June 25, 2008
4 min read
Save

Micronutrient deficiencies possible after gastric bypass

You've successfully added to your alerts. You will receive an email when new content is published.

Click Here to Manage Email Alerts

We were unable to process your request. Please try again later. If you continue to have this issue please contact customerservice@slackinc.com.

Gastric bypass is the most common bariatric procedure performed in the United States. In this procedure, a small gastric pouch is created and is anastomosed distally to a Roux limb of the small intestine. This effectively bypasses the distal stomach, duodenum and proximal jejunum. The most common deficiencies after Roux-en-Y gastric bypass are that of iron, vitamin B12, folate, calcium and vitamin D.

Iron

In one prospective study, anemia developed in 36.8% of the population at a mean time from operation of 20 months. It was more frequent in women than in men and it required transfusions in 3.5% of the population. The etiology is multifactorial. Reduced dietary intake after RYGB is thought to play a role as well as the exclusion of acid stream from ingested food. Gastric acid oxidizes dietary iron so it is more readily absorbed. Furthermore, iron absorption occurs in duodenum and with gastric bypass this segment is not in contact with ingested food. Iron deficiency is more pronounced in women of reproductive age and in patients with ongoing chronic blood losses. Current recommendations for iron supplementation after RYGB include the administration of 40 mg to 65 mg of elemental iron per day (200 mg to 400 mg of ferrous sulfate). In premenopausal women, recommendations for iron supplementation increase to 100 mg of elemental iron per day (400 mg to 800 mg of ferrous sulfate).

Vitamin B12

Sagida Ahad, MD
Sajida Ahad
Brant K. Oelschlager, MD
Brant K. Oelschlager

Vitamin B12 deficiency occurs in 39.6% of patients after a gastric bypass. Gastric acid and enzymes are required to release protein bound vitamin B12 from ingested food, while intrinsic factor is required for intestinal absorption of vitamin B12. After RYGB, the ingested vitamin B12 does not pass through the acid and intrinsic factor producing milieu of the stomach. There is also evidence that free intrinsic factor is more susceptible to intestinal enzymes than intrinsic factor bound to vitamin B12. The absorption of nonbound vitamin B12 is not affected by RYGB. Therefore supplementation with vitamin B12 can correct deficiency in 80% of cases. Another less common cause of B12 deficiency after RYGB is bacterial overgrowth in blind loop.

Oral supplementation with 350 mg/day to 600 mg/day is necessary to normalize levels in 95% of patients. Although the body’s cobalamin storage is substantial (about 2,000 mcg) and daily needs low (2 mcg/day), the deficiency is common two to nine years after bariatric surgery. Vitamin B12 deficiency, though not always symptomatic, usually presents as macrocytic anemia and neurologic disease. The latter manifests as paresthesias, peripheral neuropathy and demyelination of the corticospinal and dorsal columns.

Folate

Folate is absorbed throughout the small intestine and is also produced by bacteria in the proximal intestines. Therefore, folate deficiency is not a long-term risk. If present it is easily corrected by multivitamin supplementation. Folate deficiency may well act as a sensitive marker of noncompliance with multivitamins. Folate deficiency is associated with anemia, abnormal embryogenesis and elevated homocystine levels. A high homocystine level is also linked with cardiac diseases.

Calcium and vitamin D

Morbidly obese individuals are usually found to have hyperparathyroidism (about 20%) and a serum calcium level usually within the normal range. Since serum 25-hydroxyvitamin D levels are inversely related to parathyroid hormone levels, this relative hyperparathyroidism is thought to develop due to a deficiency of vitamin D in obese individuals. This deficiency is thought to be multifactorial and related to decreased sun exposure, reduced bioavailability of vitamin D due to storage in fat cells and end organ resistance of bone to PTH. It is therefore recommended that all patients being considered for bariatric surgery have serum PTH and vitamin D levels checked preoperatively.

Calcium is absorbed in the duodenum and proximal jejunum while vitamin D is absorbed in jejunum and ileum. Hypocalcaemia is not readily evident after RYGB. As calcium absorption from gastrointestinal tract decrease, normocalcemia is maintained at the expense of cortical bone breakdown. Decreased bone density is more evident in spinal and hip bones. Further prospective studies are needed to clarify the correct supplemental dose of calcium and vitamin D after RYGB. Calcium citrate is the preferred form to be supplemented (rather than calcium carbonate) as the latter is not bioavailable in the absence of gastric acid.

Other deficiencies

Other less common deficiencies that can occur include thiamine, zinc, copper and vitamins A and K. Severe thiamine deficiency causes Wernicke area encephalopathy that manifests as nystagmus, ocular nerve palsies, ataxia and mental confusion. It is easily correctable with parenteral thiamine. Thiamine deficiency should be considered in patients who present with intractable nausea, vomiting and dehydration. Zinc deficiency is not common but can contribute to the generalized alopecia that follows gastric bypass surgery. Copper levels are not commonly monitored after gastric bypass. Clinical presentation is similar to that of vitamin B12 deficiency. Vitamin A deficiency can present as conjunctival dryness, keratitis and corneal scarring. High dose oral supplementation will usually reverse these changes.

Sajida Ahad, MD, is a Senior Fellow in the Center for Videoendoscopic Surgery at the University of Washington Medical Center.

Brant K. Oelschlager, MD, is an Associate Professor and Director of the Center for Videoendoscopic Surgery, Director of the Swallowing Center and Director of Bariatric Surgery in the Department of Surgery at the University of Washington.

For more information:

  • Amaral JF, Thompson WR, Caldwell MD, et al. Prospective hematologic evaluation of gastric exclusion surgery for morbid obesity. Ann Surg. 1985;201:186-193.
  • Hamoui N, Anthone G, Crookes PF. Calcium metabolism in the morbidly obese. Obes Surg. 2004;14:9-12.
  • Johnson JM, Maher JW, Samuel I, et al. Effects of gastric bypass procedures on bone mineral density, calcium, parathyroid hormone, and vitamin D. J Gastrointest Surg. 2005;9:1106-1110.
  • Mallory GN, Macgregor AM. Folate status following gastric bypass surgery (The great folate mystery). Obes Surg. 1991;1:69-72.
  • Rhode BM, Tamin H, Gilfix BM, et al. Treatment of vitamin B12 deficiency after gastric surgery for severe obesity. Obes Surg. 1995;5:154-158.