[Do Vitamins Play a Role in the Pathogenesis and Therapy of Sepsis?] / Spielen Vitamine bei der Pathogenese und Therapie der Sepsis eine Rolle?

Hospital mortality of severe sepsis and septic shock is still around 40 % according to recent studies. In accordance to the current sepsis definition, sepsis is a life-threatening organ dysfunction caused by a dysregulated response of the organism to infection. Septic shock is defined by vasopressor-dependent circulatory failure and lactic acidosis. Patients with sepsis and septic shock are often old and/or characterized by severe comorbidities, e. g. tumor or liver disease. These factors also predispose to malnutrition and hence to a corresponding deficiency of essential nutritional components e. g. vitamins. A number of recent studies and reviews have addressed the question whether deficiencies in certain vitamins may facilitate the transition from infection to septic shock. In addition, studies have investigated the effect of high-dose vitamin therapies on sepsis mortality and sepsis-associated organ dysfunctions. This article would like to summarize this current discussion with a focus on vitamin B1 (thiamine), vitamin C and vitamin D.

Weight Loss and Nutritional Outcomes 10 Years after Biliopancreatic Diversion with Duodenal Switch.

BACKGROUND: Biliopancreatic diversion with duodenal switch (BPD/DS) is the most effective bariatric surgical procedure, but major concerns exist about the nutritional consequences. OBJECTIVES: The study reported weight loss and nutritional outcomes of 80 patients with a follow-up of at least 10 years. SETTING: The follow-up was conducted at a university hospital as well as in a private practice institution in France. METHODS: Eighty patients operated on between February 2002 and May 2006 were reviewed. Weight outcomes were analyzed as well as complete biological status. Revisions were reported as well as the number of patients taking vitamin supplementation. RESULTS: A follow-up of 141 ± 16 months was available for 87.7% of the patients at least 10 years from surgery. Preoperative BMI decreased from 48.9 ± 7.3 to 31.2 ± 6.2 kg/m2 with an EWL of 73.4 ± 26.7% and a TWL of 35.9% ± 17.7%. Despite weight regain ≥10% of the weight loss in 61% of the cases, 78% of the patients maintained a BMI <35. Fourteen percent of the patients had a revision. Normal vitamin D levels were found in 35.4%. The overall PTH level was 91.9 ± 79.5 ng/mL, and 62% of the patients had hyperparathyroidism. Other deficiencies were less frequent but fat-soluble deficiencies as well as a PTH >100 ng/mL were significantly associated with the absence of vitamin supplementation. CONCLUSION: BPD/DS maintains a significant weight loss, but remains associated with side effects leading to revision and multiple vitamin deficiencies. The most severe deficiencies are related to the lack of supplementation compliance.

Vitamin Status among Breastfed Infants in Bhaktapur, Nepal.

Vitamin deficiencies are known to be common among infants residing in low- and middle-income countries but relatively few studies have assessed several biochemical parameters simultaneously. The objective of the study was to describe the status of vitamins (A, D, E, B6, B12 and folate) in breastfed infants. We measured the plasma concentrations of trans retinol, 25 hydroxy vitamin D, α-tocopherol, pyridoxal 5'-phosphate, cobalamin, folate, methylmalonic acid, homocysteine, hemoglobin and C-reactive protein from 467 randomly selected infants. One in five (22%) was deficient in at least one vitamin. Mean (SD) plasma folate concentration was 73 (35) nmol/L, and no infant in the sample was folate deficient. Vitamin B6 deficiency and vitamin B12 deficiency was found in 22% and 17% of the infants, respectively. Elevated plasma methylmalonic acid or total homocysteine concentration was found in 82% and 62% of infants, respectively. Fifteen percent of infants were vitamin A deficient and 65% were marginally deficient in vitamin A. Fewer than 5% of infants had low plasma vitamin D concentration or vitamin E concentration (α-tocopherol <9.3 µmol/L). Our results illustrate the importance of continued supplementation campaigns and support the expansion of food fortification and dietary diversification programs that target children and women in Nepal.

Vitamin Supplementation in the Elderly.

Vitamin supplementation is fairly common among the elderly. Supplements are often used to prevent disease and improve health. In the United States, the use of dietary supplements has continued to increase over the last 30 years, and more than half of adults report using one or more dietary supplements. Epidemiologic evidence suggests that a diet rich in fruits and vegetables does have a protective effect on health. However, clinical trials on the use of vitamin supplements for promotion of health and prevention of disease have failed to demonstrate the strong associations seen in observational studies.

Nutritional deficiencies after sleeve gastrectomy: can they be predicted preoperatively?

BACKGROUND: Nutritional deficiencies are common among morbidly obese patients. Data are scarce for patients who have undergone laparoscopic sleeve gastrectomy (LSG). OBJECTIVES: The aim of the study is to clarify the prevalence of deficiencies and to identify risk factors for postoperative deficiencies. SETTINGS: Hebrew University, Israel. METHODS: Preoperative and 1-year postoperative data were collected. We included anthropometric parameters, obesity-related co-morbidities, and laboratory findings. RESULTS: There were 192 candidates. Seventy-seven of them completed follow-ups at 12 months. Before surgery, 15% had anemia. Deficiencies of iron, folate, and B12 were 47%, 32%, and 13%, respectively. Women were more deficient in iron (56% women, 26% men, P<.001). Before surgery, low levels of vitamin D and elevated parathyroid hormone (PTH) were 99% and 41%, respectively. One year postsurgery, the deficiencies of hemoglobin and vitamin B12 worsened (20% and 17%, P<.001, P = .048, respectively). One year postsurgery, deficiencies of iron, folate, vitamin D, and PTH improved (28%, 21%, 94%, and 10%, respectively). Deficiencies of hemoglobin, folate, and B12 before surgery were predictors for deficiencies 1 year after surgery (P = .006 OR = .090; P = .012 OR = .069; P = .062 OR = .165, respectively). CONCLUSIONS: LSG had a modest effect on nutritional deficiencies in our patients at 1-year postsurgery. Focusing on the preoperative nutritional status and tailoring a specific supplemental program for each individual should prevent postoperative deficiencies.

Prevalence of malnutrition and nutritional risk factors in patients undergoing alcohol and drug treatment.

OBJECTIVE: Chronic substance abuse is recognized to affect nutritional status and is associated with nutrient deficiencies and malnutrition. This study aimed to identify the prevalence of malnutrition and nutritional risk factors using a spread of measurements in patients undergoing alcohol and drug treatment. METHODS: Sixty-seven patients (48 male, 19 female) admitted to a public hospital detoxification unit participated: 49 were alcohol dependent (73%) and the remaining were opiate, benzodiazepine, and/or amphetamine dependent. Nutritional status was assessed by the Subjective Global Assessment. An appetite questionnaire (Simplified Nutritional Appetite Questionnaire), a diet-quality questionnaire (Australian Recommended Food Score), and blood biochemistry and hematologic tests were also applied. RESULTS: The prevalence of mild/moderate malnutrition was 24% according to the Subjective Global Assessment. Weight and body mass index were associated with nutritional status (P < 0.05). Appetite and diet quality were poor overall, with 88% of all participants requiring advice and guidance. Blood markers showed that 50% of all subjects were deficient in iron or vitamins (low vitamin A levels in 21%, low iron levels in 18%, low-range potassium in 12%, and low vitamin C levels in 8%). CONCLUSION: The prevalence of malnutrition in this patient population is likely to underestimate the prevalence of nutritional risk factors and micronutrient undernutrition. Multiple tools assessing nutritional status, appetite, diet quality, and blood test results have different advantages and can further identify the specific needs and appropriateness of nutritional education in patients during treatment for drug and alcohol use.

Nutrient deficiencies in the premature infant.

Premature infants are a population prone to nutrient deficiencies. Because the early diet of these infants is entirely amenable to intervention, understanding the pathophysiology behind these deficiencies is important for both the neonatologists who care for them acutely and for pediatricians who are responsible for their care through childhood. This article reviews the normal accretion of nutrients in the fetus, discusses specific nutrient deficiencies that are exacerbated in the postnatal period, and identifies key areas for future research.

Neurologic complications of gastric bypass surgery for morbid obesity.

BACKGROUND: The number of bariatric procedures is rapidly growing as the prevalence of obesity in the USA is increasing. Such procedures are not without complications, and those affecting the nervous system are often disabling and irreversible. We now describe our experience with these complications and review the pertinent literature. METHODS: We describe 26 patients with major neurologic conditions that seemed causally related to bariatric surgery encountered in the neurology service of a tertiary referral university medical center over a decade. RESULTS: The neurologic complications affected most regions of the nervous system: encephalopathy, optic neuropathy, myelopathy, polyradiculoneuropathy, and polyneuropathy. Myelopathy was the most frequent and disabling problem; symptoms began about a decade after surgery. Encephalopathy and polyradiculoneuropathy were acute and early complications. Except for vitamin B(12) and copper deficiencies in patients with myelopathy, we could not correlate specific nutritional deficiencies to the neurologic complications. All patients had multiple nutritional deficiencies, but their correction did not often yield dramatic results. The best result was achieved in one patient after surgical revision to reduce the bypassed jejunum. CONCLUSIONS: A wide spectrum of serious neurologic conditions may follow bariatric surgery. These complications may occur acutely or decades later.

Nutritional and metabolic complications of bariatric surgery.

Bariatric surgery is an effective treatment for patients with clinically severe obesity. In addition to significant weight loss, it is also associated with improvements in comorbidities. Unfortunately, bariatric surgery also has the potential to cause a variety of nutritional and metabolic complications. These complications are mostly due to the extensive surgically induced anatomical changes incurred by the patient's gastrointestinal tract, particularly with roux-en-Y gastric bypass and biliopancreatic diversion. Complications associated with vertical banded gastroplasty are mostly due to decreased intake amounts of specific nutrients. Macronutrient deficiencies can include severe protein-calorie malnutrition and fat malabsorption. The most common micronutrient deficiencies are of vitamin B12, iron, calcium, and vitamin D. Other micronutrient deficiencies that can lead to serious complications include thiamine, folate, and the fat-soluble vitamins. Counseling, monitoring, and nutrient and mineral supplementation are essential for the treatment and prevention of nutritional and metabolic complications after bariatric surgery.

Effects of vitamin restriction and supplementation on rat intestinal epithelial cell apoptosis.

Diet influences intestinal growth and function and vitamins modulate intestinal cell turnover. We have assessed the effects of chronic, moderate (50% of control) vitamin restriction and supplementation on intestinal epithelial cell (IEC) apoptosis and the relevance of this to alterations in tissue oxidative stress and antioxidant status. Feeding a vitamin-restricted diet to male, weanling WNIN rats for 20 weeks significantly increased IEC apoptosis, but only in the villi region, as evident from increased annexin V staining, M30 positivity, histological observations, DNA ladder formation, and reduced expression of Bcl-2. This was associated with elevated levels of lipid peroxides and protein carbonyls in the intestinal mucosa despite the increased activities of superoxide dismutase, catalase, and glutathione peroxidase. Consistent with the increased oxidative stress and apoptosis, structural and functional integrity of the villi were compromised as evident from the lowered ratio of villus height:crypt depth and the decreased activities of the membrane marker enzymes alkaline phosphatase and Lys-Ala dipeptidyl aminopeptidase. These changes were reversed by supplementation with a vitamin mixture or vitamin E alone, whereas riboflavin or folic acid supplementation reduced the apoptotic rates, but only partially. Further, oxidative stress was the least in vitamin E- or vitamin mixture-supplemented rats and correlated well with their IEC apoptotic rates. Increased tissue oxidative stress seems to mediate the vitamin-restriction-induced apoptosis of the IECs in rats.

Nutritional modulation of malaria morbidity and mortality.

This review critically examines the relationship between nutritional status and malaria. The data indicate that protein-energy malnutrition is associated with greater malaria morbidity and mortality in humans. In addition, controlled trials of either vitamin A or zinc supplementation show that these nutrients can substantially reduce clinical malaria attacks. Data for iron indicate that supplementation may minimally aggravate certain malariometric indices in some settings and also strongly improve hematologic status. Withholding of iron supplements from deficient population is, therefore, not currently indicated. Available evidence for other nutrients describe varied effects, with some deficiencies being exacerbative (e.g., thiamine), protective (e.g., vitamin E), or both exacerbative and protective in different settings (e.g., riboflavin, vitamin C). The roles of folate, other B vitamins, unsaturated fatty acids, amino acids, and selenium are also examined. Study of the interactions between nutrition and malaria may provide insight to protective mechanisms and result in nutrient-based interventions as low-cost and effective adjuncts to current methods of malaria prevention and treatment.

Vitamin A deficiency exacerbates methotrexate-induced jejunal injury in rats.

Two studies were conducted to investigate whether vitamin A-deficient rats were more susceptible to intestinal injury caused by methotrexate (MTX), since vitamin A deficiency alone causes only mild changes to jejunal structure and function. Weanling male rats were fed a vitamin A-deficient diet (-VA) for 40-42 d and compared to rats either pair-fed (PF) or with free access (+VA) to the same diet. Drinking water of PF and +VA rats was supplemented with 37.5 microg (Study 1) or 75 microg (Study 2) vitamin A (Rovimix A 500W)/d. Rats in each group received MTX (-VAMTX, PFMTX, +VAMTX) or vehicle. MTX administration reduced intestinal mucosal wet weight, protein and DNA concentrations, and sucrase and maltase activities in -VA and PF rats (P < 0.02). In Study 1, -VAMTX rats developed a severe jejunal enteropathy and had a higher incidence of diarrhea (P < 0.005), greater weight loss (P < 0.005), more disruption of villus architecture (P < 0.0001) and lower disaccharidase activity (P < 0.007) than PFMTX rats. Similar results were observed in Study 2. Liver retinol concentration (but no other variable) was greater in rats receiving 75 microg vitamin A/d (P < 0.001) than in those receiving 37.5 microg/d. The interaction of vitamin A deficiency and small intestinal injury may explain the efficacy of vitamin A supplementation in preventing childhood diarrheal disease mortality in developing countries, and highlights the need for ensuring adequate vitamin A status in people worldwide with diseases and/or treatments which may injure the gastrointestinal tract.

High-risk subjects for vitamin deficiency.

Chronic deficiency of various vitamins can influence the occurrence of some chronic degenerative diseases such as cancer, cardiovascular pathology, cataract, arthritis, disorders of the nervous system and photosensitivity. Similarly, vitamin intake can influence various disorders in infants and elderly people, in burns and in subjects following unbalanced diets or undergoing strenuous physical exercise. Among vitamins, beta-carotene, vitamin E and vitamin C have received most attention, particularly in the prevention of oxidative damage from free radicals. It is supposed that each vitamin plays a different role in the pathogenesis of various diseases, depending on the type of damage relevant to a specific disease. Results from different studies are still far from conclusive and the effects on longevity are not well defined. In industrialized countries, vitamin deficiencies seem to be related only to specific and clearly identifiable groups in the population: therefore, at the moment, it seems more advisable to target vitamin supplementation at risk groups.

Vitamin neurotoxicity.

Vitamins contain reactive functional groups necessary to their established roles as coenzymes and reducing agents. Their reactive potential may produce injury if vitamin concentration, distribution, or metabolism is altered. However, identification of vitamin toxicity has been difficult. The only well-established human vitamin neurotoxic effects are those due to hypervitaminosis A (pseudotumor cerebri) and pyridoxine (sensory neuropathy). In each case, the neurological effects of vitamin deficiency and vitamin excess are similar. Closely related to the neurological symptoms of hypervitaminosis A are symptoms including headache, pseudotumor cerebri, and embryotoxic effects reported in patients given vitamin A analogs or retinoids. Most tissues contain retinoic acid (RA) and vitamin D receptors, members of a steroid receptor superfamily known to regulate development and gene expression. Vitamin D3 effects on central nervous system (CNS) gene expression are predictable, in addition to the indirect effects owing to its influence on calcium and phosphorus homeostasis. Folates and thiamine cause seizures and excitation when administered in high dosage directly into the brain or cerebrospinal fluid (CSF) of experimental animals but have rarely been reported to cause human neurotoxicity, although fatal reactions to i.v. thiamine are well known. Ascorbic acid influences CNS function after peripheral administration and influences brain cell differentiation and 2-deoxyglucose accumulation by cultured glial cells. Biotin influences gene expression in animals that are not vitamin-deficient and alters astrocyte glucose utilization. The multiple enzymes and binding proteins involved in regeneration of retinal vitamin A illustrate the complexity of vitamin processing in the body. Vitamin A toxicity is also a good general model of vitamin neurotoxicity, because it shows the importance of the ratio of vitamin and vitamin-binding proteins in producing vitamin toxicity and of CNS permeability barriers. Because vitamin A and analogs enter the CNS better than most vitamins, and because retinoids have many effects on enzyme activity and gene expression, Vitamin A neurotoxicity is more likely than that of most, perhaps all other vitamins. Megadose vitamin therapy may cause injury that is confused with disease symptoms. High vitamin intake is more hazardous to peripheral organs than to the nervous system, because CNS vitamin entry is restricted. Vitamin administration into the brain or CSF, recommended in certain disease states, is hazardous and best avoided. The lack of controlled trials prevents us from defining the lowest human neurotoxic dose of any vitamin. Large differences in individual susceptibility to vitamin neurotoxicity probably exist, and ordinary vitamin doses may harm occasional patients with genetic disorders.(ABSTRACT TRUNCATED AT 400 WORDS)