Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AVITAMINOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources

Bilateral corneal ulcers in primary vitamin A deficiency.

PURPOSE: To report a case of bilateral corneal ulcers and perforations resulting from hypovitaminosis A in an alcoholic patient. METHODS: A 38-year-old cachetic man presented with bilateral corneal ulcerations and severe visual loss. He was hospitalized, developed bilateral corneal perforations, and was treated with bilateral corneal transplants. RESULTS: Serum vitamin A level was 0.01 microg/dL (normal, 0.30-0.75). The electroretinogram was consistent with vitamin A deficiency. His clinical status improved after vitamin A replacement. CONCLUSIONS: Although rare in developed countries, the ophthalmologist must consider avitaminosis A in the differential diagnosis of corneal ulcerations in cachetic, alcoholic, or chronically ill patients. Early diagnosis and treatment can prevent unwanted outcomes.

Adult↗

Wernicke's encephalopathy with hyperemesis and ketoacidosis.

BACKGROUND: Avitaminosis can result from the acute malnutrition associated with prolonged pregnancy-related hyperemesis. Serious complications may arise from thiamine deficiency under these circumstances. CASE: We review the relevant literature and describe a case with central nervous system involvement presenting with typical manifestations of Wernicke's encephalopathy, apparently precipitated by a combination of hyperemesis gravidarum, diabetic ketoacidosis, and intravenous glucose administration. CONCLUSION: While this life-threatening complication is rare, it is important for all who care for obstetric patients to be aware of it and alert to its development. Early recognition is critical given the need to treat affected women expeditiously to help avoid potentially fatal adverse consequences. Prophylactic thiamine supplementation should be considered in the care of gravidas with hyperemesis.

Adult↗

Orthomolecular psychiatry. Varying the concentrations of substances normally present in the human body may control mental disease.

The functioning of the brain is affected by the molecular concentrations of many substances that are normally present in the brain. The optimum concentrations of these substances for a person may differ greatly from the concentrations provided by his normal diet and genetic machinery. Biochemical and genetic arguments support the idea that orthomolecular therapy, the provision for the individual person of the optimum concentrations of important normal constituents of the brain, may be the preferred treatment for many mentally ill patients. Mental symptoms of avitaminosis sometimes are observed long before any physical symptoms appear. It is likely that the brain is more sensitive to changes in concentration of vital substances than are other organs and tissues. Moreover, there is the possibility that for some persons the cerebrospinal concentration of a vital substance may be grossly low at the same time that the concentration in the blood and lymph is essentially normal. A physiological abnormality such as decreased permeability of the blood-brain barrier for the vital substance or increased rate of metabolism of the substance in the brain may lead to a cerebral deficiency and to a mental disease. Diseases of this sort may be called localized cerebral deficiency diseases. It is suggested that the genes responsible for abnormalities (deficiencies) in the concentration of vital substances in the brain may be responsible for increased penetrance of the postulated gene for schizophrenia, and that the so-called gene for schizophrenia may itself be a gene that leads to a localized cerebral deficiency in one or more vital substances.

Aminobenzoates↗

Nutrition: prospects for the 1990s.

For many decades there has been adequate information for the elimination of acute dietary deficiency diseases. Scurvy, beri-beri, and pellagra, once serious scourges, are now seen only rarely. The severe forms of protein-energy malnutrition, kwashiorkor and marasmus, have also decreased greatly. Nonetheless, mild to moderate forms of protein-energy deficiency, exacerbated by infection, continue to impair growth and development in a majority of the low-income pre-school age populations of most developing countries. Deficiencies of iron, iodine, and vitamin A are still widespread in developing countries. Fortunately, the success of the WHO/UNICEF "Child Survival and Development Revolution" in persuading most developing countries to introduce expanded programs of immunization, growth monitoring, and appropriate feeding of young children, control of diarrheal disease, and specific campaigns against avitaminosis A, iodine deficiency disorders, and the functional consequences of iron deficiency, will accelerate the decline of acute deficiency diseases in the developing world. Diets are changing among the more affluent in these countries, however, and it is time for them to stress dietary goals for the health of rich and poor alike. For the first time there is enough information regarding dietary risk factors for chronic disease to provide an opportunity in the 1990s to accelerate the dietary changes that have already brought significant health benefits to some populations in North America and Europe. The changes, which include a lower dietary intake of fat, particularly saturated fat, less salt, and more green and yellow vegetable and whole grain cereals, can be expected to influence favorably morbidity from cardiovascular diseases and some kinds of cancer. For maximum benefit, these measures need to be combined with the avoidance of obesity, reasonable physical activity, abstention from, or moderate use of, alcohol, and avoidance of tobacco in any form. Since there is already considerable momentum toward these changes in North America and some European countries, the 1990s are likely to see substantial further progress in the reduction of chronic diseases known to be influenced by diet.

Age Factors↗

Risk factors for retrolental fibroplasia.

Besides oxygen administration and immaturity of the premature retinal vessels, there are other risk factors for retrolental fibroplasia: (1) respiratory distress syndrome; (2) multiple episodes of bradycardia apnoea; (3) exchange transfusions; (4) hyaline membrane disease; (5) anemia of prematurity; (6) hyperbilirubinemia; (7) avitaminosis E; (8) cardiovascular defects; (9) infectious diseases; (10) multiple births; (11) hypocalcemia; (12) hypothermia; (13) hemorrhagic tendency; (14) delayed coaptation of the retina, and (15) spastic diplegia.

Apnea↗

Life expectancy, infant mortality and malnutrition in preindustrial Europe: a contemporary explanation.

In Europe's preindustrial and overwhelmingly agricultural society, people did not in general live long lives. While there were exceptions, by our standards, life expectancy was appallingly low for most and almost inconceivable to a modern audience living in an advanced industrial society where longevity is constantly being revised upwards. Europe's impoverished past came to an end in the nineteenth century with the advent of the agricultural and industrial revolutions. But before then, a great deal of suffering had taken place as Europe, as a whole, was plagued by a very high rate of infant mortality that significantly reduced, statistically, overall life expectancy. Clearly many of the sad deaths from the European past were tied to poor nutrition and the apparent lack of key vitamins, substances that modern researchers would consider as absolutely critical for proper cell development and amino-acid synthesis. In fact, it could probably be argued that Europe's preindustrial era was beset by a constant avitaminosis of some kind or another.

Adult↗

Cytochemical studies of nuclear basic proteins in control and vitamin B12 starved Euglena.

In avitaminosis B12, Euglena gracilis Z is blocked in the cell cycle in the S/G2 phase. In these blocked cells, transcription and traduction go on and the amount of DNA is less than doubled and remains constant during the blockage. Chromatin clumps observed in situ with classical electron microscopic methods are always condensed in control cells but are not visualized in B12 starved cells. Two cytochemical reactions, ethanolic phosphotungstic acid and ammoniacal silver reaction, specific for lysine- or arginine-rich residues, are performed to reveal basic nuclear proteins of chromatin. With these two methods, control chromatin in situ always shows a condensed aspect, whereas the starved chromatin appears dispersed. These cytochemical differences might be considered to result from a different supramolecular organization of the two kinds of chromatin.

Animals↗

Thiamine, riboflavin and pyridoxine deficiency in psychiatric in-patients.

One hundred and seventy-two successive admissions to a district general hospital psychiatric unit were examined. Routine psychiatric, drug and dietary histories were taken and signs of avitaminosis B specifically noted. Red cell transketolase (for thiamine deficiency), glutathione reductase (for riboflavin deficiency) and aspartate transaminase (for pyridoxine deficiency) were measured. Of the patients, 53 per cent were deficient in at least one vitamin, 12 per cent in more than one (30 per cent in thiamine, 27 per cent in riboflavin and 9 per cent in pyridoxine). Schizophrenics and alcoholics were significantly over-represent in those patients low in thiamine and in more than one vitamin. Patients with an affective disorder had low riboflavin and low pyridoxine. It is suggested that affective changes are characteristic of riboflavin and pyridoxine deficiency.

Aspartate Aminotransferases↗

Reversal of prednisolone-induced inhibition of intestinal calcium-binding protein synthesis by 1 alpha-hydroxycholecalciferol in chicks.

Effects of prednisolone on the biochemical indices of blood serum, ash content in bones, calcium absorption and calcium-binding protein (CaBP) in the intestinal mucosa were studied. The oral administration of prednisolone (10 mg/kg) for 2 weeks reduced CaBP content and calcium absorption to the level typical for D-avitaminosis. The oral administration of 1 alpha-hydroxycholecalciferol (390 pmoles/day) in combination with prednisolone for a week returned calcium absorption and CaBP to the control value.

Animals↗

Change in blood vitamin levels in surgical patients given a multivitamin preparation (NK-041) for total parenteral nutrition.

We studied the utility of a trial multivitamin preparation 'NK-041' for total parenteral nutrition. This preparation was used in 260 surgical patients during total parenteral nutrition, and changes in their blood vitamin levels were analyzed. Blood levels of all vitamins administered varied within the respective normal ranges, with few exceptional patients. During the administration of NK-041, avitaminosis, hypervitaminosis and side-effects were not observed. Laboratory examinations demonstrated that no abnormalities attributable to this preparation had arisen in these patients. Thus, these results seem to warrant the conclusion that NK-041 is useful as a multivitamin preparation for total parenteral nutrition, with no adverse effects.

Adult↗

Utilization of the bone/liver alkaline phosphatase activity ratio in blood plasma as an indicator of ascorbate deficiency in salmonid fish.

The goal of this study was to test the hypothesis that the ratio of liver to bone alkaline phosphatase in blood plasma reflects the ascorbate status in scurvy-prone teleost fish (rainbow trout [Oncorhynchus mykiss]). The studies focused on finding a method for distinguishing bone alkaline phosphatase present in blood plasma from other alkaline phosphatase isoforms. We tested temperature optima and thermostability of liver, kidney, gill cartilage, and intestinal alkaline phosphatases. We did not observe differences among liver, bone, and kidney enzymes with respect to temperature optima and thermostability. We partially purified alkaline phosphatase from juvenile rainbow trout vertebrae and liver using n-butanol solubilization and ammonium sulfate fractionation. We found a difference between bone alkaline phosphatase, which precipitated in 0%-20% ammonium sulfate saturation, and liver enzyme, which required 40%-50% ammonium sulfate saturation to precipitation. We conducted a series of urea inactivation studies on partially purified enzymes from liver and vertebrae. Urea differentially inhibited the enzymes with t 1/2 = 1.1 and 0.4 min, for bone and liver, respectively. Subsequently, we subjected blood plasma alkaline phosphatase to urea inhibition, and using regression analysis we calculated the ratio of liver to bone alkaline phosphatase. We found that thus obtained ratios of bone enzyme in blood plasma correlated with liver ascorbate concentration. Bone alkaline phosphatase declined in ascorbate deficiency 10-fold, whereas low ascorbate status resulted in a 3.5-fold decrease. In order to draw a general conclusion on the linearity of the response of blood plasma/bone alkaline phosphatase as an indicator of ascorbate deficiency in fish, further studies must include analysis of individual fish followed in the process of developing avitaminosis.

Alkaline Phosphatase↗

[Stimulating effect of vitamin A on the absorption and metabolism of zinc in chicks].

Zinc metabolism and absorption were examined in chicks of two groups that differed in vitamin A supply. Five week chicks that were given a diet without an addition of vitamin A showed overt symptoms of A-avitaminosis. The condition was followed by marked changes in the zinc metabolism and absorption in the intestine and by insignificant changes in the calcium metabolism. Vitamin A was administered per os at a dose of 24,000 i. u. (in oil) and 72 hours later zinc absorption in the ileum increased noticeably and zinc balance in the body became positive.

Animals↗

[Sialadenosis of the parotid gland. Ultrastructural, clinical and experimental findings in disturbances of secretion (author's transl)].

Among the secretory disturbances ("Dyschylien") of salivary glands the sialadenosis of the parotid gland is a clinic and a morphologic definited entity. The typical clinical symptom is a bilateral, often recurrent, and painless swelling of the parotid gland. The characteristic pathological findings consist in an acinar cell hypertrophy without any inflammatory signs. According to this definition, sialadenosis has to be separated from those diseases of salivary glands, which are primarily altered by inflammation of the salivary tissue with secondary secretory disturbances. From flinical point of view it is possible to distinguish the following kinds of sialadenosis according to the syntropy with various diseases: Endocrine sialadenosis (in diabetes mellitus, dysfunction of gonads, pituitary gland, thyroid gland etc.); dystrophic-metabolic sialadenosis (malnutrition, avitaminosis, alcohilsm, chronic liver diseases etc.), and neurogenic sialadenosis (dysfunction of the vegetative nervous system, drug damages e.g. antihypertensive agents). The question arises, whether all forms of sialadenosis have a common etiology and a coincidental pathogenic factor. The following studies were carried out with the aim to find further details concerning the etiology and pathogenesis of sialadenosis. The study is based on the following material: a) 126 Biopsies of parotid glands from patients with sialadenosis (Register of salivary gland diseases at the Institute of Pathology, University of Hamburg, supported by Deutsche Forschungsgemeinschaft). This material was collected from 1965 to 1973. b) 80 Biopsies of parotid glands from patients with other diseases (parotitis [4]; acinic cell carcinoma [4]; other parotid and oral tumors [72]; for comparison. c) Experimental studies on the parotid salivary glands of Wistar-rats. The biopsies of the parotid glands were studied histologically, morphometrically, and ultrastructurally. The investigations centered on the ultrastruct of sialadenosis. Before interpreting the ultrastructural findings in view of etiology and pathogenesis of sialadenosis, it was primarily necessary to study the normal ultrastructure of the human parotid gland including the vegetative nervous system. Furthermore it was necessary to elucidate details of a functional morphology of the secretory cycle and to integrade the findings into a concept of general pathology of secretory disturbances. The following results were achieved by our investigations: 1. Normal ultrastructure of human parotid gland: The architecture of the acinar cells is identical with these of other animal species (cytoplasm with a basal standing nucleus, rough endoplasmatic reticulum, Golgi-apparatus, secretory granules etc.). Further identical elements are intercalated and striated ducts, myoepithelial cells, and the vegetative nervous system (postganglionic sympathetic and parasympathetic neurites, however no ganglionic cells in the parotid gland)...

Action Potentials↗

[Metabolism of nucleic acids in testicles of adult rats deficient in vitamin A].

Avitaminosis A, applied on deficient rats receiving retinoic acid leads to an important decrease of thymidine incorporation in testicular DNA in vivo as well as in vitro. On the contrary uridine incorporation in RNA is considerably increased in vitro as well as in vivo. The function of ribosomes, as measured by the aggregation ability in the polysomes, is not altered by vitamin A deficiency. From these results one can say that the degenerescence of rat testicle is accompagnied by a decrease of DNA anabolism and a stimulation of RNA anabolism due to an increase of its catabolism (compensatory synthesis).

Animals↗

[Mycotic disease of the mucous membranes of the head and neck].

INTRODUCTION: Candidiasis is usually a superficial infection of the moist areas of the body and is generally caused by Candida albicans. Visceral infections occur in diabetes, lymphomas and leukemias, malnutrition, avitaminosis and they are associated with antibiotic, corticosteroid and immunosuppressive therapy. Candida albicans was isolated from middle ear inflammation. The diagnosis is made on the basis of microscopic appearance of colonies and characteristic smell. Candidiasis is successfully treated with nystatin, imidazol derivatives (fluconazole, ketoconazole and intraconazole), amphotericin B, 5-fluorocystosine and 1% iodine solution. CASE DESCRIPTION: This is a case report of a 46-year-old patient with a persistent nasal, sinus and ear infection of unknown origin. The patient first received antibiotic and steroid therapy and trepanation of the right maxillary sinus was performed. As the patient's condition aggravated with increase of temperature and bad laboratory findings, he was hospitalized. Radiography revealed a pathological process in both maxillary sinuses and both mastoids, so mastoidectomy and left maxillary sinus trepanation were performed. Histopathological examination of the right mastoid revealed a mould infection. The immunologic status pointed to hypogammaglobulinemia IgG. The following diseases were excluded: systemic diseases, blood diseases, Reiter's syndrome, AIDS, Hepatitis B, other viral diseases, toxoplasmosis, trichinellosis, borreliosis, typhus, paratyphus and exanthematous typhus. The diagnosis of candidiasis caused by Candida crusei and Candida kefyr was made on the basis of macroscopic and microscopic findings and biochemical identification. Ketoconazole was introduced (400 mg/per day) as well as high doses of vitamins and povidone-iodine locally. After a period of remission the patient died due to myocarditis, sepsis, acute kidney failure associated with severe mucosal necrosis of the mouth, esophagus and throat. Differential diagnosis in fever of unknown origin must include the possibility of mycotic infection, whereas the therapy of mycotic diseases must include two antimycotics at the same time. DISCUSSION AND CONCLUSION: Candida albicans is often found in the oral cavity and skin as well as in intestines of 18% of healthy subjects. It is unknown why it causes clinical illness. Antibiotic therapy of bacterial infections enables candida colonization especially in immunosuppressed patients. In our patient two types were found: Candida krusei and Candida kefyr. It is of special importance to perform differential diagnosis in cases with fever of unknown origin in order to include the possibility of mycotic infections, whereas treatment of systemic fungal infections requires a team of physicians.

Candidiasis↗

[Influence of vitamin A on the sialoglycoproteids and the electrophoretic motility of erythrocytes].

Tests conducted on albino rats with experimental avitaminosis and hypervitaminosis A provide evidence that vitamin A has an influence on sialoglycoproteids and on the electrophoretic motility of erythrocytes. In the states under study there is observed an appreciable fall in the hemoglobin and sialic acids content in the erythrocytes, the electrophoretic motility of the latter being on the decrease. These data support the opinion according to which optimal amounts of vitamin A are needed for a normal functioning of the red blood cells.

Animals↗

[Some peculiarities of skin metabolism with vitamin A deficit].

The paper deals with studying the effect of vitamin A deficit in the rat organism on the incorporation of the C14-labelled asparaginic acid serine-3-C14 and glycine-2-C14 into different fractions of skin proteins, with determining the content of glycine cycle components (glycine, glycolic acid and glycolic aldehyde), activity of phosphatases and succinate dehydrogenase in the skin as well as the quantity of mucopolysaccharides and seromucoids in the skin and blood serum. It is established that with vitamin A deficit the intensity of the incorporation of labelled asparaginic acid and serine into the skin total proteins decreases and the incorporation of glycine-2-C14 into the total proteins and the fraction of soluble non-collagen proteins of skin increases. The intensity of the incorporation of the labelled asparaginic acid into the skin soluble collagen falls by 40% but almost twice as high into the soluble non-collagen proteins. A 47% decrease of glycine, 22% fall of glycolic acid and almost two-fold increase of glycolic aldehyde are observed in the skin of the animals with A-avitaminosis. Skin extracts manifest a higher activity of alkaline and acid phosphatases, but a lower activity of succinate dehydrogenase in comparison with control.

Animals↗

[Dynamics and causes of mortality in poultry in the Pleven district].

Studied were the various factors causing death and the dynamics of death in two broiler flocks, two parental flocks for broilers, and one flock of market egg layers. Death rate among broilers ranged between 2.17 and 2.98 per cent. It was highest during the first week after which it sharply dropped up to the end of the fattening period. In some flocks it again rose in the 4th to 6th of 8th week owing to the onset avitaminosis E, coccidiosis or Marek's disease. Noninfectious and deficiency diseases were prevailing in broilers. In the layers death rate varied within wide limits, ranging from 15 up to 23.75 per cent. It was highest during the first month and then sharply dropped. However, after the third month it again rose, reaching its maximum by the 6-7th month in connection with the outbreak of Marek's disease. In layers the infectious diseases were slightly prevailing, causing 51 to 57.39 per cent of the total number of deaths. Most widespread of the infectious diseases was Marek's disease, causing nearly 50 per cent of the deaths.

Age Factors↗