more would be excreted by the kidneys, less would be absorbed by the intestines, and more would be absorbed into the bones for long term storage.

However if 1, 25-D levels are elevated above 42 pg/mL than even if calcium levels were elevated in the blood the abnormally elevated 1, 25-D level would still be telling the bones to release more calcium and for the intestines to absorb more calcium which would lead to way too much calcium for the kidneys to be able to excrete during good health let alone during renal disease (elevated blood calcium would normally signal the body to make more of the enzyme that de-activates 1, 25-D but some microbial pathogens seem to bypass our immune system by disabling our body’s ability to make that enzyme). Adequate magnesium is necessary for the kidneys to be able to excrete calcium and elevated 1, 25-D causes the intestines to preferentially absorb calcium rather than magnesium.

And it turns out that eczema is an autoimmune disease so I may have been trying to figure out how to feel healthier since I was a baby. [8]

My mother gave up trying to spoon feed me. She said I would spit food into my hand, look at it, then put it back into my mouth before swallowing. She put cookie sheets around my highchair to block the mess (and possibly the view) and left me to feed myself from a fairly early age. I still don’t like to be fed by others, whether it’s just a taste of something on a spoon, or whether it is a dietary supplement that might cause my underlying autoimmune condition to worsen.

I’m feeling less itchy and the open wound areas are beginning to heal. The tachycardia problem is better, (having a rapid heart rate with little exercise), and an internal jittery feeling is less. The problem with trying to medicate a nutrient deficiency with psychiatric drugs is that the psychiatric drug can’t take the place of a nutrient in metabolic pathways. For years now physicians, family members and friends have been encouraging me to just take the psychiatric medication as prescribed and stop complaining about psychosomatic symptoms and imaginary problems. But the psychiatric medications that were offered all had bad side effects and while some helped slow down whirling thoughts they didn’t make the thoughts less sad or negative and they didn’t take away the internal feeling of tension.

I felt like a coiled spring internally, very jittery all the time and unable to concentrate as well as normal. I knew something was wrong and I knew feeling like a coiled spring all the time wasn’t an imaginary delusion and the feeling didn’t go away with the three different anti-psychotic medications that physicians or psychiatrists had me try.

We can’t afford ineffective health care as individuals or as a global community. Harsh medications that cause side effects in humans are probably also causing side effects in the health of the environment once the chemicals become waste products. Expensive pharmaceuticals that cause side effects in patients without addressing the person’s underlying condition are primarily helping the pharmaceutical company and may be causing the person’s condition to worsen over the long term.

Low protein intake may be involved as hypoalbuminemia is a risk factor for calciphylaxis. [9 -includes images of calciphylaxis wounds.] I don’t know for sure that my weird skin patches are early stage calciphylaxis wounds but I hadn’t been eating much protein in the weeks before my bruise like symptoms became more like open painful sores and I have probably had a low calcium intake ever since I started limiting my use of dairy products. I did take calcium supplements in the past but my chronic muscle cramps became a problem and the calcium seemed to make it worse. More recently not eating much for a couple weeks would have further reduced my intake of calcium from the sources such as sesame seeds and tree nuts that I normally do eat. Just two days of calcium supplements have helped me feel calm internally instead of jittery (I’m using about 500 mg spread out through the day in low doses). I’m also eating a more adequate amount of protein and other foods and the odd skin patches have less of a burning itchy painful feeling and the areas are starting to heal rather than remain open seeping wounds.

Twenty three and a half to fifty million Americans may have one or more types of autoimmune diseases. [10] So I don’t think that I am the only one who has been regularly told that her symptoms must all be imaginary and to go see a talk therapist or to go get stronger and stronger psychiatric medications. We can’t afford ineffective health care because it doesn’t help the patient and the medications may be bad for the environment once they become waste products. Calcium is a natural mineral that is not harmful to the environment and it is inexpensive.

6/15/15 lab values:

  • Parathyroid hormone level – PTH Intact – 154.1 pg/mL — normal range: [15.0-75.0]
  • Calcium – 8.8 mg/dL — normal range: [8.4-10.2]
  • Phosphorus was not ordered but would probably be good to check.
  • Vitamin D, 25 – 10.9 ng/mL — normal is considered: [30.0-100.0]
  • Vitamin D 1, 25 – 55 pg/mL — normal is considered: [18-72]

I did schedule an appointment with a physician but it will be a few weeks and the tachycardia was not pleasant, the internal coiled spring feeling made it hard to concentrate and hard to not over react to outside events, and the open seeping sores were painful.

I don’t see why I should not try to take care of myself rather than having to follow the orders/recommendations of physicians or psychiatrists when they are working from the premise that “we don’t know what is causing your symptoms or how to cure them but we would really like you to take these harsh medications anyway because we guess that they might reduce some of your symptoms – and please just ignore the negative side effects that the medication is actually adding to your problems because we guess that the medication might help reduce some of the symptoms that you originally came to see us about.” That is an example of circular logic based on guesses and I’m not buying it anymore now than I did when I was sitting in a highchair covered with eczema, milk based formula, and baby food.

Medications can be life saving and certainly are a modern miracle but nutrients will always be our body’s building blocks. Providing medicines to reduce symptoms of nutrient deficiency will only prolong the time the body is left without adequate nutrients and some deficiencies can cause long term damage that is not reversible once the nutrient is added back to the diet. A long term deficiency of Vitamin B12 can cause irreversible nerve damage, [11], and it turns out that calcium or vitamin D deficiency can cause osteoporosis if the deficiency is chronic enough to lead to secondary hyperparathyroidism.

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./

Bibliography:

  1. Pyroluria: anxiety and deficiency of B6 and zinc
  2. Thiamin: people with anorexia or alcoholism are more at risk for vitamin B1 deficiency
  3. Julia R Nunley, MD, “Calciphylaxis,” Medscape, July 21, 2014, [4-Overview,  4.5-Pathophysiology]
  4. Liu NQ et al., “Vitamin D and the regulation of placental inflammation.” J Immunol. 2011 May 15;186(10):5968-74. doi: 10.4049/jimmunol.1003332. Epub 2011 Apr 11, [5]
  5. Eleftheriadis T., et al., “Vitamin D receptor activators and response to injury in kidney disease.” JNephrol 2010: 23(05): 514-524 [6]
  6. Meg Mangin, Rebecca Sinha, and Kelly Fincher, “Elevated 1,25(OH)2D appears to be evidence of a disabled immune system’s attempt to activate the VDR to combat infection.” Inflamm Res. 2014; 63(10): 803–819., 2014 Jul 22. [7]
  7. by Charlotte LoBuono, “For the First Time, Study Proves Eczema Is an Autoimmune Disease.” Jan. 5, 2015, [8]
  8. Dermnet NZ, “Calciphylaxis,” [9]
  9. AARDA, “Autoimmune Statistics,” [10]
  10. Vitamin B12 deficiency can cause long term nerve degeneration.” August 21, 2013, [11]

Additional references about risk factors for calciphylaxis in dialysis patients:                   These articles are not mentioned in the text above and the research studies are not about secondary hyperparathyroidism but they do suggest that adequate protein intake may help reduce risk for calciphylaxis and that having elevated phosphorus or alkaline phosphatase levels may increase the risk.

  • Zacharias JM, Calcium use increases risk of calciphylaxis: a case-control study. Perit Dial Int. 1999 May-Jun;19(3):248-52.  [link] *This small research study is about calciphylaxis occurring in patients on kidney dialysis – calcium supplements were found to increase risk of calciphylaxis, while iron intake may have been protective, vitamin D intake made no difference between groups, (n=8 women). The study group’s parathyroid hormone and albumin levels were not found to be significantly different then the lab values of the control group of dialysis patients who did not have calciphylaxis. The conclusion includes the suggestion that “use of calcium salts as a phosphate binder” during dialysis might have something to do with the increased rate of calciphylaxis that was being seen at dialysis centers at the time.
  • A Rauf Mazhar, et. al., Risk factors and mortality associated with calciphylaxis in end-stage renal disease.  Kidney International (2001) 60, 324–332; doi:10.1046/j.1523-1755.2001.00803.x [link] *This study (n=19) found an increased risk for calciphylaxis in dialysis patients who were female, and when the patient had elevated phosphorus and/or alkaline phosphatase levels and/or low serum albumin levels. “Calciphylaxis independently increased the risk of death by eightfold.”
  • Doweiko JP, Nompleggi DJ. The role of albumin in human physiology and pathophysiology, Part III: Albumin and disease states. JPEN J Parenter Enteral Nutr. 1991 Jul-Aug;15(4):476-83. [link] *Albumin is the main protein found in blood plasma and having low albumin levels is also associated with poor wound healing and an increased risk of death.
  • Albumin levels can be low even when there is adequate protein intake in the presence of edema. Fluid imbalance can make the albumin values seem lower due to the change in concentration of the blood serum rather than due to changes in diet. However edema and low protein intake may both be problems. A low protein intake can increase the risk for edema.
  • Pickwell K, Predictors of lower-extremity amputation in patients with an infected diabetic foot ulcer. Diabetes Care. 2015 May;38(5):852-7. doi: 10.2337/dc14-1598. Epub 2015 Feb 9. [link] *Severe edema is also a sign of ill health. the presence of edema increased the risk of poor wound healing and the need for amputation for patients with a diabetic foot ulcer.