Results for : "thyroid"
Question : “Do I have to take higher dose of thyroid medication after the duodenal switch? ”
Answer : “Maybe”
With all weight loss surgical procedures, there may be changes to absorption of medications. It is easily understood why duodenal switch may results in decreased absorption of fat-soluble medication. What is not as clear is the reduction in absorption of other medication with procedures that do not explicitly change the absorption at the level of the small bowel directly.
The research data is all over on this topic. There is published literature that shows improvement in the thyroid function after gastric bypass and the sleeve gastrectomy. However, the exact mechanism is not completely understood.
There is research that reports “…decreased postoperative levothyroxine requirements.” Other have shows no correlation between the length of the bowel distal to duodenum to absorption of thyroid medication.
With all this confusing data, the best course would be to always “treat the patient and not the lab results.”
If a patients who has been on medications with stable number and symptoms, suddenly presents with complaints of hypothyroidism after weight loss surgery, it’s possible the medications should be up adjusted even if the thyroid lab values may not be as defining.
A Parathyroid scan or Sestamibi scan may be needed if the typical weight loss surgical reasons for elevated PTH levels have been addressed. Sestamibi is a small protein which is labeled with the radio-pharmaceutical technetium-99. This very mild and safe radioactive agent is injected into the veins of a patient with overactive parathyroid and is absorbed by the overactive parathyroid gland. If the parathyroid is normal it will not absorb the agent. The scan below shows the uptake of the agent.
Calcium, Vitamin D and Parathyroid hormone are routinely measured on yearly follow up for most post weight loss surgical (WLS) patients. Elevated parathyroid hormone (PTH) may be caused by Vitamin D deficiency or calcium deficiency (most common in post WLS) or by over active parathyroid gland(s). In the latter case, if one of the four glands is overactive then this is knows as a parathyroid Adenoma. If all 4 are over active and are secreting too much PTH, this is known as hyperplasia. Ultrasound of the neck, may identify an enraged parathyroid gland (adenoma) which is located behind the thyroid gland. Given the large area where the parathyroid gland may be located, additional tests are needed to not only identify the location of the gland(s) but also to distinguish between single gland (adenoma) or multiple glands (hyperplasia) cause for the elevated PTH. It is important to investigate all avenues and testing in parathyroid hormone elevation and in some cases, not to rely on one test for your diagnosis. It is also imperative that weight loss surgical patients take their supplements routinely and consistently and have their laboratory studies followed at least yearly.
Hypoparathyroidism refers to elevated level of parathyroid hormone levels (elevated or high PTH). Parathyroid glands are two small glands that are located behind the thyroid gland. The primary function is regulation of the calcium level in the bloodstream. Parathyroid levels may be abnormally elevated for a number of reasons.
There may be abnormalities within the parathyroid glands themselves including benign and malignant tumors. Laboratory studies to assist in identifying Parathyroid hyperplasia are calcium, phosphorus, magnesium, PTH (parathyroid hormone), Vitamin D and possibly a 24 hour urine, kidney x-ray, and Dexa scan. The calcium levels in parathyroid hyperplasia are usually elevated and Vitamin D levels low. Patients can present with hypercalcemia symptoms such as kidney stones, nausea, vomiting, peptic ulcer, constipation, bone pain, bone weakness, depression, lethargy, fatigue. There are two types of Primary Hyperparathyroidism parathyroid hyperplasia and parathyroid adenomas. These both can at times be genetically linked.
Once the cause of elevated parathyroid hormone has been identified as primary hyperparathyroidism, the treatment involves surgical removal of one or more of the adenoma(s) or removal of 3.5 off all of the parathyroid glands if hyperplasia is diagnosed.
Parathyroid hyperplasia: When the growth involves all 4 of the glands. These may effect either one of the glands or all 4 of them. Majority of these are benign.
Parathyroid adenoma(s) refers to the abnormality or benign growth of one or more of the parathyroid glands.
2- Secondary Hyperparathyroidism
This is probably the most common cause of hyperparathyroidism imposed on a weight loss surgical patient. The elevated parathyroid hormone is the physiologic response all of the parathyroid glands to low calcium level. The parathyroid hormone is elevated in order to favor bone breakdown and make available for calcium to be circulating in the bloodstream. Parathyroid hormone also facilitates reabsorption of the calcium from the urine and improve absorption of the calcium from the GI tract.
The most common causes of secondary hyperparathyroidism is Vitamin D deficiency, weight loss surgery, kidney failure, Celiac or Crohn’s Disease. Lower levels of Vitamin D decrease the intestinal calcium absorption and thereby increasing PTH secretion. Vitamin D is the transport molecule for calcium. Symptoms may include bone or joint pain, muscle weakness, osteomalacia, low to normal blood calcium levels. The treatment of secondary hyperparathyroidism is correction of the underlying low calcium, low vitamin D levels. We have our Duodenal Switch patients take calcium citrate and dry water miscible type of Vitamin D3. Some people may require vitamin D injection in order to overcome deficiencies. You can find a list of supplements on our website and/or our starting point supplement recommendation in our patient workbook
Articles on Secondary Hyperparathyroidism following Weight Loss Surgery:
Calcium is measured to evaluate function and adequacy of a physiologic processes. Calcium plays a critical role in several body functions such as, coagulation pathways, bone health, nerve conduction, and other functions. It is important whenever you are evaluating laboratory results that you look at the whole picture of the person, including medications, other laboratory studies and health history. One value is not a stand alone result. There are many factors that effect calcium results.
Factors that effect calcium results: (not an all inclusive list)
The two most common issues following Weight loss Surgery or Duodenal Switch may be albumin level and Vitamin D level. Please see past blogs on Vitamin D. Magnesium may also play a role in a Duodenal Switch patient.
The most common calcium result drawn is the total calcium level. Laboratory results may not explicitly label it as such, however, it measures the calcium that is bound to protein. Ionized calcium is the free calcium that is representative of the true total calcium. Ionized Calcium can be measured by ordering specific lab. Alternatively, the Ionized calcium can be calculated by the following formula: Corrected calcium mg/dL = (0.8 * (Normal Albumin – Pt’s Albumin)) + Serum Ca ) or use the calculator at the bottom of this post.
The low Albumin level accounts for the low calcium level. This may be the reason for a patient with a low albumin/protein level, also having their calcium level reported as low. However, when adjusted for the protein deficiency the corrected calcium comes into normal range. Video of Trouseau’s sign of a patient with calcium deficiency.
The first step in a patient who has low calcium reported, is to make sure their protein and albumin levels are normal, along with Vitamin D.
Calcium levels are managed by two processes major regularly hormones and influencing hormones. Controlling or major regulatory hormones include PTH, calcitonin, and vitamin D. In the kidney, vitamin D and PTH stimulate the activity of the epithelial calcium channel and the calcium-binding protein (ie, calbindin) to increase calcium absorption. Influencing hormones include thyroid hormones, growth hormone, and adrenal and gonadal steroids.
Corrected calcium = 0.8 * (4.0 – serum albumin) + serum calcium
Thank you to Contributor: Mariam Michelle Gyulnazaryan
Vitamins are organic, essential nutrients that are necessary to keep your body in good health. Most vitamins must be obtained through diet because they cannot be synthesized in the body. However, the human body is able to make its own vitamin D in the skin through sun exposure or it can be obtained by food and supplements of Vitamin D3.
Vitamin D is a fat-soluble vitamin that is responsible for regulating muscle contraction, immune function, bone health, and intestinal absorption of magnesium, calcium, phosphate, iron, and zinc. Good sources of Vitamin D include sun exposure, dairy products, fatty fish, fortified orange juice, cod liver oil, mushrooms, and supplements.
There are two types of Vitamin D: D2 (ergocalciferol) and D3 (cholecalciferol). Both types have the same mechanism of action, but different sources and kinetics.
Ergocalciferol is easily obtained through Vitamin D-rich foods in normal anatomy. However, a post Duodenal Switch patient will have less absorption of Vitamin D via food due to fat malabsorption. Ergocalciferol is hydroxylated to ercalcidiol [25(OH)D2] in the liver. Its second hydroxylation takes places in the kidney, where it is converted to the active form of Vitamin D2 known as ercalcitriol [1,25(OH)2D2]. Now in it’s active form, Vitamin D2 can bind to the Vitamin D receptor (VDR) and help the body where it’s needed.
In the epidermis of the skin, precursor 7-dehydrocholesterol (7-DHC) forms cholecalciferol as a result of UVB radiation. Several factors such as increased skin pigmentation, age, and sunscreen application reduce the skin’s production of choleciferol (6). Cholecalciferol is hydroxylated in the liver to become calcidiol [25(OH)D3]. It is then moved to the kidney for further hydroxylation to Vitamin D3’s active form known as calcitriol [1,25(OH)2D3], also called calcifediol. The active form allows binding to VDR for biological activity.
Both forms of Vitamin D have been shown to effectively increase 25(OH)D levels. Research shows that after administering a single dose of 50,000 international units (IU) Vitamin D2 or D3, both experienced a similar increase in serum 25(OH)D concentration. However, Vitamin D2 levels rapidly declined while Vitamin D3 levels remained high (1). Further studies have confirmed that Vitamin D3 is more effective in elevating and maintaining 25(OH)D levels for a longer amount of time (5). Scientists believe the most reasonable explanation for Vitamin D3’s substantial efficacy is its higher affinity to metabolites, which results in a longer circulating half-life than Vitamin D2 making it more potent(4). For a post Duodenal Switch patient, due to fat malabsorption, it is important to use “Dry” Water Miscible form of Vitamin D3.
A 25-hydroxy Vitamin D blood test is the most accurate way to measure levels. A level between 20 ng/mL-50 ng/mL may be considered sufficient, however in our bariatric practice we would like to keep the levels in 60-80 ng/mL. It is worth nothing that recently the reference ranges was increase to 30-100 ng/mL. Treatments of Vitamin D deficiency include frequent sun exposure, fortified foods, supplements, and injectables. in addition to 50000IU of vitamin D on daily basis in emulsified (water soluble) formulary or unto 600,000IU in injection form. The parallel guide for adequate vitamin D supplementation is normalization of PTH levels. Monitoring these levels is imperative in a post bariatric patient.
In conclusion, studies have shown that Vitamin D2 and D3 are not interchangeable. Although they have comparable absorption, Vitamin D2 has a shorter duration of action which makes it less potent than Vitamin D3. Researchers have shown that neither form is harmful to treat Vitamin D deficiency, but they should not be considered bio-equivalent.
1. Armas LAG, Hollis BW, Heaney RP. Vitamin D2 is much less effective than Vitamin D3 in humans. Journal of Clinical Endocrinology & Metabolism. 2004; 89(11) 5387-5391.
2. Creighton D, Ignaszewski A, Francis G. Vitamin D: new d-fence against cardiovascular disease. BCMJ. 2012; 54(3) 136-140.
3. Holick MF, Schnoes HK, DeLuca HF. Identification of 1,25-Dihydroxycholecalciferol, a form of Vitamin D3 metabolically active in the intestine. PNAS. 1971; 68(4) 803-804.
4. Hollis BW. Comparison of equilibrium and disequilibrium assay conditions for ergocalciferol, cholecalciferol and their major metabolites. J Steroid Biochem. 1984; 21(1) 81-86.
5. Houghton LA, Vieth R. The case against ergocalciferol (Vitamin D2) as a vitamin supplement. Am J Clin Nutr. 2006; 84 (4): 694-697.
6. Howick Mf, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, Murad MH, Weaver CM. Evaluation, treatment and prevention of Vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2011; 96(7) 1911-1930.
7. Johal M, Levin A. Vitamin D and Parathyroid Hormone in general populations: understandings in 2009 and applications to chronic kidney disease. CJASN. 2009; 4(9) 1508-1514.
8. Tetley EA, Brule D, Cheney MC, Davis Cd, Esslingen KA, Fischer PWF, Friedl KE, Green-Finestone LA, Guenther PM, Klurfeld DM, L’Abbe MR, McMurry KY, Starke-Reed PE, Trumbo PR. Dietary reference intakes for Vitamin D: justification for a review of the 1997 values. Am J Clin Nutr. 2009; 89(3) 719-727.
9. Tripkovic L, Lambert H, Hard K, Smith CP, Bucca G, Penson S, Chope G, Hypponen E, Berry J, Vieth R, Lanham-New S. Comparison of Vitamin D2 and Vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: a systematic review and meta-analysis. Am J Clin Nutr. 2012; 95(6) 1357-1364.
Obesity is a multifactorial disease process that affects nearly every organ system in the body and is the one of the largest health crises in the United States. Obesity was long thought to be an issue with will power and eating habits. However, we have learned that obesity is a much more complex and insidious health issue that is both uncontrollable and controllable.
These may include the following:
- Health conditions
- Gut micro biome
- Activity level
- Environmental toxins
- Mental or emotion trauma
- Social Economic
- Sleep Deprivation
In the United States more than one third of the population is facing obesity, it’s side effects and possible metabolic derangement. Contrary to popular misconceptions, body weight is not regulated by diet alone. Scientists have found that a number of factors determine one’s body weight, such as genetics, environment, emotional trauma, and daily activity. Obesity is a complicated world wide health concern.
It’s important to note that obesity is not yours to manage alone and there is help that is tangible and manageable.
While there are other factors involved, a healthy and non-excessive diet is still very important. Each individual still needs to examine the causes of obesity that can be controlled. There isn’t cure all for obesity but, Bariatric Surgery can counter the effects of some of the causes and may improve some health risks.
Common Obesity Related Health Risks:
- High blood pressure
- High cholesterol
- Type 2 diabetes
- Heart disease
- Gallbladder disease
- Sleep apnea
- Respiratory problems
- Fatty Liver disease
- Venous disease
- Acid reflux
- Menstrual irregularities and infertility
- Meningioma (brain tissue and spinal cord)
- Adenocarcinoma of the esophagus
- Multiple myeloma (blood cells)
- Breast (post-menopausal women)
- Upper stomach
- Colon and rectal
There are a a number of skin conditions that are associated with the disease of obesity. Acanthosis Nigricans is characterized as areas of thickened, dark, velvety discoloration in body folds and creases. Usually seen in the armpits, neck, under the breasts, in the skin folds of the abdomen and groin. The exact cause of it at the molecular level is not clear other than seen frequently with insulin excess in the case of benign conditions. This symptom can give a warning about health conditions that require further investigation.
Patients may assume excessive sweating and poor hygiene are the causes of this condition- both of which are incorrect.
Acanthuses Nigerians is caused by acanthosis and papillomatosis of the epidermis (the outer most layer of the skin) pigmentation is usually not in this area, rather than pigment-producing cells. The skin proliferation abnormalities in acanthosis nigrcans are frequently associated with hyperinsulinemia and insulin resistance. This probably presents the best understanding of the pathology behind it. It suggests that the layer of skin gets thicker probably caused by some stimuli- as indicated above seen with insulin excess.
There are two forms of this condition: Benign and Malignant.
Benign forms are associated with obesity, insulin resistance, and type II diabetes.
Insulin resistance: Insulin is a hormone secreted by the pancreas that allows your body to process sugar. Resistance predisposes to type II diabetes.
Hormonal disorders: Hypothyroidism, Polycystic Ovarian Disease, and other endocrine disorders of adrenal glands are ovaries
Drugs: Certain drugs and supplements such as high-dose niacin, birth control pills, steroids, may cause acanthosis nigricans.
Malignant forms may be an indication of Gastro-intestinal cancer such as stomach, colon, or liver cancer.
Treatment: No specific treatment is available for acanthosis nigricans. Treating the underlying conditions may restore some of the normal color and texture to affected areas of skin.