Bsm1 vitamin D receptor polymorphism and calcium homeostasis following bariatric surgery.

PURPOSE/AIM: To evaluate the association between the Bsm1 vitamin D receptor polymorphism and the calcium-vitamin D-parathormone axis following bariatric surgery. MATERIALS AND METHODS: This cross-sectional study included 86 morbidly obese patients, who underwent either gastric bypass or sleeve gastrectomy, with a mean follow-up of four years. Calcium metabolism indices and bone turnover markers were assessed according to the presence of secondary hyperparathyroidism and the Bsm1 vitamin D receptor genotypes. RESULTS: Secondary hyperparathyroidism (42.2% of sample) was associated with lower levels of 25hydroxyvitamin D and elevated markers of bone turnover. In subjects without secondary hyperparathyroidism, presence of the unfavorable B allele resulted in higher levels of parathormone (Bb and BB vs. bb genotype: 50.3 ± 8.2 pg/dl vs. 44.4 ± 10.7 pg/dl, p = .011, adjusted for weight loss, baseline body mass index, 25hydroxyvitamin D, surgical procedure, and duration after surgery). In the whole sample, patients bearing the unfavorable B allele exhibited lower weight loss, a parameter that was negatively associated with markers of bone resorption. CONCLUSIONS: Secondary hyperparathyroidism is highly prevalent after bariatric surgery. Bsm1 vitamin D receptor polymorphism may have an effect in early stages of calcium metabolism imbalance, while no association is detected in patients who have already developed secondary hyperparathyroidism. Moreover, vitamin D receptor polymorphism is associated with post-surgery weight loss, a process related to bone turnover.

[Nutritional support in surgical treatment of patients with post-gastroresection and post-gastrectomy syndromes].

The aim of the research determine the character and peculiarities of nutritional support in surgical treatment of patients with gastroresection--and total gastrectomy syndromes. Analyzed are the results of the evaluation nourishing status of 68 patients who have had a resection intervention on the stomach. It was noted that the 26.5% of patients with clinical manifestations of diseases of operated stomach arise sub- and decompensated forms of disorders metabolism and nutrition, entailing numerous violations of homeostasis and requiring compliance with reconstructive surgical interventions. We studied the results of the implementation of the reconstructive operations with the formation of functionally active (see text for symbol) in 18 patients, suffering from the disease of stomach operated on. It is proved, that the rational nutritional support in the perioperative period allows to avoid gross violations of metabolism and provides a reasonably good compensation digestive function, significantly improving the quality of life of this category of patients.

[Abnormalities of bone metabolism in bariatric surgery]. / Alteraciones del metabolismo óseo en la cirugía bariátrica.

Obesity is an ever-increasing disease in our environment, and a major risk factor for the development of other chronic diseases that increase morbidity and mortality. Bariatric surgery is an effective treatment for obesity, since it not only allows a significant and sustained loss of weight, but also an important reduction of its co-morbidities. However, this treatment is not free of complications, since along with weight loss, frequent nutritional and metabolic deficiencies have been described. These complications are particularly frequent when mixed surgical procedures with a restrictive and malabsortive component such as Roux-en-Y gastric bypass and biliopancreatic diversion are performed. The nutritional deficiencies observed include, to a greater or lesser extent, malabsorption of fat and liposoluble vitamins, as well as other micronutrients such as calcium. As a result, disorders of bone mineral metabolism with skeletal manifestations that include bone mass reduction, increased bone turnover and defective bone mineralization may develop.

Nitrous oxide-induced B12 deficiency myelopathy: Perspectives on the clinical biochemistry of vitamin B12.

Beginning with a case report of nitrous oxide (N2O)-induced B12 deficiency myelopathy, this article reviews the clinical biochemistry of vitamin B12, and examines the pathogenetic mechanisms by which B12 deficiency leads to neurologic damage, and how this damage is potentiated by N2O exposure. The article systematically examines the available experimental data relating to the two main coenzyme mechanisms that are usually suggested in clinical articles, particularly the deficient methylation hypothesis. The article demonstrates that neither of these mechanisms is fully consistent with the available data. The article then presents a novel mechanism based on new data from the neuroimmunology basic science literature which suggests that the pathogenesis of B12 deficiency myelopathy may not be related to its role as a coenzyme, but rather to newly discovered functions of B12 in regulating cytokines and growth factors.

[The enterochromaffin-serotonin system and Helicobacter infection in the mechanisms of the staged development of peptic ulcer]. / Enterokhromafinno-serotoninova systema i khelikobaktriina infektsiia v mekhanizmakh stadiinoho rozvytku vyrazkovoï khvoroby.

Submitted in this article are scientific propositions and problems concerning the way ulcer disease (UD) of the gastroduodenal system (GDS) develops through its particular stages, and pathosanogenous role which the enterochromaffin-serotonin system (ECSS), a part of the diffusive neuroendocrine APUD-system of the organism, has in it, along with etiopathogenetic role Helicobacter infection plays in the gastroduodenal mucosa (M). Experience gained by the authors with prospective comprehensive evaluation and treatment of 310 patients with chronic gastroduodenitis (CGD), 198 UD GDS patients and 350 of those surgical patients who had undergone resection of the stomach for complicated UD GDS, indicates that all above pathological states share common etiopathogenetic, clinical, histomorphological and microbiological (Helicobacter infection) features, which facts suggest a common pathomorphogenesis of CGD, erosive GD, UD GDS and postgastroresectional UD, and a staged character of erosive-ulcerous transformation in the GDS M, with the hypercoagulative sings being present at the level of hemomicrocirculation. Progressing structural and functional changes in ECSS parallel to stages of development and severity of the UD GDS course suggest their interrelationship to pathosanogenesis during all stages of erosive-ulcerous transformation. At the molecular level, this may reflect directly the course of staged ulceration and a point of activation of processes of physiological defence, this being of diagnostic as well as prognostic value. The enterochromaffin-serotonin conception of pathosanogenesis of staged erosive-ulcerous transformation in GDS M supplements, rather than contradicts to a current infectious Helicobacter hypothesis of ulcerogenesis. Thus, evaluation of ECSS structural and functional status in UD GDS is to be part of a diagnostic algorithm testing severity of the course as well as of a monitoring of treatment and prognostication.

Calcium regulating hormones and bone mineral content in patients after subtotal gastrectomy.

Twenty-nine men who had undergone Billroth I gastrectomy and 19 men who had undergone Billroth II gastrectomy were studied to examine the changes in their calcium regulating hormones and bone mineral content following surgery. The serum calcium and phosphate concentrations in the patients with Billroth I and Billroth II were normal. The Billroth II group had an elevated level of serum alkaline phosphatase and reduced bone mineral content. The 24,25(OH)2D concentration was reduced (P < 0.01) and 25(OH)D and 1,25(OH)2D concentrations were increased (P < 0.01, P < 0.05, respectively) in the Billroth II group. It was suggested by our study that the Billroth II patients had a reduced bone mineral content and an elevated 1,25(OH)2D concentration. Therefore, the pathophysiology of postgastrectomy bone metabolic disease is not due to vitamin D deficiency, but may instead be due to reduced calcium absorption in the intestine.

The value of sham-feeding tests in patients with postgastrectomy syndromes.

OBJECTIVE: The value of gastric secretory testing in surgical practice has been questioned. Sham feeding (SF) is a test of gastric secretion that determines the status of gastric vagal innervation or incomplete vagotomy. Our purpose was to show that the results of SF tests affect operative strategy and/or clinical management. DESIGN: The medical records of 30 consecutive patients studied with SF in our laboratory were reviewed to determine if patient management was affected by the results of SF. PATIENTS: All 30 patients had prior vagotomies. Sham feeding was performed in patients (1) before planned reoperation for postgastrectomy syndromes (n = 17), (2) with peptic ulcerations/pain of unclear etiology (n = 8), or (3) postoperatively in those who were at high risk for recurrent ulcer (n = 5). RESULTS: Sham feeding indicated complete vagotomy in 16 patients and incomplete vagotomy in 14 patients. In 17 patients studied before planned reoperation, operative strategy was affected by results of SF in 15 cases; five patients had revagotomies performed at reoperation, 11 did not, and one patient had her operation canceled. In patients with atypical postoperative ulcers/pain, management was changed in only two of eight patients. In the high-risk patients studied postoperatively, management was affected in four of five patients. CONCLUSIONS: (1) We believe that our results justify the performance of SF before any reoperation on the stomach, since an operative plan was nearly always affected. (2) In patients with atypical peptic complaints after gastric surgery, SF usually (80%) confirmed acid hypersecretion, thereby affecting management less often. (3) Although unproved, we believe SF results can guide the use of "prophylactic" H2-blockers in treating selected high-risk postgastrectomy patients.

[Study of postgastrectomy fatty liver].

Fatty liver was often found concomitantly by the ultrasound during the follow up study of the gastric cancer operation. By ultrasound, development of postgastrectomy fatty liver was seen in 29 out of 176 patients (16.5%) with several gastrectomies. The number of the patients with postgastrectomy fatty liver was 12 out of 104 patients (11.5%) with distal partial gastrectomy with B-I reconstruction, while that was 17 of 72 patients (23.6%) with total gastrectomy with several reconstructions. The incidence of postoperative fatty liver change was significantly higher in the patients under 59 years old compared to the elders. Seventy-five g oral glucose test induced oxyhyperglycemia and hyperinsulinemia in patients with gastrectomy, especially with total gastrectomy. Integrated plasma insulin and triglyceride responses during first one hour in postgastrectomy patients were significantly higher than preoperative values. Moreover, plasma insulin and blood sugar in response to oral glucose test were significantly higher in patients with postgastrectomy fatty liver, compared to those in patients without fatty liver. These results suggested that the postgastrectomy fatty liver was resulted from the abnormality of the glucose metabolism.

[The late complications and nutritional follow-up in 96 patients who underwent a total gastrectomy]. / Complicanze tardive e follow-up nutrizionale in 96 pazienti sottoposti a gastrectomia totale.

Clinical and nutritional follow-up was performed in 96 patients who had undergone total gastrectomy. We studied the incidence of clinical complications and alterations of nutritional parameters in those patients who had undergone curative resection and were alive and free of neoplastic disease 1 year (36 patients) and 2 years (26 patients) after operation. We observed a very low incidence of late complications, and nutritional parameters, 1 year and 2 years after operation, were normal in almost all the patients. We obtained these results because we performed a Roux en Y esophagojejunostomy using an at least 60 cm-loop; we also adopted a strict and rigorous follow-up, able to guarantee an adequate daily calorie intake. In fact, a close relationship between calorie intake and the variations of nutritional parameters was observed.

Malabsorption of fat after partial gastric resection. A study of pathophysiologic mechanisms.

The causes of fat malabsorption after gastric resection were studied in patients randomized to Billroth I gastroduodenostomy or Roux-en-Y gastrojejunostomy after antrectomy and selective gastric vagotomy for intractable prepyloric peptic ulcer. Eighteen patients were studied 2 years or more postoperatively. Assessment of food intake concerning protein, fat, carbohydrate, vitamins and minerals showed deficiency in seven cases, but without significant difference between the two operation types. Postoperative weight loss did not differ significantly between the two study groups, but the faecal excretion of fat was significantly larger (p less than 0.05) after gastrojejunostomy than after gastroduodenostomy. Since both the oro-caecal transit time and the breath excretion of hydrogen after a standardized test meal showed no intergroup difference, the results suggest that duodenal exclusion may be of particular pathophysiologic importance for the observed malabsorption of fat after gastric resection.

[Metabolic disorders in the gastrectomized patient]. / Estudio de los trastornos metabólicos en el enfermo gastrectomizado.

The present study attempts on one hand to study the metabolic disorders which may present themselves in the gastrectomized patient, such as the malabsorption of fat, vitamin B12, folic acid and iron as well as the possible correlation between steatorrhea and the presence of exocrine pancreatic insufficiency. For this purpose a group of 71 patients have been studied who have undergone a subtotal gastrectomy (70.42%) or total (29.58%) in the General Surgery Services of Elche. The results obtained show the presence of ferropenic or megaloblastic anemia in 61.97% of the group, serious steatorrhea in only 3 patients (4.22%) and calciumphosphorous metabolism alterations appeared in 21.13%. With this we conclude that anemia is the most frequent ferropenic alteration in the gastrectomy patient; steatorrhea does not seem to be produced exclusively by the presence of exocrine pancreatic insufficiency and bone alterations in the gastrectomized patient appear in an insidious manner, being more a question of biochemical alterations than actual clinical lesions.

[Bone disorder after gastrectomy--clinical & experimental studies].

To study the pathophysiology of bone disorder after gastrectomy, 320 patients and 40 Wistar male rats were used. Clinically, patients who had received gastrectomy 1-15 years previously, were examined for skeletal symptoms, serum biochemistry, microdensitometry of second metacarpal bone, and 20 of them were then studied in a calcium infusion test. Using microdensitometry, abnormality of bone metabolism was observed in 38% of the patients. In severe cases, a significant decrease of serum Ca. and increase of alkaline phosphatase were observed (p less than 0.05), 65% complained of joint pain. In the calcium infusion test, severe cases showed a low urinary excretion of Ca, like osteomalacia, and unlike osteoporosis. Experimentally, body weight & amount of food intake decreased and fatty diarrhea was observed in rats after total gastrectomy. Skeletal changes including thinning of the cortex, loss of medullary trabeculation & decrease of bone ash and biochemical changes such as low serum Ca. 25(OH)D3, 24, 25(OH)2D3 and high iPTH levels were observed. Also the bone formation rate was lower than control as detected by tetracycline double labelling method. As low food intake & fatty diarrhea after gastrectomy which result in Ca. & vit. D insufficiency may be the major etiology of bone disorder.

The influence of the duodenal passage on postprandial neurotensin release in dogs.

All types of gastric resections induce an abnormal release of gastrointestinal hormones. The missing duodenal passage seems to be the most important factor for these disturbances. In the present study we have examined the effect of exclusion and restoration of the duodenal passage on the postprandial release of neurotensin in dogs. After feeding a standard canned dog meal, exclusion of the duodenal passage by a Billroth-II-resection caused a significant increase in postprandial neurotensin release compared to the control group (peak levels 52 +/- 5.6 to 29 +/- 6 pg/ml preoperatively, integrated output 2132 +/- 228 to 3604 +/- 213 pg/ml x 150 min. p less than 0.05). Reconstruction of the duodenal passage by the Biebl-Henly-Soupault-procedure tended the elevated neurotensin levels towards normal (peak levels 36 +/- 4.8 pg/ml, integrated output 2448 +/- 236 pg/ml x 150 min., p less than 0.05). From our data we conclude that changes in intestinal transit time are responsible for the pathological increase in neurotensin release after exclusion of the duodenal passage.

Gastric outlet loss and enterogastric reflux after gastrectomy.

The relationship of gastric secretion in response to a single injection of insulin and in response to a histamine infusion, before and after partial gastrectomy, was analysed in 58 patients. The aspirated gastric juice was corrected for gastric outlet loss and enterogastric reflux. Gastrectomy drastically reduced the stimulated gastric secretion by a similar proportion for the two secretagogues, thereby implying that antral gastrin plays no greater part in one than in the other. Gastric outlet losses were also reduced after gastrectomy, but as a fraction of gastric contents, both gastric outlet loss and enterogastric reflux more than doubled; the possible relationship of these findings to the aetiology of gastric ulcer is discussed.

Correlation between lowered PgE2 levels and alkaline reflux gastritis in patients subjected to Billroth II. Pylorogastrectomy: possible improvement with sulglycotide.

In patients subjected to pylorogastrectomy with anterior gastroenterostomy (Billroth's operation II) the remaining gastric mucosa is exposed to the damaging action of bile with consequent reduction of locally generated prostaglandins. The purpose of the present study was to explore the correlation between PgE2 levels in such postgastrectomy patients before and after treatment with sulglycotide. Twelve patients with clinical, endoscopic and histological evidence of alkaline reflux gastritis were treated with sulglycotide in daily doses of 1600 mg for 30 days. At termination there was a definite clinical, endoscopic and histological improvement with significant (p less than 0.001) increase of PgE2 levels.