Other Micronutrient Deficiencies in Bariatric Surgery


Thiamine

Males

Females

RDA* (India) [16]

1.2–1.7 mg/day

1.0–1.4 mg/day

RDA*(US) [17]

1.2 mg/day

1.1 mg/day

RNI**(UK) [18]

1.3 mg/day

1.1 mg/day

NRV***(Australia/New Zealand) [19]

1.2 mg/day

1.1 mg/day


RDA* recommended dietary allowances, RNI** reference nutrient intake, NRV*** nutrient reference value





36.1.2 Thiamine Recommendation Post-bariatric Surgery


Dietary sources of thiamine are whole grain cereals (brown rice and bran), meat (pork, poultry), eggs, nuts, legumes (dried beans, peas), soybeans and vegetables (green leafy vegetables, beetroot, and potatoes).

Thiamine should be part of a routine multivitamin with mineral preparation prescribed post bariatric surgery. Also routine thiamine screening is not recommended following bariatric surgery [11]. Empiric thiamine supplementation and/or screening for thiamine deficiency should be considered in post bariatric surgery patients with rapid weight loss, protracted vomiting, parenteral nutrition, excessive alcohol use, neuropathy, encephalopathy, or heart failure [11].

Patients with severe thiamine deficiency (suspected or established) should be treated with intravenous thiamine, 500 mg/day, for 3–5 days, followed by 250 mg/day for 3–5 days or until resolution of symptoms, and then to consider treatment with 100 mg/day, orally, usually indefinitely or until risk factors have resolved. Mild deficiency can be treated with intravenous thiamine, 100 mg/day, for 7–14 days. It is important to note that thiamine supplementation requires in addition 300–400 mg/day of elemental magnesium supplementation [11].

For Wernicke’s encephalopathy most authors agree on a dosage scheme of 500 mg of intravenous thiamine three times daily for 2–3 days, followed by 250 mg intravenously daily until improvement [4, 10]. Dramatic improvement with thiamine administration practically confirms the diagnosis. Timely recognition of affected patients can be difficult but is of utmost importance, since intense supplementation of thiamine may completely reverse symptoms. Thiamine administration should not be delayed until diagnosis is confirmed as delay in treatment inadvertently leads to permanent neurological deficits or even death [9]. However, even with replacement therapy, almost half the patients will still exhibit permanent cognitive impairment [9].



36.2 Copper


Copper is an essential micronutrient which acts as a cofactor in several oxidative enzymes vital to the function of hematopoietic, skeletal, vascular tissues as well as the structure and function of the nervous system [12].

Copper is mainly absorbed in the stomach and duodenum. In the small intestine, copper is bound to metallothionein with greater affinity than zinc or other metal ions. Excessive intake of zinc may result in decreased copper levels and sideroblastic anaemia [13].

Due to the malabsorptive nature of procedures like RYGB, biliopancreatic diversion with/without duodenal switch (BPD-DS) copper deficiency is more common in these procedures. Gastric acid is involved in freeing copper from food, and the risk of copper deficiency increases as the stomach and duodenum are bypassed. Diarrhea caused by BPD-DS can cause excess loss of copper in addition to malabsorption [14]. One study reported that in post BPD-DS patients 50.6 % of 89 BPD patients had at least once, a low copper level, and half of them repeatedly had low levels during a 5-year period. Several cases of copper deficiency after RYGB have also been reported [14, 15]. The prevalence and incidence of copper deficiency following RYGB surgery was determined to be 9.6 % and 18.8 %, respectively, with many patients experiencing mild-to-moderate symptoms.

The symptoms of copper deficiency include hematologic abnormalities like anaemia, neutropenia, leucopenia and myeloneuropathy. Myeloneuropathy is rare and often unrecognized complication of copper deficiency.

Also copper and vitamin B12 deficiency may coexist as acquired copper deficiency in humans has been described, causing a syndrome similar to the subacute combined degeneration of vitamin B12 deficiency. Ataxia and myelopathy secondary to acquired copper deficiency are rare complications. Early recognition and therapy with oral or parenteral copper may lead to a decrease in both neurologic and hematologic consequences.


36.2.1 Copper Recommendation After Bariatric Surgery


The highest diet rich sources of copper include organ meats, shellfish, nuts and seeds like sesame seeds, cashew, sunflower seeds, walnuts, pumpkin seeds, peanuts, almonds, flax seeds, chocolate soy beans, shiitake mushroom, crimini mushroom, spinach, kale, summer squash, tempeh, tofu, kidney beans, sweet potatoes, grapes, pineapple, tomatoes and egg plant.



The recommended Dietary Allowance for Copper




























Copper

Males

Females

RDA* (India) [16]

1.35 mg/day

1.35 mg/day

RDA*(US) [17]

0.9 mg/day

0.9 mg/day

RNI**(UK) [18]

1.2 mg/day

1.2 mg/day

NRV***(Australia,New Zealand) [19]

1.7 mg/day

1.2 mg/day


RDA* recommended dietary allowances, RNI** reference nutrient intake, NRV*** nutrient reference value

Despite the lack of consensus concerning supplementation dosing, routine copper supplementation is recommended. At least 2 mg of copper per day is advised in the form of copper gluconate or sulfate as part of a vitamin and mineral supplement for BPD-DS and RYGB patients. Patients being treated for zinc deficiency or using supplemental zinc for hair loss should receive 1 mg of copper for each 8–15 mg of zinc as zinc replacement can cause copper deficiency. Copper levels are not routinely monitored but need to be evaluated in patients with neuropathy and normal vitamin B12 levels [16, 17]. The literature reports the use of oral copper gluconate in mild to moderate deficiency and IV copper infusion in severe deficiency [1822]. For mild to moderate deficiency, the recommended oral administration is of 3–8 mg/d of copper gluconate until copper indices return to normal. Severe deficiency should be treated with 2–4 mg/d IV copper for 6 days or until neurological symptoms resolve and serum levels return to normal. Continuous monitoring of copper status is necessary every 3 months after deficiency is treated [23].


36.3 Selenium


Selenium is an essential trace element and a vital constituent of antioxidant enzymes that participate in various physiological activities and protects the cell against the deleterious effects of free radicals by modulating the cell response. The role of selenium has been explored in normal thyroid functioning, enhancing immune function, carcinogenesis, cardiovascular diseases, in the prevention of pre-eclampsia, diabetes mellitus and male reproduction etc.

It has been reported that obese people have lower serum selenium levels [23]. The actual incidence of selenium deficiency after bariatric surgery is not well documented, hence it’s difficult to get a clear picture of its deficiency state but post bariatric patients can be at a risk of selenium deficiency secondary to reduction in nutrient intake and altered absorption as selenium is mainly absorbed in the duodenum.

Selenium is assimilated more effectively from plant food than animal products but some dietary constituents (vitamin C and vitamin E) generally affect its absorption. Also, other factors like, copper, magnesium, zinc, vitamin B, lipoic acid and some amino acids such as cysteine, glutamine, and methionine may play a role that affect the level of selenium.

A recent study following bariatric surgery showed that even with multivitamin and mineral supplements, a reduction in selenium concentration was noted in the early post-operative period which normalised during the first year after surgery [24].

Selenium deficiency is uncommon, but severe deficiency can cause symptoms and diseases including myopathy, cardiomyopathy, arrhythmia, muscle wasting, impaired immunity, low thyroid function, loss of skin and hair pigmentation, whitened nail beds, and progressive encephalopathy. There is an indication that selenium deficiency may contribute to the progression of viral infections.

Plasma erythrocyte and whole blood selenium, plasma selenoproteins P, and plasma platelet and whole blood glutathione activity are good biomarkers of selenium status in the body. In humans the selenoenzyme methionine sulfoxide reductase B1 (MsrB1) is the most sensitive protein marker of selenium status [25].



The recommended Dietary Allowance for Selenium




























Selenium

Males

Females

RDA* (India) [16]

40 mcg

40 mcg

RDA*(US) [17]

55 mcg

55 mcg

RNI**(UK) [18]

75 mcg

60 mcg

NRV***(Australia,Newzealand) [19]

70 mcg

60 mcg


RDA* recommended dietary allowances, RNI** reference nutrient intake, NRV*** nutrient reference value


36.3.1 Selenium Recommendation After Bariatric Surgery


Plant foods are the major sources of selenium and it varies tremendously according to its concentrations in soil which varies regionally. Animals that eat grains or plants that were grown in selenium rich soil have higher levels of selenium in their muscle and is widely distributed in all tissues. Selenium is present in foods like brazil nuts, walnuts, almonds, peanuts, cashew nuts, pistachios, pine nuts, hazelnuts, sunflower seeds, grains (wheat germ, barley, brown rice, oats), fresh water and salt water fish (tuna, halibut, sardines, flounder, salmon), shellfish (oysters, mussels, shrimp, clams, scallops), meat (beef, lamb, pork, liver), poultry (chicken, turkey), eggs andmushroom (button, crimini, shiitake) [45].

A prospective pilot study (n = 39) showed that RYGB and laparoscopic adjustable gastric banding (LAGB) procedures increase the risk for disturbances of selenium and GTP homeostasis and suggested that consideration of selenium supplementation at higher levels of current RDA (i.e. 55 mcg) during the first 3 months and perhaps longer may be needed [26].

However, there is insufficient evidence for routine selenium screening or supplementation but patients with malabsorptive bariatric surgeries who have unexplained anemia or fatigue, persistent diarrhea, cardiomyopathy or bone metabolic diseases, selenium levels should be checked.


36.4 Zinc


Zinc is an abundant essential trace element and important for cell function as well as metabolism, protein synthesis, detoxification, thyroid function, blood clotting, cognitive functions, fetal growth, immune response, growth and maintenance, sperm production, signaling transduction and gene regulation and essential for over 300 enzymatic reactions. Zinc is also an essential antioxidant and anti-inflammatory agent [27].

Zinc deficiency can either be genetic or can be acquired and can happen due to low intake, intestinal malabsorption (e.g. RYGB, inflammatory bowel disease (IBD), celiac disease, chronic diarrhea) or increased depletion (infection, pregnancy, burns, alcoholism, stress) [28, 29]. Serum zinc levels can also be lowered by medicines like penicillamine, diuretics, antimetabolites and valproate [28].

A moderate zinc deficiency can be seen as growth retardation, male hypoganadism in adolescents, rough skin, poor appetite, mental lethargy, delayed wound healing, cell mediated immune dysfunctions and abnormal neurosensory changes. Manifestations of severe deficiency include bullous pustular dermatitis, alopecia, diarrhea, pica, significant dysgeusia, emotional disorders, weight loss, intercurrent infections. If the deficiency is not treated then it may lead to a fatal situation [27].


36.4.1 Zinc Deficiency and Bariatric Surgery


Zinc deficiency is common after bariatric surgery as the main absorption sites such as duodenum and proximal jejunum are being bypassed and also the deficiency rates may vary depending on the type of surgery. After surgery, reduced stomach acid which is essential for zinc bioavailability, reduced protein intake, food intolerance and impaired zinc absorption may worsen the situation and may lead to zinc deficiency [30, 31]. In addition, regular iron and calcium supplementation can also contribute to insufficient zinc absorption [32, 33]. Zinc deficiency can also be associated with pregnancy and can lead to reduced birth weight, preterm delivery and congenital abnormalities and can induce hypertension in the mother [3436].

A recent retrospective study showed that patients (n = 272) who underwent RYGB, LSG and BPD-DS, 99 % had zinc deficiency preoperatively [31]. Studies at 2 years follow up after RYGB reported 20–35 % and Sleeve with 18–34 % and higher deficiency rates were found with BPD (74–91 %) with serum or plasma zinc levels [15, 37, 38]. It was found that, zinc deficiency persisted in patients even after 5 years follow up with 12.5 % after sleeve, 21–33 % after RYGB and 45 % after BPD. Rojas et al. stated that at 6 months, post bariatric surgery patients have an increased hair loss with lower intakes of zinc and iron requiring monitoring and supplementation [39].


36.4.2 Zinc Recommendation After Bariatric Surgery


Liver (beef, chicken, lamb, pork), red meat (beef, lamb, pork), sea foods like crab, lobsters, oysters and scallops, wheat germ, spinach, pumpkin, sesame and squash seeds, cashew nuts, mushrooms, chick peas, lentils, black beans, tofu, and whole grains are good dietary sources of zinc.

Copper and zinc compete for the same transport mechanism, so the excess of one might determine the deficiency of the other. Hence post bariatric patients should be advised oral zinc gluconate or acetate to provide 8–15 mg of zinc and 1 mg of copper for each 8–15 mg of zinc given.



The recommended Dietary Allowance for Zinc




























Zinc

Males

Females

RDA* (India) [18]

12 mg

10 mg

RDA*(US) [19]

11 mg

8 mg

RNI**(UK) [20]

11.3 mg

14.8 mg

NRV***(Australia/New Zealand) [21]

14 mg

8 mg


RDA* recommended dietary allowances, RNI** reference nutrient intake, NRV*** nutrient reference value


36.5 Vitamin A


Vitamin A (includes retinol, B-carotene and caroteniods), is an essential fat soluble vitamin absorbed through the small intestine either as retinal (animal derived) or carotene (plant and vegetable derived) and is stored in the liver. Vitamin A is essential to eyes and immune system and it plays an important role in the cellular proliferation process and also in the protection against free radicals hence protecting against development of certain chronic diseases. Vitamin A can also affect iron metabolism contributing to iron deficiency. Zinc deficiency can affect vitamin A metabolism as it is essential for the synthesis of retinol binding protein (RBP) in both the liver and the plasma and the oxidation of retinol to retinal [40]. Iron deficiency also compromises the function of the intestinal mucosa, affecting the absorption of vitamin A and iron deficiency should be corrected in order to normalize vitamin A levels [41].

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Nov 18, 2017 | Posted by in ENDOCRINOLOGY | Comments Off on Other Micronutrient Deficiencies in Bariatric Surgery

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