PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “DEFICIENCY DISEASES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 577 records · Page 32Linked to original sources

[Iodine deficiency in cardiovascular diseases].

The thyroid hormone deficiency on cardiovascular function can be characterized with decreased myocardial contractility and increased peripheral vascular resistance as well as with the changes in lipid metabolism. 42 patients with cardiovascular disease (mean age 65 +/- 13 yr, 16 males) were investigated if iodine insufficiency can play a role as a risk factor for the cardiovascular diseases. The patients were divided in 5 subgroups on the ground of the presence of hypertension, congestive heart failure, cardiomyopathy, coronary disfunction and arrhythmia. Urine iodine concentration (5.29 +/- 4.52 micrograms/dl) was detected with Sandell-Kolthoff colorimetric reaction. The most decreased urine iodine concentration was detected in the subgroups with arrhythmia and congestive heart failure (4.7 +/- 4.94 micrograms/dl and 4.9 +/- 4.81 micrograms/dl, respectively). An elevated TSH level was found by 3 patients (5.3 +/- 1.4 mlU/l). An elevation in lipid metabolism (cholesterol, triglyceride) associated with all subgroups without arrhythmia. In conclusion, the occurrence of iodine deficiency in cardiovascular disease is frequent. Iodine supplementation might prevent the worsing effect of iodine deficiency on cardiovascular disease.

Aged↗

Screening tests for cell-mediated immunodeficiency diseases.

As our knowledge of immunology has become more sophisticated we have had to alter our ideas of the etiology of many immune deficiency diseases. Indeed, current concepts now prevalent have led to reclassification of a number of disease entities. In order to keep our diagnostic efforts abreast of the information being generated by the extensive immunology research programs now in progress, the clinical laboratory has been required to offer a new array of sophisticated tests on a relatively routine basis. This article is intended to serve as a brief review of immunobiology and immunodeficiency diseases with an indepth coverage of specialized tests generally available at the large centers. With an understanding of the principles, procedures, and pitfalls of the tests carried out the laboratory scientist is in a better position to assist the clinician in reaching the correct diagnosis. The detailed review is concerned with methods available to separate, classify, and subclassify lymphocytes and thereby allow a categorization of immune deficiency diseases. Toward that end there is a discussion of surface markers, rosetting, mitogenic and antigenic responsiveness as well as lymphokine production. With a view to present day research tests that might eventually find their way into the armamentarium of the clinical laboratory in the future, there is brief discussion of the methods presently used to classify T-cells as helper, suppressor, or effector cells, assays of some of the lymphokines, and measurement of antibody synthesis in cell culture.

Antigens, Surface↗

Complement components and receptors: deficiencies and disease associations.

The complement system, accessory to many immunological functions, consists of a number of interdependent components and receptors. Numerous in vitro approaches have elucidated the biological role of these components and receptors. However, it is the in vivo "natural" experiments that underscore their importance. The phagocytosis and subsequent digestion of pyogenic bacteria is significantly enhanced by the fixation of the third complement component to the bacterial cell wall. Equally important is the intact expression of a receptor (CR3) for the C3b cleavage fragment. Breakdown in this ligand-receptor interaction due to either C3 or CR3 deficiency leads to pyogenic infection. Interestingly, C3-deficient individuals do not demonstrate leukocytic infiltration at the site of infection. Undoubtedly, this is due to the lack of C5 convertase and failure to produce C5a. CR3-deficient individuals, on the other hand, do demonstrate leukocytosis since the third complement component is functional. C3 deficiency is not necessarily a primary lesion and may be secondary to factor I deficiency. In this case, the C3b fragment, along with factor B, acts as a C3 convertase. Inefficient inactivation of C3b, due to factor I deficiency, leads to the uncontrolled consumption of the third component, resulting in C3 deprivation. It appears that phagocytosis by neutrophils and monocytes followed by enzyme-interaction is not sufficient for destruction of the Neisseria organisms. In addition to this leukocyte activity, an intact membrane attack complex, composed of the late complement components C5, 6, 7, 8, and 9, is required for the lysis of these bacteria. This is supported by findings that individuals deficient in late components are highly susceptible to systemic Neisseria infections. Diseases of an autoimmune nature are frequently associated with a deficiency of one of the early complement components C1, C2, or C4 and a deficiency of erythrocytic CR1 receptors as well. This may suggest that proper interaction between a complement fragment of the immune complex with the complement receptor expressed on the erythrocyte is important for proper management and clearance of the complex. Deficiency of the early complement components would prevent the activation of C3 and the fixation of a resulting C3 cleavage product. In this case, erythrocytes would be unable to participate in the transport of the immune complex to the reticuloendothelial system. Instead, tissue deposition of the complex would occur more readily, contributing to the pathologic process. Provided that the early complement cascade were intact, deficiency of erythrocytic CR1 receptors would contribute to the pathologic response for the same reason.(ABSTRACT TRUNCATED AT 400 WORDS)

Autoimmune Diseases↗

Drug development for neglected diseases: a deficient market and a public-health policy failure.

There is a lack of effective, safe, and affordable pharmaceuticals to control infectious diseases that cause high mortality and morbidity among poor people in the developing world. We analysed outcomes of pharmaceutical research and development over the past 25 years, and reviewed current public and private initiatives aimed at correcting the imbalance in research and development that leaves diseases that occur predominantly in the developing world largely unaddressed. We compiled data by searches of Medline and databases of the US Food and Drug Administration and the European Agency for the Evaluation of Medicinal Products, and reviewed current public and private initiatives through an analysis of recently published studies. We found that, of 1393 new chemical entities marketed between 1975 and 1999, only 16 were for tropical diseases and tuberculosis. There is a 13-fold greater chance of a drug being brought to market for central-nervous-system disorders or cancer than for a neglected disease. The pharmaceutical industry argues that research and development is too costly and risky to invest in low-return neglected diseases, and public and private initiatives have tried to overcome this market limitation through incentive packages and public-private partnerships. The lack of drug research and development for "non-profitable" infectious diseases will require new strategies. No sustainable solution will result for diseases that predominantly affect poor people in the South without the establishment of an international pharmaceutical policy for all neglected diseases. Private-sector research obligations should be explored, and a public-sector not-for-profit research and development capacity promoted.

Anti-Infective Agents↗

[Surveillance of patients with chronic inflammatory intestinal diseases: problems relevant to clinical practice].

For control of activity of inflammatory bowel diseases, clinical signs and acute-phase proteins are of higher value compared to endoscopy; however this method is necessary for supervision of patients with ulcerative colitis for detection of malignancies. In patients with longstanding and extensive ulcerative colitis, a consequent supervision permits to prevent cancer development markedly. New aminosalicylates are effective in preventing relapse in ulcerative colitis and perhaps in Crohn's disease. Deficiency in vitamins and minerals has to be recognized and balanced. Patients suffering from Crohn's disease should quit smoking because nicotine is worsening the course of the disease.

Colitis, Ulcerative↗

Hereditary zinc deficiency (Adema disease) in cattle, an animal parallel to acrodermatitis enteropathica.

Adema disease and acrodermatitis enteropathica, two parallel syndromes in calves of Friesian descent and in man, are described. Both are congenital zinc deficiency disorders with a lethal course if left untreated. Complete recovery follows oral zinc therapy. Symptoms and findings are set out in Table I. Diseased calves may serve as animal models for further studies on acrodermatitis enteropathica and the biological role of zinc.

Acrodermatitis↗

Evidence for nutritional benefits in prolonging wellness.

Healthy aging involves the interaction between genes, the environment, and lifestyle factors, particularly diet and physical activity. Worldwide, the increase in life span has led to an increase in morbidity and mortality as the result of chronic, lifestyle-influenced diseases such as type 2 diabetes, cardiovascular disease, and cancer. Nutrient deficiency diseases are giving way to energy imbalances, and links between diet and chronic disease are becoming clearer. The global demographic, epidemiologic, and nutrition transitions are dramatic and point to an urgent need to focus on preventive approaches in health care. Thus, nutrition research has shifted from focusing exclusively on alleviating nutrient deficiencies to also stressing chronic disease prevention. Ongoing initiatives to optimize long-term health and promote healthy aging are based on the concept of functional fitness, ie, the ability to lead an active and healthy life. The Dietary Reference Intakes provide a framework for assessing nutrient adequacy at the population and individual levels. In addition, the Healthy Eating Index provides a single summary measure of diet quality. To effect changes in lifestyles to optimize health as we age, health care providers need to consider all the lifestyle and environmental factors contributing to suboptimal eating and lifestyle patterns.

Aged↗

Safety of megavitamin therapy.

Carbon compounds that are needed in small amounts in the diet because they are not made in the body of vertebrates are defined as vitamins. Excluded from this definition are vitamins D, K, and niacin which can be synthesized by the organism or, as in the case of vitamin K, by the host's intestinal bacteria. Lack of such vitamins can result in characteristic deficiency diseases. The therapeutic use of such compounds (megavitamin intake) is based on the spectacular effect of vitamins on deficiency diseases; however, evidence that the ingestion of large amounts of vitamins beyond the "Recommended Daily Allowances" (RDA) is beneficial is not within the basic concept of nutrition. Vitamins, like many substances, may be toxic when taken in large quantities, especially the fat-soluble vitamins, and the concept of "more is better" is a common misconception. Vitamin supplements can be suggested only in the unusual cases of patients having inadequate intake, disturbed absorption (genetic or otherwise), or increased tissue requirements. A well-balanced diet that includes a wide variety of foods from each of the four food groups is adequate for the supply of vitamins, as well as other nutrients, in healthy people. This paper will review some of the recent findings regarding vitamin toxicity and the mechanisms of toxicity.

Ascorbic Acid↗

Isoflavones extracted from Sophorae fructus upregulate IGF-I and TGF-beta and inhibit osteoclastogenesis in rat bone marrow cells.

Isoflavones have been a central subject in research on the natural phytoestrogens found in Leguminosae. Their effects on bone formation and remodeling are important in that they can act like estrogen by binding on estrogen receptors on the target cell surface. We, therefore, believed that isoflavones may help in the treatment of patients with estrogen deficiency disease such as estrogen replacement therapy (ERT) for osteoporosis. As commonly known, osteoporosis is one of the hormonal deficiency diseases, especially in menopausal women. When estrogen is no longer produced in the body a remarkable bone remodeling process occurs, and the associated events are regulated by growth factors in the osteoblast lineage. In the present study, we investigated whether isoflavones (Isocal) extracted from Sophorae fructus affect the growth factors IGF-I and TGF-beta that have been known to be related with bone formation. In the study, we found that the active control (PIII) effectively enhanced the level of nitric oxide (NO) and growth factors, and thereby inhibited osteoclastogenesis. The most efficient concentration was 10(-8)% within five days, whereas the comparative control (soybean isoflavone) was not as effective even at a lower concentration. In conclusion, the products which contain enriched glucosidic isoflavone and nutrient supplements such as shark cartilage and calcium can be used for osteoporosis therapy by enhancing the production of IGF-I and TGF-beta. Furthermore, the NO produced through endothelial constitutive NO synthase (ecNOS) may play a role in inhibiting bone reabsorption.

Animals↗