After BPD, the reduction of protein digestion, resulting from the reduction of the time of contact between digestive enzymes and the bolus (due to asynchronia and the delayed meeting between the alimentary bolus and the biliopancreatic secretions, the reduction of enzyme secretion, the faster intestinal transit time, and limited contact with the brush border of enterocytes) and the reduction of intestinal absorption area, causes a decrease in protein absorption of around 30 %. Furthermore, Scopinaro demonstrated in BPD subjects an endogenous nitrogen loss of about 5 g/day, which greatly exceeds what is considered to be the maximum normal in intact GI tract individuals. Both events play a significant role in the pathogenesis of protein malnutrition (PM) after BPD [16].

Protein malnutrition represents a dangerous potential complication of malabsorptive operations. Scopinaro describes two types of protein malnutrition: the sporadic and the recurrent one. The sporadic protein malnutrition can occur in the early postoperative period, because of too drastic protein intake reduction or the preference for carbohydrate intake, and at any time after the operation, because of prolonged diarrhea or reduced food intake for any reason. Of much greater importance is the recurrent form of protein malnutrition. A number of different factors, alone or in combination, can lead to this condition. Patient–dependent factors are insufficient protein intake, insufficient protein absorption per unit of intestinal surface, and excessive loss of endogenous nitrogen. Operation–dependent factors are too small stomach (causing too rapid emptying and too rapid intestinal transit with permanently reduced absorption) and too short alimentary limb (causing insufficient protein absorption). One or more of these factors can be responsible for the complication. The concept is that specific operation as it is, in that specific subject as he/she is, is incompatible with good protein nutritional status. After two or more episodes of protein malnutrition, the decision for surgical revision is made, consisting of elongation of the common limb. Because, protein absorption depends on the length of the small bowel from the GEA to the ICV, the elongation must not be done along the alimentary limb, but along the biliopancreatic one. The standard which in our hands guarantees the solution of all protein nutritional problems is to add 150 cm, for a final total length of 400 cm. This obviously entails the restabilization of body weight at an average level which corresponds to about 25 % regain of the original excess weight [3].

The incidence of PM in the initial series of Scopinaro is included between 7 and 21 % [17].

On the contrary, another study by Trotte on 180 patients submitted to standard-BPD demonstrated a protein deficiency, requiring parenteral nutrition and the elongation of the common limb, only in two patients [18].

Marinari in 2004 reviewed the experience of our group, in the last 858 patients with “ad hoc stomach ad hoc alimentary limb” BPD, 5 years after the operation, and found mild hypoalbuminemia in 11 % and severe in 2.4 % of BPD patients. Reoperations were performed in 6 % of the total patient population, mainly for late recurrent protein malnutrition [19].

Nanni found that the main specific complication after “ad hoc stomach ad hoc alimentary limb” BPD was PM, which was observed in 3.4 % of operated patients [20].

According to Marceau, the BPD-DS procedure, due to the conservation of antrum and pylorus, would be expected to reduce diarrhea and risk of PM, when compared with standard-BPD. On the contrary, the author observed a high incidence of protein deficiency 79 months after BPD (11 % of the patients revealed albumin levels <3.5 g/dL, and 2.4 % <3.2 g/dL), needing revisional surgery in 6 % of them [21].

Dolan also found that 18 % of patients were hypoalbuminemic at a median follow-up of 28 months with no significant differences between BPD and BPD-DS with a common channel length of 50 cm [22].

Rabkin, in a study on 589 consecutive patients, showed that after BPD-DS, protein metabolism markers were normal within the first 3 postoperative years, but with a common channel of 100 cm [23].

Marceau had similar results, with the length of the common channel of 100 cm instead of 50 cm, in a subsequent study on 465 patients who underwent BPD-DS at 4 years [4].

In condition of normal GI anatomy, half of protein absorption occurs in the duodenum, the majority of protein uptake occurring within the mid-jejunum. It is therefore obvious that protein deficiency may occur after RYGBP as well.

This complication, indeed quite rare after standard RYGBP (with 75–150 cm Roux limb lengths), is observed more frequently after longer Roux limbs, with a reported incidence of 7–12 % [24]^.

In the randomized series of Brolin, no protein deficit was showed at a minimum of 2 years after standard RYGBP, while 13 % of the patients submitted to a distal RYGBP had PM [25].

Kalfarentzos confirmed this difference with a 5.9 % protein deficiency rate 20 months after distal RYGBP, but no deficiency after the standard RYGBP [26].

After standard and distal RYGBP, 1.4 and 3 % of patients, respectively, showed an albumin level <3 g/dL in the study of Skroubis [27].

Clinical manifestations of PEM are hypoalbuminemia, asthenia, anemia, loss of muscle mass, anomalies of the skin mucosa and nails (hair loss, striated nails, dermatitis), and edema. Protein depletion is very easy to recognize by following albumin (albumin <3.5 g/dL).

An intake of 1.0–1.5 g/kg ideal body weight (60–80 g/day total protein) in the early postoperative period is recommended after any bariatric operation. Due to the loss of endogenous nitrogen greater than normal, alimentary protein requirements in BPD patients have to be increased by 30 %, that is approximately 90 g/day. During the postoperative visits, the assessment of protein intake has to be performed, and protein supplementation should be given when protein intake remains inferior to 60 g/day.

Mild-to-moderate cases of PM are usually corrected by more frequent dietetic counseling and increased protein intake [27].

In case of severe PM, a prompt rehospitalization and the initiation of parenteral nutrition is mandatory. Three weeks of total parenteral nutrition (TPN) are usually sufficient to correct the acute problem, whether PM occurs after the BPD or RYGBP.

In condition of normal GI anatomy, while bile salts are absorbed only in the terminal ileum, fat and fat-soluble vitamins absorption occur all along the small intestine, the majority of lipids uptake occurring in the proximal two thirds of the jejunum.

Following BPD and distal RYGBP, the meeting between the food and biliopancreatic secretions and the absorption occurs in the common channel, resulting in a reduction of lipid absorption of around 70 %. Based on this, Scopinaro showed, after standard-BPD, a maximum threshold of 40 g/day of the dietary fat absorption.

If it is true that the shorter the length of the common channel (generally varying between 50 and 100 cm), the greater the fat malabsorption, the consequent weight loss and maintenance are, it is equally true that longer common channels are better tolerated, being associated with less steatorrhea and diarrhea.

Fat-soluble vitamins and essential fatty acid deficiencies are common following malabsorptive procedures. Linoleic and α-linoleic acids are fundamental components for the prostaglandin and leukotriene synthesis. Therefore, deficit of essential fatty acids can induce anemia, thrombocytopenia, alopecia, and dermatitis, even if this topic has not been studied in depth.

Fat malabsorption, clinically expressed by steatorrhea, never present after ASGB and SG, frequently present after RYGBP, is always present after BPD, being the principal mechanism by which BPD promotes weight loss. Therefore, special attention to the quality of alimentary fat should be given after any malabsorptive operation.

Ingested iron is solubilized, ionized, and reduced from the alimentary ferric form to its ferrous form by acid gastric juices, and subsequently actively transported into the cell. Iron absorption may occur throughout the small bowel, but it is best absorbed in the duodenum and in upper jejunum.

There are several mechanisms that cause iron malabsorption after RYGBP and BPD, including a relatively achlorhydric gastric pouch, with limited exposure of food to acid, and the exclusion of duodenum and proximal jejunum (where iron is maximally absorbed) from digestive continuity. After gastric restrictive procedures, a reduction of red meat intake, the major source of heme, and of iron-rich foods can be an important factor in such deficiency.

SG, entailing the removal of most of the stomach, so reducing the production of hydrochloric acid, is followed by iron deficiency [28]. Indeed, hemoglobin and hematocrit were less than normal in, respectively, 28.6 and 25 % of the 82 patients submitted to SG at 5 years, in a study by Saif et al. [29]. A Dutch study confirmed a decrease in iron levels in 43 % of patients 1 year after SG [30]. On the contrary, a report from Saudi Arabia showed no occurrence of iron deficiency 1 year after sleeve gastrectomy [31].

Although there is no solid data regarding iron deficiency after purely restrictive operations, this complication occurs surely after RYGBP and BPD.

The American Society of Bariatric Surgery surgeons showed the incidence of iron deficiency of 14–16 % after RYBG and 21–26 % after BPD [32].

Brolin demonstrated an iron deficiency in 49–52 %, and anemia in 35–74 % in a series of 298 superobese patients, 3 years after RYGBP, depending on the Roux limb length [25].

Skroubis found an iron deficiency after RYGBP increasing from 26 % preoperatively, to 39 % at 4 years, and then decreasing to 25 % at 5 years [27].

BPD also reduces the iron absorption, and many studies showed a higher prevalence of iron deficiency when compared with other bariatric operations, particularly in young women [23].

In the aforementioned study by Skroubis, iron deficiency rates increased from 32.6 % preoperatively to 44.4 % at 4 years and 100 % at 5 years, following BPD [27].

Marceau after BPD-DS showed abnormal ferritin levels (<20 μg/L) in 4 % of the 92 patients preoperatively, and in 25–40 % at 5 years [21].

Dolan reported an iron deficiency in 22.9 % of his patients at mean follow-up of 28 months. This complication was similar in patients submitted to BPD with or without a duodenal switch, in spite of the respect of antrum, pylorus, and a cuff of duodenum entailed with the latter operation [22].

Skroubis demonstrates no differences in the incidence of iron deficiency, in a study comparing patients submitted to RYGBP or BPD at a 5-year follow-up [27].

Brolin demonstrated a significant decline in the iron status in 63 % of 140 subjects followed for 2 years after RYGBP in spite of a correct standard supplementation. This suggests that additional prophylactic iron supplements should be provided for women to prevent iron deficiency, in addition to the standard supplementation [33].

The laboratory diagnosis for iron deficiency includes anemia with a low MCV, low serum iron, high TIBC, and low serum ferritin level.

Subjective manifestations are fatigue, reduced exercise tolerance and dyspnea. On examination, the patient has pale conjunctiva, koilonychia (spoon nails), hair loss, and possibly atrophic glossitis.

Though malabsorption is the obvious reason to explain any iron deficiency after bariatric surgery, an additional mechanism for iron deficiency after RYGBP and BPD is the gastrointestinal blood loss. Typical sites of bleeding are a marginal ulcer (on the anastomosis between the jejunum or ileum and the gastric pouch), an iron-losing enteropathy of bypassed loop, an overgrowth of intestinal bacteria phenomenon in the small bowel excluded, or hemorrhoids. But any pathology of the GI tract (such as a gastrointestinal cancer) should be excluded in refractory cases.

Oral treatment usually consists of 325 mg of ferrous sulfate or 200 mg of ferrous fumarate (providing about 65 mg of iron), one to two tablets a day as prophylaxis, and three to four tablets a day to correct iron deficiency. The bypass of the antrum and duodenum makes the iron absorption very difficult in deficient patients. Preparations containing elemental iron complexed with a polysaccharide are well absorbed and can be assumed in single daily doses of 100–200 mg. The dosage may be increased if iron parameters do not improve within a few months of starting therapy. The addition of vitamin C enhances the absorption.

Sometimes, parenteral iron infusion with iron dextran, ferric gluconate, or ferric sucrose is needed either in patients who have poor response to oral iron therapy or in case of intolerance or noncompliance. Intramuscular iron is not tolerable in the long run. On the contrary, intravenous iron dextran can be well tolerated by patients, also as an outpatient procedure, and can be used regularly.

After bariatric surgery, iron deficiency can occur early after surgery or after some time. Patients submitted to RYGBP and BPD require postoperative screening for iron status, including blood count with MCV, serum iron, ferritin, and TIBC. After the first year, these values should be checked yearly or biyearly throughout life.

Thiamin absorption is maximal in the small bowel, thanks to a mechanism of active transport, mediated by a specific sodium and energy-dependent carrier, and a mechanism of passive diffusion. The vitamin B1 deficiency has a low prevalence: only 29 cases were identified in a study on 168,010 bariatric operations, (0–0.002 %) [34], but it is a major complication of all bariatric operations.

As vitamin B1 is contained in all aliments, the deficit occurs as a consequence of the association of frequent episodes of vomiting and a reduced intake. It is not evident if the decreased absorption plays a role in the development of the deficiency. Symptomatic thiamine deficiency has been observed both after restrictive and malabsorptive procedures. The small amount of liver thiamine stored (which last approximately 30 days) contributes to this deficiency weeks or months after surgery.

Since vitamin B1 is involved in carbohydrate metabolism, administration of intravenous glucose or dextrose in patients complicated or dehydrated from vomiting, who have low vitamin B1 reserves, has been reported to be a precipitating factor for Wernicke’s encephalopathy (bariatric beriberi).

A few cases of the deficiency have been reported after ASGB [35].

Low levels of thiamine were demonstrated in 0–11 % of patients 1 year after SG and in 31 % of patients after 5 years [36].

In a series of 141 patients submitted to RYGBP, the prevalence of thiamine deficiency was 18 % after 1 year and 11 % after 2 years [37].

A study on 1,663 patients submitted to BPD demonstrated an incidence of 0.18 % of Wernicke’s encephalopathy 3–5 months after the operation [38].

The laboratory diagnosis for deficiency includes a low serum thiamine level and a reduced erythrocyte transketolase activity.

Wernicke’s encephalopathy classically presents with a clinical triad: ocular manifestations, (such as nystagmus and ocular palsies), ataxia, and mental disturbances such as confusion. More often, an isolated peripheral neuropathy is described (dry beriberi) with symptoms of pain, burning, or tingling in the distribution of the affected sensory nerves, or peripheral extremity weakness in case of motor impairment.

In case of suspected deficiency, prompt recognition and immediate treatment with 50–100 mg of parenteral thiamine every 8 h can resolve ocular symptoms within a few days, but neurologic sequelae need months to completely regress, and are often not totally reversible.

In patients with protracted vomiting, aggressive supplementation with thiamine for 1 month after surgery avoids the deficiency.

Compliance to a multivitamin supplement is usually sufficient to prevent thiamine deficiency in most of the cases.

The presence of a bacterial overgrowth in the bypassed bowel must be considered when patients do not respond to an adequate oral therapy, due to an increased consumption. In these cases, the diagnosis can be confirmed by elevation of serum folate level or by the increase in hydrogen or methane in breath after an oral load of glucose.

Folate deficiency, defined as serum folate levels <3 ng/mL, is the most common nutrient deficiency after gastric restrictive procedures, usually caused by a decrease in the intake of vegetables in the immediate postoperative period. After RYGBP and BPD, the deficiency is produced by a reduction of acid and pepsinogen secretion (responsible for the vitamin bioavailability) and the lack of contact of food with the duodenum and the proximal third of the jejunum, primary sites of its absorption.

Gasteyger found a significant decrease in serum folate in 44 % of 36 women submitted to ASGB 2 years after surgery [39].

Folate deficiency has an incidence of 9–35 % after bypass surgeries [40].

Halverson demonstrated that 1 year after gastric bypass, 63 % of patients have folate deficiency [41].

Another study by Brolin showed folate deficiency in 22 % of patients 2 years after the operation [33].

On the contrary, the risk of folate deficiency is negligible in the long term, because an important bacterial synthesis of the vitamin occurs in the small intestine, progressively colonized after most bariatric operations.

Clinical manifestations of folate deficiency are megaloblastic anemia or a normocytic anemia, characterized by increased red cell distribution width. On the contrary, high serum folate levels are a specific marker for intestinal bacterial overgrowth.

Unlike iron and vitamin B12, routine multivitamin preparation (400 μg/day) is sufficient to maintain a good folate status.

The correction of folate deficit consists of oral folic acid 1–5 mg daily, even if the deficiency is as a rule corrected with multivitamin supplements alone.

A folate supplement of 1 mg/day is particularly important in pregnant women, in order to avoid risks of fetal neural-tube defects in case of deficiency.

Vitamin B12 deficiency is a common consequence both of restrictive procedures and malabsorptive ones, and involves multifactorial origin.

RYGBP and BPD, but also SG, excluding the majority of parietal cell mass and chief cells, primarily located in the fundus and body of the stomach, cause a significant vitamin B12 bioavailability reduction and a decreased production of intrinsic factor, a glycoprotein produced by parietal cells, required for absorption of the vitamin in the terminal ileum.

Further potential mechanisms for the vitamin malabsorption after RYGBP and BPD are the bypass of duodenum and the rapid transit time in the ileum. The risk of B12 deficiency is also increased after purely restrictive surgery, if patients reduce their intake of meat or milk products.

In a group of 100 patients planned for bariatric surgery, the incidence of vitamin B12 deficiency has been demonstrated in 5 % of subjects [42].

SG should have a more important effect on B12 status, compared with other restrictive procedures, due to resection of the fundus and the body of the stomach. Indeed, deficiencies in vitamin B12 have been showed at 1 and 3 years following SG [28], but not in the study by Saif [29].

Abnormal serum B12 levels (<180 pg/mL) were observed in 154 of 429 patients (36 %) at an average of 22 months after gastric bypass surgery in a study [43].

Another study confirmed that 33 % of patients have vitamin B12 deficiency (<250 pg/mL) 1 year after gastric bypass [41].

Brolin also showed vitamin B12 deficiency in 37 % of patients 2 years after gastric bypass [33].

Comparing 45 and 25 patients submitted, respectively, to BPD-DS and RYGBP at 2 years, Breton showed that vitamin B12 deficiency was more common in patients with gastric bypass [44].

The prevalence of vitamin B12 deficiency after bariatric surgery ranges from 4 to 62 % [45], whereas clinical symptoms are less common. This variability from study to study can be explained both by the different length of follow-up of studies, conditioning the time necessary to deplete the considerable body storage of vitamin, and by the differences in regime and adherence to supplementation.

Vitamin B12 is synthesized by bacteria and it is present in all forms of animal tissues, but not in fruits and vegetables. The recommended dietary intake is about 5 μg per day. The normal human body storage of the vitamin is about 2,000 μg, so the deficiency occurs years after surgery.

Clinical manifestations of vitamin B12 deficiency are the pernicious (megaloblastic) anemia and development of disorders of both CNS and PNS. These can include paresthesias, sensory abnormalities, spastic paraparesis, visual loss, cognitive, and neuropsychiatric manifestation.