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
Malnutrition is one of the most feared complication of the duodenal switch operation. It may present years after surgery. What is common is a mix of nutritional deficiencies which include fat soluble vitamins, and protein calorie malnutrition. These all point to possible excessive shortening of the common channel. In my practice we have seen patients that have had lengthening of their common channel to improve their metabolic picture. What is very obvious to us, is that we see disproportionately higher number of cases coming to us for revision from practices where the common and alimentary lengths are done as a “standard” numbers with no specific adjustments made for the patient, their anatomy and situation. I have said for years, that the length of the bowel that is measured to be become the common and the alimentary limb should be a percentage of the total length of small bowel, rather than a pre-determined measurement. Here is a visual description of how this works.
If a common channel and the alimentary limb is measured to be a percent of the total length then the chance of protein calorie malnutrition is minimized since this will take into account the bowels absorptive capacity which is being reduced. This decrease in the absorption is done as a fraction of the total length.
Raines et al. published a study in 2014, that showed how small bowel length is related more closely to a patient’s height and not weight. And yet, some surgeons totally based the length of the common channel and the alimentary limb arbitrarily based on the patient pre operative BMI and nothing else. Could this be the cause of why I see some patients coming to us for revision of their duodenal switch for malnutrition?
Vitamin K1 is a found in dark green leafy vegetables, asparagus, brussels sprouts, some grains, olive oil, prunes, soy bean oil, and canola oil. The body has limited storage capacity for Vitamin K and uses a recycle system to reuse it.
Vitamin K1 is a fat-soluble vitamin that after Duodenal Switch is not as easily absorbed due to the limiting contact of the food product with the bile until the common channel. Bile is needed to absorb fatty acids and fat-soluble vitamins.
Duodenal Switch patients in need of Vitamin K1 supplements should take “Dry” or water miscible type of Vitamin K1, such as Biotech brand. The patients laboratory studies will determine if a patient requires Vitamin K1 supplement. Duodenal Switch patients should have laboratory studies drawn and evaluated at least on a yearly basis. Vitamin K works in a delicate balance with other supplements and should be monitored by a physician, in at risk people.
Vitamin K1 is most know for it’s coagulation effect and the clotting cascade. Vitamin K1 works with calcium and proteins in order to accomplish coagulation synethesis. Care should be taken with Vitamin K supplementation and anti-coagulation (blood thinners) therapy. Please see your physician regarding any supplementation of Vitamin K and blood thinner medications.
A discovery of Vitamin K dependent proteins has led to research on Vitamin K1 in bone health. Bone matrix proteins, specifically osteocalcin, undergo gamma carboxylation with calcium much the way coagulation factors do; this process also requires Vitamin K. Osteocalcin is a Gla-protein that is regulated by Vitamin D. The calcium binding ability of osteocalcin requires several Vitamin K carboxylations to exert it’s effects on bone mineralization.
In adults, the causes of Vitamin K1 deficiency include the following :
Multiple abdominal surgeries
Long-term parenteral nutrition
Parenchymal liver disease
Inflammatory bowel disease
Medications: Antibiotics (cephalosporin), cholestyramines, warfarin, salicylates, anticonvulsants, Cefamandole, cefoperazone, salicylates, hydantoins, rifampin, isoniazid, barbiturates, and certain sulfa drugs, higher Vitamin E can antagonized Vitamin K)
Disseminated intravascular coagulation (DIC) – Severe
Chronic kidney disease/hemodialysis
Additional information: https://lpi.oregonstate.edu/infocenter/vitamins/vitaminK/
As always, discuss with your physicians and/or surgeon any changes in medications and supplements. This is not meant to be an all inclusive discussion of Vitamin K.
An Example of Medications that may cause bone loss
It should be noted that this list is NOT all inclusive and gives the type of medication but does not list all the medications in that category that may affect bone health. I would also like to point out that the Proton Pump Inhibitor labels should probably be changed to “Acid Reducers” as reducing acid is the issues. https://americanbonehealth.org
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