Deficiencies in micronutrients in morbidly obese patients are frequently diagnosed. Due to a limited diet for certain micronutrients, a great number of patients already develop these deficiencies prior to a bariatric procedure [14, 15]. Because LSG is a restrictive procedure and therefore lacks the malabsorptive component of for example a RYGB, the risk for developing deficiencies after surgery is considered low and therefore often not tested. However, because of the resection of the fundus, a number of micronutrients like iron and vitamin B12 are less likely to be absorbed, and the low risk status for developing deficiencies can be questioned [11, 16–18].
In the past, a number of publications presented data on micronutrient deficiencies found after partial gastrectomy for the treatment for ulcer disease. Iron, folate, and vitamin B12 deficiencies were most frequently reported. Long-term follow-up was advised to identify anemia, vitamin, and mineral deficiencies [19–23].
During the first year of follow-up, we found that anemia was identified in almost a third of patients. This implicates that preventing and screening for anemia and possible deficiencies leading to anemia should be one of the priorities in postoperative care. Although only eight patients developed abnormal MCVs it is likely that, with 23 (43%) patients developing iron deficiency and eight (15%) patients developing folate deficiency, these two deficiencies eventually contribute to the number of anemic patients. The iron deficiencies found can be partially explained by pre-existing shortage [14], but also by the LSG itself. Iron needs to be transformed to an absorbable form by hydrochloric acid in the normal stomach [11, 14]. The quantity of hydrochloric acid produced in the stomach is reduced and nutrients may pass the stomach faster after an LSG, thus making it more difficult to absorb iron [5]. Folic acid stores deplete quickly when intake is insufficient. This is also the most likely explanation for the eight patients (15%) who were found to have folate deficiency [24]. A normal individual has an average store of 2 mg of vitamin B12 that should last for 2 years when intake is insufficient. Morbidly obese patients have a higher risk of having a pre-existing vitamin B12 deficiency or lower storage levels, due to insufficient intake. Vitamin B12 uptake after LSG can become inadequate due to the lower production of hydrochloric acid which is needed to release bounded vitamin B12 in food [16, 17]. In the first year, five patients were diagnosed with a vitamin B12 deficiency, but it can be expected that this number will increase over the years when vitamin B12 stores have depleted.
Bone metabolism can change during the first year after LSG. Part of this change is explained by the weight loss itself due to the loss of pressure on the weight bearing bones, thus losing a potent stimulant for bone preservation. Furthermore, normal levels of vitamin D are essential for an adequate intestinal calcium uptake. A shortage in vitamin D eventually leads to a negative calcium balance and causes a compensatory rise in PTH to promote bone resorption [25, 26]. Although calcium levels were almost all within acceptable margins, 39% of the patients were diagnosed with elevated PTH levels and 39% were diagnosed with vitamin D deficiency. Suboptimal vitamin D levels (<50 nmol/L) occurred in 30 (55.5%) patients. The rise in PTH is, in some cases, most likely due to secondary hyperparathyroidism and not solely explained by a decreased uptake of calcium by insufficient calcium intake or low vitamin D levels. Albumin levels dropped in the first year resulting from protein malnutrition especially in the first months after the LSG. This is a second explanation for these results. Clearly, these patients are at risk for osteoporosis in the long-term when not corrected or treated for their calcium, vitamin D, and albumin deficiencies.
Another phenomenon arises when patients who underwent LSG are supplemented with multivitamins. Some vitamins showed a significant rise in serum levels. Serum vitamin A was elevated most frequently (48%). It is known for its function in cell differentiation and phototransduction. An excess in serum vitamin A can lead to ataxia, alopecia, dry skin, hepatotoxia, hepatomegaly, and might have an effect on bone metabolism by increasing bone resorption [27, 28]. Furthermore, high serum levels of vitamin A can be harmful in pregnant women due to the teratogenic effects on the fetus [13, 29, 30]. The serum levels in our patients, however, did not exceed 4 μmol/L after 1 year.
Vitamin B1 was low in six (11%) patients, but was found too high in 17 (31%) patients with a maximum of 230 nmol/L. Neurological abnormalities like Wernicke–Korsakoff can occur when thiamin levels are below the adequate level [11]. There has even been a report on Wernicke's encephalopathy after an LSG [31]. Reports on anaphylactic shock after intake of high doses of vitamin B1 have been published, but complications due to high levels seem rare [32, 33].
As vitamin B6 plays a role in amino acid metabolism, gluconeogenesis, and neurotransmitter synthesis, it is important to ensure adequate serum levels [32]. No patients had deficient serum vitamin B6, which is less than after a RYGB [34]. During this study, one patient developed neuropathy in hands and feet, which can be a symptom of high levels of vitamin B6 [35]. This patient had taken extra vitamin B6 on his own initiative, and serum levels had risen to seven times the maximum normal serum level. Supplements were stopped, and the symptoms vanished after a few weeks.