Multiple vitamin deficiencies in a patient with a history of chronic alcohol excess and self-neglect in the UK.

We report a case of inadequate diet (caused by extreme self-neglect and alcohol excess) which led to chronic severe deficiencies of vitamins A, D and E. At presentation the patient had widespread follicular hyperkeratosis of the skin, keratomalacia of both eyes and a severe cognitive impairment. He responded well to treatment including high dose parenteral vitamins, but lasting impairments in his vision and cognition have caused permanent disability.

[Effects of dietary fibers on hepatocyte apoptosis in rats with alimentary polyhypovitaminosis].

The effect of dietary fibers (DF) of wheat bran on hepatocyte apoptosis in rats adequately provided with vitamins or insufficiently supplied with vitamins has been investigated. 48 male Wistar rats (initial body mass--58.1 +/- 0.5 g) were randomly divided into 6 groups and fed with semi-synthetic diet, containing 100% or 20% of vitamin mixture (Vit) with or without addition of DF in the dose corresponding to the upper allowable level of its consumption (5% of diet mass) for 4 weeks. The animals of the 1 group received 100% of vitamin mixture (100% Vit); 2 group--100% Vit + DF; 3 group--20% of vitamin mixture with full exclusion of vitamins E, B1 and B2 (20% Vit); 4 group--20% of vitamin mixture and DF (20% Vit + DF). The next 5 days rats from vitamin-deficient groups were fed with diets supplemented with 80% of vitamins from their content in control group: (5 group--20% Vit + 80% Vit; 6 group--20% Vit + DF + 80% Vit). The suspension of hepatocytes was received by Becton Dickinson Medimachine System (USA). Hepatocyte apoptosis was assessed by the method of flow cytometry using Beckman Coulter FC 500 (USA) cytometer by stained cells with Annexin V-FITC/ 7-Amino-Actinomycin D Kit (Beckman Coulter, USA). In rats fed complete semi-synthetic diet supplemented with DF (100% Vit + DF) the hepatocyte apoptosis was higher by 22% (p < 0.10) than that in rats of control group (4.99 +/- 1.82%). In rats fed diets with low vitamin content (groups: 20% Vit and 20% Vit + DF) the hepatocyte apoptosis was significantly higher (p < 0.05) than that in the control group and reached 7.03 +/- 1.74 and 7.26 +/- 1.13% accordingly. Normalization of vitamin content in the diets of rats from deficient groups during 5 days had no effect on the severity of apoptosis regardless from presence (8.02 +/- 2.18%) or absence of the DF (8.04 +/- 1.66%). Adding DF in dose corresponding to the upper allowable level of consumption, on the background of adequate vitamin content in the diet is accompanied by a tendency to develop hepatocyte apoptosis, which may be the result of a direct action of short chain fatty acids generated from the DF and the deterioration of vitamin sufficiency.

[The influence of dietary fibers on cell immunity under the adequate nutrition and in the presence of alimentary polyhypovitaminosis in rats].

The effect of wheat bran on cell immunity in rats adequately provided with vitamins or insufficiently supplied with vitamins has been investigated. 48 male Wistar rats (58.1 +/- 0.5 g) were divided into 6 group and fed with complete semi-synthetic diet, containing 100% or 20% of vitamin mixture (Vit) with or without supplement of insoluble dietary fiber (DF) in the dose corresponding to the upper allowable level of its consumption (5% wheat bran of diet mass) for 4 weeks. The animals of the 1 group received 100% of vitamin mixture (100% Vit); 2 group--100% Vit+DF; 3 group--20% of vitamin mixture (20% Vit); 4 group--20% of vitamin mixture and DF (20% Vit+DF). The next 5 days rats from vitamin-deficient groups were fed with diets supplemented with 80% of Vit: (5 group--20% Vit+80% Vit; 6 group--20% Vit+DF+80% Vit). The contents of lymphocytes, relative quantity of B-(CD45RA+) and T-lymphocytes (CD3+), subpopulations of T-lymphocytes: T-helper (CD3+CD4+) and cytotoxic T-lymphocytes (CD3+CD8+), NK-cells (CD161a+) in the peripheral blood of rats were determined by the method of flow cytometry using Beckman Coulter FC 500 (USA) cytometer. In rats fed complete semi-synthetic diet supplemented with DF (100% Vit+DF) the reduction of relative contents of T-lymphocytes and the increase of the fraction of cytotoxic T-lymphocytes in peripheral blood has been found. The analogous changes and more pronounced degree of immunosupression, that appeared in a lymphocytopenia, much smaller level of T-lymphocytes, T-helper and increase of cytotoxic T-lymphocytes content in rats fed a low vitamins diet (20% Vit) in comparison with these parameters of control group, have been detected. In rats received 20% Vit+DF the suppressed cell immunity was accompanied with decreased level of NK-cells. Normalization of vitamins content in the diets of rat deficient groups led to an almost complete recovery of cell immunity indicators to the level of the animals from the corresponding control groups. Inclusion in the diet of fiber requires its further enrichment with vitamins. Special studies of fiber diet influence on are needed to clarify the upper allowable level of insoluble dietary fiber in human nutrition.

Niacin status and genomic instability in bone marrow cells; mechanisms favoring the progression of leukemogenesis.

Niacin deficiency causes dramatic genomic instability in bone marrow cells in an in vivo rat model. The end result is seen in the increased incidence of sister chromatid exchanges, micronuclei, chromosomal aberrations and the eventual development of nitrosourea-induced leukemias. From a mechanistic perspective, niacin deficiency delays excision repair and causes double strand break accumulation, which in turn favor chromosome breaks and translocations. Niacin deficiency also impairs cell cycle arrest and apoptosis in response to DNA damage, which combine to encourage the survival of cells with leukemogenic potential. Niacin deficiency also enhances the level of oxidant damage found in cellular proteins and DNA, but not through depression of GSH levels. Pharmacological supplementation of niacin decreases the development of nitrosourea-induced leukemias, while short term effects of high niacin intake include a large increase in cellular NAD+ and poly(ADP-ribose) content and enhanced apoptosis. These results are important to cancer patients, which tend to be niacin deficient, are exposed to large doses of genotoxic drugs, and suffer short-term bone marrow suppression and long-term development of secondary leukemias. The data from our rat model suggest that niacin supplementation of cancer patients may decrease the severity of short and long-term side effects, and may also improve tumor cell killing through activation of poly(ADP-ribose)-dependent apoptosis pathways.

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.

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.

A fine structural demonstration that some benzopyrones act as vitamin P in the rat.

In rats fed a diet lacking flavonoids (but which had supplementary vitamin C) definite fine structural alterations were found in blood capillaries and tissues. These fine structural alterations were quite different from those reported in C-avitaminosis and imply a different deficiency. They were largely prevented by feeding the benzopyrones, coumarin or coumarin plus troxerutin, thus pointing to the specificity of the lesions. This implies that, for the rat, benzopyrones are vitamins and that vitamin C and "vitamin P"-deficiency states are qute distinct. In "P-avitaminosis" the basic lesion is the opening of some blood capillary endothelial intercellular junctions. Unlike in C-avitaminosis, the endothelial cells are intact, without pale, grossly swollen cytoplasms.