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Secondary Hyperparathyroidism

Posted by: Cleo Libonati, RN, BSN in A LISTING OF ALL HEALTH CONDITIONS, Calcium, Complications, Malabsorption Disorders, Parathyroid Disorders, System - Glandular 0 3,144 Views

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Courtesy Wikipedia.com

Parathyroid Glands in the Neck. Courtesy Wikipedia.com

What Is Secondary Hyperparathyroidism?

Secondary hyperparathyroidism is a parathyroid disorder resulting from hypocalcemia (low blood calcium level) that is characterized by excessive production of parathyroid hormone in the attempt to normalize the low blood calcium by releasing calcium from bone.

Parathyroid hormone is produced by the four pea sized parathyroid glands that are located on the thyroid gland in the front of the neck. In part, because the thyroid and parathyroid glands share the same anatomic place in the body and because they have similar names, they are often confused although they have completely different actions.

Parathyroid hormone regulates calcium and the opposing mineral phosphorus in the blood. In secondary hyperparathyroidism, calcium blood levels are low to normal while phosphorus levels are increased which stimulates the outpouring of parathyroid hormone.

Q: How does secondary hyperparathyroidism differ from primary hyperparathyroidism?

A: In primary hyperparathyroidism blood calcium is high and phosphorus is low, which is the opposite of secondary hyperparathyroidism.

The most common cause of secondary hyperparathyroidism is kidney disease causing failure to reabsorb calcium followed by vitamin D deficiency and malabsorption.

What Is Secondary Hyperparathyroidism In Celiac Disease and/or Gluten Sensitivity?

  • Relationship between secondary hyperparathyroidism and celiac disease. Secondary hyperparathyroidism in untreated celiac disease is characterized by excessive levels of parathyroid hormone (PTH) that do not respond to medical treatment because it results from ongoing malabsorption. patients with secondary hyperparathyroidism were found to have celiac disease.
  • Relationship between secondary hyperparathyroidism and celiac antobodies. When grouping the serological test results of study subjects as negative, borderline or positive, there was a significant difference between the secondary hyperparathyroidism group and the controls for anti-tissue transglutaminase and anti-gluten IgA (p<0.05.1
  • Relationship between secondary hyperparathyroidism and vitamin D deficiency. Vitamin D deficiency is a cause of secondary hyperparathyroidism because it is required for absorption of calcium from the small intestine and this explains the calcium deficiency that results.
  • Relationship between secondary hyperparathyroidism and normal vitamin D. Isolated hypocalcemia with hypocalciuria and secondary hyperparathyroidism without  vitamin D deficiency can be initial manifestations of celiac disease. In a case report below, correction was demonstrated after dietary gluten withdrawal.2
  • Relationship between secondary hyperparathyroidism and bone mineral density. Secondary hyperparathyroidism is associated with decreased bone mineral density in celiac disease patients.3
  • Relationship between secondary hyperparathyroidism and diet. Gluten free diet reverses secondary hyperparathyroidism. Normal parathyroid function with increased bone mineral density (BMD) is suggestive of continuing long term benefit of gluten withdrawal on bone metabolism in celiac disease patients.4,3

How Prevalent Is Secondary Hyperparathyroidism In Celiac Disease and/or Gluten Sensitivity?

  • Secondary hyperparathyroidism is common in untreated celiac disease.
  • Of 54 consecutively diagnosed patients with celiac disesse, 12 (22.2 %) had secondary hyperparathyroidism.5
  • In the reverse, 4% of 97 patients with secondary hyperparathyroidism were found to have celiac disease. When grouping the serological test results as negative, borderline or positive, there was a significant difference between the secondary hyperparathyroidism group and the controls for anti-tissue transglutaminase and anti-gluten IgA.1

What Are The Symptoms Of Secondary Hyperparathyroidism?

Secondary hyperparathyroidism is marked by these symptoms:

  • Emotional instability.
  • Depression.
  • Insomnia.
  • Anxiety.
  • Bone pain.
  • Itching.
  • Muscle weakness.
  • Bone weakness (osteomalacia in adults and rickets in children in severe vitamin D deficiency).

How Does Secondary Hyperparathyroidism Develop In Celiac Disease and/or Gluten Sensitivity?

  • Secondary hyperparathyroidism results as a consequence of calcium deficiency resulting from malabsorption and/or vitamin D deficiency and steatorrhea in celiac disease. Vitamin D is required for adequate absorption of calcium from the small intestine.6

Does Secondary Hyperparathyroidism Respond To Gluten-Free Diet?

Yes. Parathyroid function normalizes in treated patients.7

Normal parathyroid function with increased bone mineral density (BMD) is suggestive of continuing long term benefit of gluten withdrawal on bone metabolism in celiac disease patients.8

6 Steps To Improve Secondary Hyperparathyroidism In Celiac Disease and/or Gluten Sensitivity:

Treatment. This condition responds to the complete elimination of gluten, which is the required treatment that improves both secondary hyperparathyroidism and gut health.

  • Gut health is the foundation to restore ALL health. Restored health will enable you to maintain a strict gluten free diet, just as other life tasks will be easier.
  • A strict gluten free diet means removing 100% of wheat, barley, rye and oats from the diet.
  • Cutting out bread and other obvious sources of gluten is not good enough for recovery. Even 1/8th teaspoon of flour or bread crumb is enough to sustain the inflammation that is damaging your small intestine, causing increased permeability (leaky gut) and allowing undigested gluten to enter your body where it can damage structures and function, and instigate immune inflammatory responses.

Correct Your Individual Nutritional Needs.

Recovery. You should begin to feel better within a week and notice more energy as inflammation subsides and the  absorbing cells that make up the surface lining of your small intestine are better able to function.

  • Intestinal lining cells are replaced every 5 days. The healing process is like sunburn where the damaged surface layer of skin sloughs off and is replaced with new normal cells.
  • Leaky gut normally resolves in two month after starting a gluten free diet and brings about a big improvement in health. Improvement in intestinal permeability precedes morphometric recovery (cell appearance and structure) of the small intestine in celiac disease.9
  • The intestinal lining may take up to a year to heal.
  • 2 Reduce Inflammation. Foods to Eat and Foods Not to Eat:

Because gluten is inflammatory, eliminate OTHER inflammatory foods from your diet to reduce an additive effect to gluten. At the same time, try to eat foods that reduce inflammation (anti-inflammatory).

Here Are Major Inflammatory Food Types That Reduce Healing:

  • Damaging Foods. In susceptible persons, includes corn, dairy (cow), and soy. Lactose, the sugar in any animal milk disrupts intestinal permeability causing leaky gut.10
  • Allergenic Foods. Includes foods that trigger the immune sytem to produce IgE antibodies. Allergy testing is the usual way to discover these offending foods.
  • Shelf Stable Processed Foods. Includes any that contain additives and preservatives. Look for them on the nutrition label of the box or package. Additives and preservatives also disrupt intestinal permeability causing leaky gut.10
  • Fats. Limit deep fried foods, trans-fats, saturated fats (animal fat/butter), and EXCESSIVE omega-6 fatty acid oils like corn oil. Rancid fats, sodium caprate (a medium chain fat), and sucrose monester fatty acid (a food grade surfactant) induce significant disruption of the intestinal barrier that causes leaky gut.10.
  • Excessive Refined White Flours (bran layer removed). Includes products made from them such as cookies, bread, cakes, pies. Bran contains the vitamins and minerals that metabolize grains and slows the otherwise rapid entry of sugar from their digestion into the bloodstream. Also disrupt intestinal permeability causing leaky gut.10
  • Refined Sugars.  Includes white sugar, corn fructose and high fructose corn syrup.
  • Certain Spices. Includes paprika and cayenne pepper which disrupt intestinal permeability causing leaky gut.10
  • Alcohol and Caffeine. Disrupt intestinal permeability causing leaky gut.10

Here Are Important Anti-Inflammatory Food Types to Promote Health:

  • Fruits. Contain ample amounts of vitamins, minerals and phytochemicals which are naturally occuring components in plants that detoxify toxins, carcinogens (reducing the risk by 50%) and mutagens.
  • Non-Starchy Vegetables. Support intestinal integrity and provide ample amounts of vitamins, minerals and phytochemicals. Includes green leafy vegetables such as lettuce and kale, also onion, broccoli, garlic, and others.
  • High Quality Complex Carbohydrates. Provide vitamins, minerals, and fiber while boosting serotonin levels to help you relax and feel calm. Includes whole grains, legumes, and root vegetables such as carrots, parsnips, sweet potatoes, turnips, red beets, and others.
  • Antioxidants. Protect the body from inflammatory oxidant molecules that continually occur and help us handle stress and reduce irritability. Includes vitamin C-containing foods such as lemon, grapefruit, apricot, Brussels sprouts and strawberries, and others. Also, includes vitamin E-containing foods such as nuts, seeds, avocado, olive oil, and others. Cocoa is good, too.
  • Omega-3 Fatty Acids. Balance opposing omega-6 fatty acids and bad fats. Fish sources includes tuna, salmon, cod, and others. Plants sources include flax, chia seeds, canola oil, and others.
  • Probiotics. Supply normal microbes needed for colon health and health of the body such as these fermented foods: yogurt, kefir, and unpasteurized apple cider vinegar.
  • Prebiotics/ High Fiber Foods.  Food with fiber keeps our population of colonic microbes healthy.
  • Protective Herbs and Spices.  See below #6 below for examples.
  • 3 Information Sheet You Can Take to Your Doctor or Other Health Professional:

Click here.

  • 4 Manage Your Medications Safely:

Certain medications deplete calcium and vitamin D that exacerbate secondary hyperparathyroidism.  Ask your doctor or pharmacist about this possible adverse effect if you are taking any of the drugs listed below. Do not stop prescribed medications without supervision.

This is not a complete listing.

ANTACIDS / ULCER MEDICATIONS

ANTIBIOTICS disrupt intestinal permeability which complicates celiac disease.

ANTI-INFLAMMATORIES disrupt intestinal permeability which complicates celiac disease.

  • Corticosteroids (Prednisone, Medrol®, Aristocort®, Decadron) deplete Calcium, Vitamin D.
  • Aspirin and Salicylates deplete Calcium.

ANTICONVULSANTS

  • Phenobarbital and Barbituates; and Dilantin®, Tegretol®, Mysoline®, Depakane/Depacon® deplete Calcium, Vitamin D.

ANTIVIRAL AGENTS

CHOLESTEROL DRUGS

  • Colestid® and Questran® deplete Vitamin D.

DIURETICS

  • Loop Diuretics (Lasix®, Bumex®, Edecrin®) depletes Calcium.
  • Potassium Sparing Diuretics (Midamor®, Aldactone®, Dyrenium® and others) deplete Calcium.

  • 5Nutritional Supplements To Help Correct Deficiencies:

The type and quantity of nutritional supplements that may be needed depend on which nutrients are deficient.

  • Multivitamin/mineral combination once a day is useful to improve overall nutrient levels. This is a safe dose, but always check with your doctor to avoid interactions with medications.
  • Calcium citrate is the best absorbed of calcium supplements. Calcium carbonate is a poor choice.
  • Vitamin D3 as prescribed following blood test for status.

Storage Note: Store container tightly sealed, away from heat, moisture and direct light to avoid loss of potency. That is, in a safe kitchen cabinet – not in the bathroom or on the kitchen table.

  • 6Manage Natural Remedies: 

Hydration:

  • Eight glasses of water are recommended per day unless there is a contraindication such as kidney or heart disease. The Institute of Medicine recommends approximately 2.7 liters (91 ounces) of total water, from all beverages and foods, each day for women and 3.7 liters (125 ounces) daily of total water for men.
  • If you are thirsty, drink water. Add fresh, squeezed lemon to water. Lemon is anti-inflammatory, alkalizing and provides vitamin C.
  • Hydration Test: Urine should be pale yellow. Fingertips should be plump, without pruning but this may not be reliable when fingers are swollen with edema. Lips should be plump, without puckering. The feeling of thirst can be unreliable.
  • What is wrong with soda, coffee, tea, and alcohol? These drinks are dehydrating, increase acid, and deplete nutrients.

Carminatives. The following  anti-inflammatory plant sources called carminitives help heal the digestive tract. They also tone the digestive muscles which improves peristalsis, thus aiding in the expulsion of gas from the stomach and intestine to relieve digestive colic and gastric discomfort.

Carminative Food Remedies:

  • Raspberry.
  • Carrot is also a cleansing digestive tonic.
  • Grape is also bile stimulating and a cleansing remedy for sluggish digestion and laxative.
  • Redbeets also stimulate and improve digestion and are easily digested.
  • Cabbage also stimulates and improves digestion and is also a liver decongestant.
  • Lettuce also stimulates and improves digestion and is also an alterative, meaning it improves the function of organs involved with the digestion and excretion of waste products to bring about a gradual change.
  • Potatoes are antispasmodic (due to atropine like properties) and a liver remedy.

Carminative Herb Remedies:

  • Sage is also a digestive, astringent, bile stimulant and energy tonic that heals the mucosa.  Drink as tea or use in cooking.
  • Chamomile, lemon balm, and fennel, (as a tea) also help relieve nervous tension.
  • Parsley also relieves indigestion.
  • Rosemary as a tea and in cooking also is a nervous system tonic for stress and fatigue, bile stimulant, and can relieve headaches and indigestion.
  • Thyme is also soothing remedy useful for stimulating digestion of rich, fatty foods.

Carminative Spice Remedies:

  • Cloves are also antispasmodic.
  • Nutmeg is also useful for indigestion.
  • Ginger.

Exercise Helps: Exercise improves circulation and rids the body of toxins.

Note: Exercise is important, but the amount and type of exercise undertaken depends on your health. Your first priority is to heal.

What Do Medical Research Studies Tell About Secondary Hyperparathyroidism In Celiac Disease and/or Gluten Sensitivity?

RESEARCH STUDY SUMMARIES

Prevalence and predictors of abnormal bone mineral metabolism in recently diagnosed adult celiac patients.” This study investigating the prevalence of low bone mineral density (BMD) in recently diagnosed adult celiac patients and aiming to identify the factors associated with this found that low BMD is common in newly diagnosed adult celiac patients with approximately one fifth of them having osteoporosis and low vitamin D level.

BMD was measured in 54 newly diagnosed adult celiac patients between February 2008 and April 2009 and its correlation with clinical and biochemical parameters was analyzed. Fifty-four (24 male) newly diagnosed celiac patients ages 18-50 were included. Thirty-nine (72.2 %) presented with intestinal symptoms and the rest with extraintestinal symptoms.

Low vitamin D levels were seen in 11 (20.3 %) patients and elevated iPTH (secondary hyperparathyroidism) in 12 (22.2 %) patients. Twenty-one (39 %) patients had normal BMD, 23 (43 %) had osteopenia (T-score -1 to -2.5), and 10 (18 %) patients had osteoporosis (T-score <-2.5). A statistically significant association was seen between BMD and age of onset, duration of illness, serum tTGA levels, serum vitamin D levels, and cellular changes seen on biopsy.5

“Celiac disease in subjects with secondary hyperparathyroidism.” This study investigating the prevalence of celiac disease in subjects with secondary hyperparathyroidism found that subjects with secondary hyperparathyroidism, at least when secondary hyperparathyroidism is persistent, should be tested for celiac disease.

In the Tromsø study 2001, serum parathyroid hormone (PTH) and calcium were measured in 7954 subjects of whom 6061 were eligible for follow-up. From this group, 97 subjects with secondary hyperparathyroidism (serum PTH less than or equal to 6.5 pmol/l and serum calcium less than 2.40 mmol/l) and 104 matched control subjects were re-examined with serological tests for celiac disease (anti-tissue transglutaminase, anti-gluten IgA and IgG).

Celiac disease was diagnosed in 4 subjects, all from the original secondary hyperparathyroidism group. At the re-examination, only 29 of the 97 subjects with secondary hyperparathyroidism still had elevated serum PTH levels. Among these were 3 of the subjects with celiac disease. When grouping the serological test results as negative, borderline or positive, there was a significant difference between the secondary hyperparathyroidism group and the controls for anti-tissue transglutaminase and anti-gluten IgA (p<0.05.1

“Normal parathyroid function with decreased bone mineral density in treated celiac disease.” This study investigating whether parathyroid hormone (PTH) remained elevated and whether abnormalities of parathyroid function were still present in celiac disease patients after treament with gluten free diet demonstrated higher basal 1-PTH values with normal parathyroid function in treated celiac disease.11

CASE REPORT SUMMARIES

“Carpopedal spasm in an elderly man: an unusual presentation of celiac disease.” This case report describes diagnosis of celiac disease in a 68-year-old single Caucasian man admitted to the hospital with a 24-hour history of carpopedal spasm of both hands. Apart from generalized weakness, he reported no other symptoms. Physical examination revealed carpopedal spasm, clubbing of fingers and cachexia (body mass index 14 kg/m2). This patient was found to have several unusual features of celiac disease, including a low vitamin D level, severe hypocalcemia, and elevated parathyroid hormone levels in the presence of minimal gastrointestinal symptoms and negative tTG-antibodies

Blood tests showed severe hypocalcemia, with a total serum calcium of 1.06 mmol/L (normal range [NR] 2.05-2.55 mmol/L). He also had low serum potassium (2.8 mmol/L; NR 3.5-5.5 mmol/L) and magnesium (0.36 mmol/L; NR 0.65-1.05 mmol/L). Other significant results included hemoglobin 10.6 g/dL (NR 13-18 g/dL), mean corpuscular volume 98.1 fl (NR 82-98 fl), vitamin B12 157 ng/L (NR > 165 ng/L), folate 2.8 g/L (NR 3.1-17.5 μg/L), ferritin 252 μg/L (NR 30-250 μg/L), prothrombin time 20 s (NR 11-14 s), thyroid stimulating hormone 0.87 mu/L (NR 0.35-4.5 mu/L), phosphate 0.57 mmol/L (NR 0.8-1.45 mmol/L), albumin 32 g/L (NR 34-48 g/L) and alkaline phosphatase 313 IU/L (NR 47-141 IU/L). Subsequent results revealed vitamin D deficiency with a low serum 25-OH vitamin D of < 7 μg/L (NR 7-40 μg/L), a low 24-hour urinary calcium excretion of 0.9 mmol (NR 2.5-7.5 mmol) and a raised serum parathyroid hormone of 22.7 pmol/L (NR 1.6-6.9 pmol/L). Serology for tissue transglutaminase (tTG) antibodies was negative, and a serum IgA level of 4.95 g/L (NR 0.8-4.0 g/L) excluded selective IgA deficiency. Electrocardiograph at admission showed prolonged QT interval.

In view of cachexia, clubbing and negative tTG-antibodies, he was further investigated for an occult malignancy. Barium meal and follow through showed dilated proximal bowel loops and absence of normal feathery pattern of the jejunum, features suggestive of a malabsorptive state. Upper gastroscopic examination was normal; however, the duodenal biopsy showed partial and subtotal villous atrophy with increased intra-epithelial lymphocyte infiltration, consistent with the diagnosis of celiac disease.12

“Celiac disease manifesting as isolated hypocalcemia.” This case report of a patient describes isolated hypocalcemia with hypocalciuria, and secondary hyperparathyroidism as initial manifestations of celiac disease. Vitamin D was normal. Correction was demonstrated after dietary gluten withdrawal.13

  1. Jorde R, Saleh F, Sundsfjord J, Haug E, Skogen B. Coeliac disease in subjects with secondary hyperparathyroidism. Scand J Gastroenterol. 2005 Feb;40(2):178-82. [↩] [↩] [↩]
  2. Rickels MR, Mandel SJ. Celiac disease manifesting as isolated hypocalcemia. Endocrine Practice: Official Journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. May-Jun 2004;10(3):203-7. [↩]
  3. Pantaleoni S, Luchino M, Adriani A, Pellicano R, Stradella D, Ribaldone DG, Sapone N, Isaia GC, Di Stefano M, Astegiano M. Bone mineral density at diagnosis of celiac disease and after 1 year of gluten-free diet. ScientificWorldJournal. 2014;2014:173082. doi: 10.1155/2014/173082. [↩] [↩]
  4. Ciacci C, Cirillo M, Giorgetti G, et al. Low plasma cholesterol: a correlate of nondiagnosed celiac disease in adults with hypochromic anemia. American Journal of Gastroenterology. Jul 1999;94(7):1888-91. [↩]
  5. Chakravarthi SD, Jain K, Kochhar R, Bhadada SK, Khandelwal N, Bhansali A, Dutta U, Nain CK, Singh K. Prevalence and predictors of abnormal bone mineral metabolism in recently diagnosed adult celiac patients. Indian J Gastroenterol. 2012 Jul;31(4):165-70.. [↩] [↩]
  6. Abboud B, Daher R, Boujaoude J. Digestive manifestations of parathyroid disorders. World J Gastroenterol. 2011 Sep 28;17(36):4063-6. doi: 10.3748/wjg.v17.i36.4063. [↩]
  7. Molteni N, Bardella MT, Vezzoli G, Pozzoli E, Bianchi P. Intestinal calcium absorption as shown by stable strontium test in celiac disease before and after gluten-free diet. American Journal of Gastroenterology. Nov 1995;90(11):2025-8. [↩]
  8. Ciacci C, Cirillo M, Giorgetti G, et al. Low plasma cholesterol: a correlate of nondiagnosed celiac disease in adults with hypochromic anemia. American Journal of Gastroenterology. Jul 1999;94(7):1888-91. [↩]
  9. Cummins AG, Thompson FM, Butler RN, et al. Improvement in intestinal permeability precedes morphometric recovery of the small intestine in coeliac disease. Clinical Science. Apr 2001;100(4):379-86. [↩]
  10. Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease. Journal of Gastroenterology and Hepatology. 2003;18:479-91. [↩] [↩] [↩] [↩] [↩] [↩]
  11. Lemieux B, Bolvin M, Brossard JH, et al. Normal parathyroid function with decreased bone mineral density in treated celiac disease. Canadian Journal of Gastroenterology. May 2001;15(5):302-7. [↩]
  12. Schmidt K, Powari M, Shirazi T, Vaidya B. Carpopedal spasm in an elderly man: an unusual presentation of coeliac disease. J R Soc Med. 2007 Nov;100(11):524-5. [↩]
  13. Rickels MR, Mandel SJ. Celiac disease manifesting as isolated hypocalcemia. Endocrine Practice: Official Journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. May-Jun 2004;10(3):203-7. [↩]

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