[Efficiency of vitamin D deficit correction depending on rats' supply with B vitamins].

Despite the presence of combined deficiency of vitamins D and group B among the population of Russia, the intake of cholecalciferol is often recommended without correcting the supply with B group vitamins, which are involved in ensuring the biological functions of vitamin D. The aim of the study was to compare the effectiveness of vitamin D deficit correction by replenishing its content in the diet to an adequate level without eliminating the deficit of B vitamins and by restoring vitamin D level in combination with B vitamins. Material and methods. The experiment was carried out on male Wistar rats (n=33) with an initial body weight of 69.5±0.8 g. Combined deficit of vitamins D and B group in rats (n=24) was caused by a 5-fold decrease in their content in the vitamin mixture of a semi-synthetic diet for 23 days. Over the next 7 days, in order to correct vitamin deficiency, 12 rats (group «-B+D¼) were fed a diet, replenished up to 100% for vitamin D with continued deficiency of B group vitamins, and 12 rats (group «+B+D¼) were fed a diet replenished for all missing vitamins. Animals of the control group (n=9) received a full semi-synthetic diet during the entire experiment. The concentration of vitamins A and E in blood plasma and lyophilized liver and whole brain was determined by HPLC, vitamins B1 and B2 in the liver, brain and urine, riboflavin in plasma and 4-pyridoxic acid in urine - by fluorimetric methods, 25(OH)D in blood plasma was determined by ELISA. The content of calcium, magnesium, iron, manganese, zinc and copper in freeze-dried liver and brain was determined by atomic absorption method, biochemical parameters of blood and urine were determined using a biochemical analyzer. Results. The only vitamin D addition to the feed with a persisting deficiency of B vitamins did not restore the concentration of 25(OH)D and osteocalcin to the level in control animals sufficiently provided with all vitamins. In animals of the "-B+D" group, 25(OH)D plasma level was reduced by 17.3% (p<0.10), osteocalcin - by 11.7% (p<0.05), the activity of aspartate aminotransferase was 1.5 fold less, alanine aminotransferase - 2.3 fold (p<0.05), lactate dehydrogenase - by 14.9% (p<0.10), while the concentration of iron exceeded 2.7 times, glucose - by 15.0%, calcium - by 8.0%, creatinine - by 8.7% (p<0.05), urea - by 32.1%, direct bilirubin - by 24.2% (p<0.10 ) compared with corresponding indicator in rats of the control group. The level of cholesterol and HDL cholesterol was 14.7% and 15.9% higher (p<0.10) than in animals of the «+B+D¼ group. Conclusions. Deficiency of B vitamins inhibits the restoration of adequate supply with vitamin D. In the presence of a lack of B vitamins in rats, vitamin D deficit and its consequences cannot be completely eliminated. Adequate supply with vitamins D and B group are synergistic factors in maintaining the level of glucose, cholesterol in blood plasma and other diagnostically significant parameters.

Nutritional neuropathies.

Neuropathies associated with nutritional deficiencies are routinely encountered by the practicing neurologist. Although these neuropathies assume different patterns, most are length-dependent, sensory axonopathies. Cobalamin deficiency neuropathy is the exception, often presenting with a non-length-dependent sensory neuropathy. Patients with cobalamin and copper deficiency neuropathy characteristically have concomitant myelopathy, whereas vitamin E deficiency is uniquely associated with a spinocerebellar syndrome. In contrast to those nutrients for which deficiencies produce neuropathies, pyridoxine toxicity results in a non-length-dependent sensory neuronopathy. Deficiencies occur in the context of malnutrition, malabsorption, increased nutrient loss (such as with dialysis), autoimmune conditions such as pernicious anemia, and with certain drugs that inhibit nutrient absorption. When promptly identified, therapeutic nutrient supplementation may result in stabilization or improvement of these neuropathies.

Micronutrient Depletion in Heart Failure: Common, Clinically Relevant and Treatable.

Heart failure (HF) is a chronic condition with many imbalances, including nutritional issues. Next to sarcopenia and cachexia which are clinically evident, micronutrient deficiency is also present in HF. It is involved in HF pathophysiology and has prognostic implications. In general, most widely known micronutrients are depleted in HF, which is associated with symptoms and adverse outcomes. Nutritional intake is important but is not the only factor reducing the micronutrient availability for bodily processes, because absorption, distribution, and patient comorbidity may play a major role. In this context, interventional studies with parenteral micronutrient supplementation provide evidence that normalization of micronutrients is associated with improvement in physical performance and quality of life. Outcome studies are underway and should be reported in the following years.

Nutritional Status in the First 2 Years of Life in Cystic Fibrosis Diagnosed by Newborn Screening.

OBJECTIVE: To evaluate nutritional status and associated factors in a cystic fibrosis (CF) cohort diagnosed by newborn screening and followed up to month 24. METHODS: A prospective longitudinal multicenter study assessing nutritional status according to pancreatic status, feeding modalities, prescriptions, pulmonary outcome, and biological nutritional parameters. RESULTS: One hundred and five infants were recruited and 99 completed the study. Nutritional care management prevented undernutrition and stunting in those with exocrine pancreatic sufficiency (EPS), but affected (13/87) 15% and (21/86) 24%, respectively, of infants with exocrine pancreatic insufficiency (EPI). The logistic regression model found a positive association between both weight and length z scores "at risk" at month 24, and initial pulmonary symptoms (odds ratio [OR] 0.06, P < 0.01 and OR 0.08, P < 0.01, respectively); these symptoms were less frequent when age at first visit was earlier than 1.2 months (33% vs 67%, P = 0.02); stunting was also associated with high-calorie density intake and Staphylococcus aureus (OR 0.05, P = 0.01 and OR 0.17, P < 0.01). Pulmonary outcome did not differ according to pancreatic status; breast-feeding for at least 3 months delayed first acquisition of Pseudomonas aeruginosa. Despite sodium and fat-soluble vitamin supplementation, half of both cohorts had low urinary sodium output and half of the EPI cohort had low vitamin D levels. CONCLUSIONS: Our data shed light on the fact that stunting was more frequent than undernutrition, while both parameters involved only patients with pancreatic insufficiency. Modalities of feeding were not associated with nutritional status; breast-feeding may provide some protection against acquisition of P aeruginosa.

Effects of nutrition intervention on the nutritional status and outcomes of pediatric patients with pneumonia.

BACKGROUND: This study aims to explore the correlation between nutrient level and pneumonia via the analysis and intervention of nutrient levels in pediatric patients with pneumonia. METHODS: Nutrient deficient children with pneumonia were randomized into intervention and non-intervention groups, and healthy children with the same age served as controls. Serum vitamin and trace element levels were determined. The nutrient levels, average hospital stay and nutrient deficiency rate were compared between groups. RESULTS: The pneumonia group showed significantly higher rates of iron, zinc and vitamin A deficiencies than the control group. The serum vitamin D level in asthmatic pneumonia group was lower than that in non-asthmatic pneumonia group and control group. Serum zinc, iron and vitamin A levels in the pneumonia group distinctly increased after intervention therapy. After vitamin D supplementation, the serum vitamin D level in asthmatic pneumonia group was significantly improved. Children in the intervention group had shorter hospital stays than children in the non-intervention group, whose hospital stays were longer than pediatric patients with normal nutrient levels. However, the difference between the intervention and normal nutrient groups was insignificant. CONCLUSION: Clinical nutrition intervention could improve the efficacy of pneumonia in pediatric patients and shorten hospital stay.

Trace element supplementation in hemodialysis patients: a randomized controlled trial.

BACKGROUND: People with kidney failure are often deficient in zinc and selenium, but little is known about the optimal way to correct such deficiency. METHODS: We did a double-blind randomized trial evaluating the effects of zinc (Zn), selenium (Se) and vitamin E added to the standard oral renal vitamin supplement (B and C vitamins) among hemodialysis patients in Alberta, Canada. We evaluated the effect of two daily doses of the new supplement (medium dose: 50 mg Zn, 75 mcg Se, 250 IU vitamin E; low dose: 25 mg Zn, 50 mcg Se, 250 IU vitamin E) compared to the standard supplement on blood concentrations of Se and Zn at 90 days (primary outcome) and 180 days (secondary outcome) as well as safety outcomes. RESULTS: We enrolled 150 participants. The proportion of participants with low zinc status (blood level <815 ug/L) did not differ between the control group and the two intervention groups at 90 days (control 23.9% vs combined intervention groups 23.9%, P > 0.99) or 180 days (18.6% vs 28.2%, P = 0.24). The proportion with low selenium status (blood level <121 ug/L) was similar for controls and the combined intervention groups at 90 days (32.6 vs 19.6%, P = 0.09) and 180 days (34.9% vs 23.5%, P = 0.17). There were no significant differences in the risk of adverse events between the groups. CONCLUSIONS: Supplementation with low or medium doses of zinc and selenium did not correct low zinc or selenium status in hemodialysis patients. Future studies should consider higher doses of zinc (≥75 mg/d) and selenium (≥100 mcg/d) with the standard supplement. TRIAL REGISTRATION: Registered with ClinicalTrials.gov (NCT01473914).

Vitamin and zinc status pretreatment and posttreatment in patients with inflammatory bowel disease.

Vitamin deficiencies are common in inflammatory bowel disease. Here we present 5-year follow-up data of 61 patients. No folate or vitamin B12 deficiency was identified throughout the study. A daily multivitamin supplement was sufficient to replete 100% of vitamin A-deficient and vitamin E-deficient patients. A total of 52% of vitamin D-deficient patients corrected, but 15% who had normal vitamin D levels at diagnosis developed deficiency. A total of 63% of zinc-deficient patients normalized their zinc status, but 15% developed zinc deficiency at follow-up despite supplementation.

Vitamins in dialysis: who, when and how much?

Despite the significant technical evolution of the blood purification methods, cardiovascular morbidity and mortality in dialysis patients is still several times higher than that observed in the general population. Vitamins are playing a crucial role in multiple key metabolic pathways. Due to multiple factors, dialysis patients present very often hypo- or hypervitaminosis for a broad range of vitamins. Dialysis in the context of renal replacement therapy is associated with a non-physiological potassium-sparing dietetic regime. Additionally, there is a non-selective intradialytic loss of micro- and macronutrients, deranged intracellular kinetics and gastrointestinal malabsorption due to uratemia. Frequent treatment with antibiotics due to infections associated with the acquired uremia-related immunosuppression may derange the vitamin-producing intestinal microflora. Certain agents prescribed in the context of renal failure or other conditions may reduce the absorption of vitamins from the gastrointestinal tract. These factors may deplete a dialysis patient from vitamins, especially the ones with antioxidant activity that may be associated with cardioprotective properties. In other cases, vitamins metabolized and excreted by the kidneys may be accumulated and exert toxic effects. The scope of this paper is to describe the main issues on vitamin therapy in dialysis patients in view of the ever contradictory opinions and practices.

Learning the oral and cutaneous signs of micronutrient deficiencies.

Wound healing is a complex process that is influenced by multiple systemic factors, including nutritional status. While nutritional support is commonly recognized as an important aspect of comprehensive wound management, the focus is typically on replacement of macronutrients, specifically calories and protein. Our experience strongly suggests that micronutrients are equally important, that micronutrient deficiencies are common, and that correction of these deficiencies frequently leads to wound healing when incorporated into a comprehensive wound management program. This article provides guidelines for assessment and management of micronutrient deficiencies.

Efficiency of various vitamin doses for polyhypovitaminosis correction in rats.

A 5-fold decrease of the content of vitamin mixture in the ration and exclusion of vitamin E from this mixture over 4 weeks led to a significant growth delay in rats initially weighing 58.1±0.5 g, but was inessential for the growth rates of animals weighing 107.1±1.1 g. The decrease in the levels of vitamins A and B2 in the liver and of 25-hydroxyvitamin D in the plasma of younger rats was more significant, this indicating their higher sensitivity to alimentary vitamin deficit. The increase in vitamin content in the ration to 100% over 5 days led to a significant body weight increment but did not restore vitamin levels in the liver, restoring, however, plasma levels of vitamins E and 25-hydroxyvitamin D. Addition of 50% vitamin content of the vitamin mixture for controls to vitamin-deficient rations of older rats for 2 weeks improved the levels of vitamins B1 and B2, but was virtually inessential for the liver content of vitamins A and E. High dose (158-200%) vitamins in animals of both age groups repaired the deficit of all vitamins, except vitamin A, despite the fact that its doses were the highest. These results validate long-term vitamin consumption for repair of their deficit.

[Correction of the combined vitamin deficiency in growing rats fed fiber enriched diets with different doses of vitamins].

The effect of 5% dietary wheat bran (WB) on the correction of combined vitamin deficiency by two doses of vitamins (physiological and enhanced) has been analyzed using a rat model (8 groups, n = 8/group). Vitamin deficiency in male weanling Wistar rats (58.1 ± 0.5 g) was induced by 5-fold reduction of vitamin mixture amount in the feed and complete vitamin E, B1 and B2 exclusion from the mixture for 30 days, then deficit was corrected within 5 days. Rats from control group were fed a complete semisynthetic diet containing microcrystalline cellulose 2%. Vitamin deficient diet for 35 days resulted in reduced (p < 0.05) levels of vitamin A in the liver by 25 fold, vitamin E and B1--2.0-2.3 fold, vitamin B2--by 40%, 25(OH)D blood plasma concentration--by 21% compared with the control. Feed consumption of the animals treated with vitamin deficient diet and WB was higher by 43% than in rats with vitamin deficit. Their rate of weight occupied the intermediate position between the rates of weight in deficit and in control animals, and they could not serve a full control to evaluate the WB impact on vitamin sufficiency. After filling the vitamin diet content to an adequate level vitamin E liver content was fully restored. To restore vitamins B1 and B2 liver level higher doses of vitamins (120-160% of adequate content) were required, and to restore the reduced levels of vitamin A in rat liver even 2-fold increased dose of vitamin A was insufficient. The diet enrichment with WB had no effect on vitamin B1 and B2 liver content, regardless of the amount of vitamins in the diet. Adding fiber to the diet of animals adequately provided with vitamins resulted in significantly 1,3-fold increase of 25(OH)D blood plasma concentration and a slight but significant decrease of α-tocopherol liver level by 16% as compared to rats not receiving WB. The enrichment of rat diet with dietary fibers worsened restoration of the reduced vitamin E status not only by filling vitamin content in the diet to an adequate level, but also by using 2-fold enhanced dose of vitamin. Within 5 days deficiency of vitamins A, B1, B2 was not eliminated with increasing vitamin diet content to an adequate level. Higher doses of vitamins are needed for the complete correction of vitamin status. The addition of vitamins to an adequate level was sufficient to normalize the elevated liver levels of MDA in rats with combined vitamin deficiency that may be associated with vitamin E status improvement. The diet enrichment with fiber did not affect on the intensity of lipid peroxidation in rat liver regardless of their provision with vitamins.

Multivitamin supplements have no effect on growth of Tanzanian children born to HIV-infected mothers.

Growth faltering and micronutrient deficiencies commonly coexist in HIV-exposed children in sub-Saharan Africa, and correcting deficiencies, such as those of vitamins B-complex, C, and E, may improve HIV-related endpoints and child growth. We therefore examined the effect of daily oral supplementation of vitamins B-complex, C, and E on growth among 2341 children born to HIV-infected mothers in Tanzania. HIV-infected women pregnant at ≤32 wk of gestation were enrolled in the study. Children were randomized at age 6 wk to receive multivitamins or placebo until age 104 wk. All women received the same types of vitamins pre- and postnatally. At 6 wk, 256 children (11.1%) were HIV infected and the mean (SD) Z-scores for length for age (LAZ), weight for length (WLZ), and weight for age (WAZ) were -0.39 ± 1.20, -0.21 ± 1.23, and -0.52 ± 1.11, respectively. There was no overall treatment effect on LAZ, WLZ, or WAZ profiles during the follow-up (P ≥ 0.15). There was no treatment effect from 6 to 104 wk on LAZ [(95% CI: -0.14, 0.13); P = 0.94], WLZ [(95% CI: -0.17, 0.13); P = 0.78], or WAZ [(95% CI: -0.15, 0.16); P = 0.97] or on the incidence of growth failure, defined as respective Z-scores < -2 (P ≥ 0.29). Among the subgroup of HIV-uninfected children, there was no treatment effect from 6 to 104 wk on LAZ, WLZ, and WAZ (P ≥ 0.71) or on the incidence of growth failure (P ≥ 0.16). Multivitamin supplements had no effect on growth among children born to HIV-infected women who were themselves receiving multivitamins.

[Vitamins and oxidative stress].

The central and local stress limiting systems, including the antioxidant defense system involved in defending the organism at the cellular and systemic levels from excess activation response to stress influence, leading to damaging effects. The development of stress, regardless of its nature [cold, increased physical activity, aging, the development of many pathologies (cardiovascular, neurodegenerative diseases, diseases of the gastrointestinal tract, ischemia, the effects of burns), immobilization, hypobaric hypoxia, hyperoxia, radiation effects etc.] leads to a deterioration of the vitamin status (vitamins E, A, C). Damaging effect on the antioxidant defense system is more pronounced compared to the stress response in animals with an isolated deficiency of vitamins C, A, E, B1 or B6 and the combined vitamins deficiency in the diet. Addition missing vitamin or vitamins restores the performance of antioxidant system. Thus, the role of vitamins in adaptation to stressors is evident. However, vitamins C, E and beta-carotene in high doses, significantly higher than the physiological needs of the organism, may be not only antioxidants, but may have also prooxidant properties. Perhaps this explains the lack of positive effects of antioxidant vitamins used in extreme doses for a long time described in some publications. There is no doubt that to justify the current optimal doses of antioxidant vitamins and other dietary antioxidants specially-designed studies, including biochemical testing of initial vitamin and antioxidant status of the organism, as well as monitoring their change over time are required.

Fat-Soluble Vitamins Deficiency in Pediatric Cholestasis: A Scoping Review.

BACKGROUND: This review aims to identify the current indications and gaps in the management of fat-soluble vitamins in pediatric patients with cholestasis. METHODS: A comprehensive review of the literature using PubMed, Scopus, Web of Science and Embase was performed. Two authors independently identified the most relevant studies published over the past 20 years up to February 2022, including original papers, narrative reviews, observational studies, clinical trials, systematic reviews and meta-analyses. The literature was screened, and preclinical studies about pathogenetic mechanisms were also included. Keywords searched for each fat-soluble vitamin (A, D, E and K), alone or in combination, were "cholestasis", "chronic liver disease", "biliary atresia", "malnutrition" and "nutritional needs". Studies published prior to the selected time range were searched manually and, when considered relevant, included within the list of references. RESULTS: Eight hundred twenty-six articles were initially screened. From these, 48 studies were selected. A comparison of the recommended methods of supplementation for fat-soluble vitamins was then carried out. The causes of malabsorption were explained and current methods for defining deficiency and monitoring complications were summarized. CONCLUSIONS: According to the literature, children with cholestasis are at a higher risk of fat-soluble vitamin deficiency. Although there are general recommendations, the treatment for vitamin deficiency is not uniformly validated.

Oral absorbable fat-soluble vitamin formulation in pediatric patients with cholestasis.

OBJECTIVE: Fat-soluble vitamin (FSV) deficiencies are common complications in pediatric patients with chronic cholestasis. The aim of the present study was to evaluate the status of FSV deficiencies in patients under present practice and to test the effect of an oral, absorbable, fat-soluble vitamin formulation (OAFSV) in these patients. METHODS: We recruited a total of 23 pediatric patients receiving conventional FSV supplementation in a single medical center, with diagnosis of biliary atresia (10), progressive familial intrahepatic cholestasis (9), Alagille syndrome (2), and other conditions (2). Ten patients switched to OAFSV and continued for 3 months. Plasma levels of vitamins A, D, and E and an international normalized ratio (INR) for prothrombin time (PT), a surrogate marker for vitamin K deficiency, were measured. RESULTS: The proportion of patients with FSV A, D, E, and K deficiencies under conventional supplementation was 73.9%, 81.8%, 91.3%, and 20.0%, respectively. In patients with total bilirubin levels ≥3.0  mg/dL, the proportion of at least 1 FSV deficiency was 100%; and the deficiency rates of vitamin A, D, E, and K were 78.6%, 100.0%, 100.0% and 21.4%, respectively. Of the 10 patients receiving standard daily dose of OAFSV for 3 months, no adverse events or overdose effects were found. The rates of vitamin A, D, and E deficiency in the patients receiving OAFSV decreased from 80.0%, 100%, and 100%, respectively, to 70.0%, 60.0%, and 60.0% after 3 months of oral supplementation. CONCLUSIONS: High rates of FSV deficiency were found in pediatric patients with chronic cholestasis under present follow-up. OAFSV supplementation is safe and potentially effective in pediatric patients with cholestasis.

On the 'discovery' of vitamin A.

Vitamin A is essential for normal growth, reproduction, immunity, and vision. The characterization of vitamin A spanned a period of about 130 years. During this long, incremental process, there is no single event that can be called the 'discovery' of vitamin A. The physiologist François Magendie conducted nutritional deprivation experiments with dogs in 1816 that resulted in corneal ulcers and high mortality - a finding similar to the common clinical situation in poorly fed, abandoned infants in Paris. In the 1880s, Nicolai Lunin showed that there was an unknown substance in milk that was essential for nutrition. Carl Socin suggested that an unknown substance for growth in egg yolk was fat soluble. Frederick Gowland Hopkins proposed in 1906 that there were 'unsuspected dietetic factors' that were necessary for life. In 1911, Wilhelm Stepp demonstrated that this essential substance in milk was fat soluble. The following year, Hopkins showed that there were 'accessory factors' present in 'astonishingly small amounts' in milk that supported life. Contrary to the dogma that all fats had similar nutritional value, in 1913, Elmer McCollum and Marguerite Davis at Wisconsin and Thomas Osborne and Lafayette Mendel at Yale showed butter and egg yolk were not equivalent to lard and olive oil in supporting the growth and survival of rats. The growth-supporting 'accessory factor' became known as 'fat-soluble A' in 1918 and then 'vitamin A' in 1920. Paul Karrer described the chemical structure of vitamin A in 1932. Harry Holmes and Ruth Corbet isolated and crystallized vitamin A in 1937. Methods for the synthesis of vitamin A came with the work of David Adriaan van Dorp and Jozef Ferdinand Arens in 1946 and Otto Isler and colleagues in 1947. Further work on the role of vitamin A in immunity and child survival continued until through the 1990s.

Vitamins - wrong approaches.

Deficiencies of essential nutrients have been responsible for many epidemic outbreaks of deficiency diseases in the past. Large observational studies point at possible links between nutrition and chronic diseases. Low intake of antioxidant vitamins e. g. have been correlated to increased risk of cardiovascular diseases or cancer. The main results of these studies are indications that an intake below the recommendation could be one of the risk factors for chronic diseases. There was hardly any evidence that amounts above the RDA could be of additional benefit. Since observational studies cannot prove causality, the scientific community has been asking for placebo-controlled, randomized intervention trials (RCTs). Thus, the consequences of the epidemiological studies would have been to select volunteers whose baseline vitamin levels were below the recommended values. The hypothesis of the trial should be that correcting this risk factor up to RDA levels lowers the risk of a disease like CVD by 20 - 30 %. However, none of the RCTs of western countries was designed to correct a chronic marginal deficiency, but they rather tested whether an additional supplement on top of the recommended values would be beneficial in reducing a disease risk or its prognosis. It was, therefore, not surprising that the results were disappointing. As a matter of fact, the results confirmed the findings of the observational studies: chronic diseases are the product of several risk factors, among them most probably a chronic vitamin deficiency. Vitamin supplements could only correct the part of the overall risk that is due to the insufficient vitamin intake.

Vitamins.

• Based on strong research evidence, all infants should receive 400 IU/day of vitamin D beginning in the first few days of age to prevent vitamin D deficiency and rickets. • Based on strong research evidence, children and adolescents age >1 year may require as much as 600IU/day of vitamin D. • Based on strong research evidence, all newborns should receive 1 mg of vitamin K at birth to prevent vitamin K deficiency bleeding. • Based on strong research evidence, preconceptional and pregnant women should be supplemented with folate to decrease the likelihood of neural tube defects.

[Thiamine, pyridoxine and cobalamine. From myths to pharmacology and clinical practice]. / Die Vitamine B1, B6 und B12. Vom Mythos zur Pharmakologie und klinischen Praxis.

Vitamins are not uncommonly uncritically prescribed by neurologists and other medical professions. The effects of vitamins are, however, often pharmacologically and biochemically well-defined. This offers the opportunity for a rational scientific approach to treatment. In this article the biochemical and pharmacological mode of action of vitamins B1 (thiamine), B6 (pyridoxine) and B12 (cobalamine) will be discussed and modern approaches to the diagnosis and treatment of clinical states of hypervitaminoses (B6) and vitamin deficiencies (B1, B6, and B12) will be presented.

Hepatobiliary complications of inflammatory bowel disease.

Several hepatobiliary abnormalities have been described in association with inflammatory bowel disease (IBD), including primary sclerosing cholangitis (PSC), small duct PSC, chronic hepatitis, cryptogenic cirrhosis, cholangiocarcinoma, and cholelithiasis. PSC is the most common biliary condition in patients with IBD, with an incidence ranging from 2.5% to 7.5%. PSC usually progresses insidiously and eventually leads to cirrhosis independent of inflammatory bowel disease activity. There is a very high incidence of cholangiocarcinoma and an elevated risk for developing colon cancer in patients with PSC. Medical therapy has not proven successful in slowing disease progression or prolonging survival. Treatment of symptoms due to cholestasis, such as pruritis and steatorrhea, is an important aspect of the medical care of patients with PSC. Our preferred treatment of pruritis due to cholestasis is with bile acid binding exchange resins, such as cholestyramine or colestipol. Endoscopic manipulation is recommended for treating complications of recurrent cholangitis or worsening jaundice in the setting of a dominant stricture, but endoscopic approaches have not been conclusively demonstrated to improve survival or decrease the need for liver transplantation. Liver transplantation remains the only effective treatment of advanced PSC, and should be considered in patients with complications of cirrhosis or intractable pruritis or fatigue.