Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidemic dropsy is a clinical state resulting from use of edible oils adulterated with Argemone mexicana oil. Sanguinarine and dehydrosanguinarine are two major toxic alkaloids of Argemone oil, which cause widespread capillary dilatation, proliferation and increased capillary permeability. Leakage of the protein-rich plasma component into the extracellular compartment leads to the formation of oedema. The haemodynamic consequences of this vascular dilatation and permeability lead to a state of relative hypovolemia with a constant stimulus for fluid and salt conservation by the kidneys. Illness begins with gastroenteric symptoms followed by cutaneous erythema and pigmentation. Respiratory symptoms such as cough, shortness of breath and orthopnoea progressing to frank right-sided congestive cardiac failure are seen. Mild to moderate anaemia, hypoproteinaemia, mild to moderate renal azotemia, retinal haemorrhages, and glaucoma are common manifestations. There is no specific therapy. Removal of the adulterated oil and symptomatic treatment of congestive cardiac failure and respiratory symptoms, along with administration of antioxidants and multivitamins, remain the mainstay of treatment. Selective cultivation of yellow mustard, strict enforcement of the Indian Food Adulteration Act, and exemplary punishment to unscrupulous traders are the main preventive measures.
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PMID:Epidemic dropsy in India. 1062 75

Long slow hemodialysis (3 x 8 hours/week) has been used in Tassin for 30 years without significant change in the method. It provides excellent results in terms of morbidity and mortality. The better survival than usually reported on shorter dialysis is mainly due to lower cardiovascular mortality. The nutritional state of the patient is good, as well as the correction of anemia with low doses of EPO. But the main feature concerns blood pressure; hypertension is very well controlled without need for antihypertensive medications. The gentle ultrafiltration provided by a long session time associated with a low salt diet and a moderate interdialytic weight gain allows for normalization of the extracellular fluid space in most patients (dry weight) without important intradialytic morbidity. This low salt diet has paradoxically been forgotten in recent years while shortened dialysis time renders it more necessary than ever.
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PMID:Long, slow dialysis. 1068 72

The objective of the study was to outline the characteristics of the development of hypertension and some neurohumoral, haematological and morphological factors contributing to development of high blood pressure in a genetic model of salt-sensitive rat. Characteristics of Dahl salt-sensitive (DS) rats, as compared to their Dahl salt-resistant (DR) controls were as follows: 1) DS rats display higher blood pressure and lower heart rate compared to DR rats as early as 1 month of age at weaning). They gradually develop hypertension at 2 months of age, irrespective of diet. Low-Na diet (0.5% NaCl) does not prevent hypertension but delays its development and ameliorates it. High Na-diet (8% NaCl) exacerbates hypertension. 2) DS rats have retardation in body weight gain. They develop mild hypochromic anaemia. 3) After 2 months of Na loading (3 months of age), DS rats express significantly increased Na and water retention and increased plasma volume by 15% compared to 2.8% increase in DR rats on high-Na diet. 4) DS rats showed renal parenchymal lesions, more pronounced after Na-loading, focal atrophy of cortical tubules, mesangial matrix expansion and glomerulosclerosis. Consistent with high blood pressure were changes in renal arterioles, fibromuscular proliferation, deposition of fibrinoid material in intima. 5) Sodium loading produced increased activity of the sympathetic nervous system (SNS), and sodium restriction reduced SNS responsiveness.
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PMID:An experimental rat model of salt-sensitive hypertension; biochemical and morphological parameters and sympathetic nervous system. 1085 16

Impairment of haemoglobin synthesis occurs in the genetic diseases known as thalassaemia. The consequent chronic anaemia leads to increased dietary iron absorption which results in iron overload. Treatment through regular blood transfusions increases oxygen capacity, but also adds iron from haemoglobin. An essential treatment, in parallel with transfusions, is the use of chelating agents to remove the excess iron. Thalassaemia patients are particularly at risk of free radical damage. Human lymphocytes from normal individuals can be investigated in vitro as a model system in the presence of free radicals in the Comet assay. This assay measures DNA damage, particularly DNA strand breakage. We examined cells from an Australian thalassaemic patient (sickle/beta thal double heterozygote-sickle phenotype) who had not yet received chelation therapy to determine if the cells were more sensitive to simulated iron overload and to haemosiderins. Lymphocytes from the patient were received as frozen samples after 28 h on dry ice and then placed in liquid nitrogen. Normal lymphocytes frozen under the same conditions and normal nonfrozen lymphocytes were compared. The lymphocytes from a normal female did not respond in vitro to ferric chloride (FeCl(3)) or haemosiderin but did to ferrous chloride (FeCl(2)) and ferrous sulphate (FeSO(4)). Deferoxamine appeared to reduce the response to FeCl(2) and FeSO(4) but deferiprone did not. When the lymphocytes from the nonchelated patient were treated with FeSO(4) and hydrogen peroxide, deferoxamine and deferiprone both reduced the response. Over the same dose range of iron salt (FeSO(4)), the lymphocytes from the thalassaemic patient were more sensitive, with much higher background levels of damage and induced damage. When deferiprone and deferoxamine were compared over a nontoxic range, deferiprone appeared to produce a greater reduction of damage in lymphocytes of the thalassaemia patient. Ferritin iron appears to be more available than haemosiderin iron in reactions leading to DNA damage. Haemosiderin containing higher amounts of the goethite-like (alpha-FeOOH) iron oxide phase leads to lower levels of DNA damage.
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PMID:Effect of iron salts, haemosiderins, and chelating agents on the lymphocytes of a thalassaemia patient without chelation therapy as measured in the comet assay. 1099 72

Autosomal dominant familial nephropathies with adult onset, no macroscopic cysts, and progressive deterioration include medullary cystic disease (ADMCKD) as well as other less specific entities. We studied a kindred of Jewish ancestry in which 15 members (both male and female) have suffered from chronic renal failure. The first evidence of renal involvement was observed between 18 and 38 years. It included hypertension followed by progressive renal insufficiency. No polyuria, anemia, gout, hematuria, nor proteinuria were seen. An average of 4.5 years elapsed from diagnosis to end-stage renal disease. Renal pathology at early stages of the disease showed extensive tubulointerstitial fibrosis and global glomerulosclerosis. Linkage analysis was performed at the two known loci of ADMCKD, on Chromosomes 1 and 16. Linkage to the chromosome 16 locus was excluded. However, linkage to the chromosome 1q21 locus of ADMCKD was established with a maximum two-point LOD score of 3.82 to D1S394. The disease interval could be narrowed to about 9 cM/7.4 Mb between D1S1156 and D1S2635. Multiple-point linkage analysis revealed a maximum LOD of 4.21, with a broad peak from markers D1S2858 and D1S2624. This report establishes linkage between a familial nephropathy characterized by hypertension and progressive renal failure to the locus described for ADMCKD, a disease classically associated with macroscopic corticomedullary cysts, salt-losing tubulointerstitial nephropathy, and anemia. This finding broadens the clinical spectrum of ADMCKD positioned on chromosome 1q21 locus.
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PMID:Clinical and genetic characterization of an autosomal dominant nephropathy. 1124 91

Congestive heart failure describes a syndrome with complex and variable symptoms and signs, including dyspnea, increased fatigability, tachypnea, tachycardia, pulmonary rales, and peripheral edema. Although this syndrome usually is associated with low cardiac output, it may occur in a number of so-called high output states, when the cardiac output is normal or greater than normal. A high output state may occur in chronic severe anemia, large arteriovenous fistula or multiple small arteriovenous shunts as in Paget's bone disease, some forms of severe hepatic or renal disorders, and acutely in septic shock. The syndrome of systemic congestion in a high output state is traditionally referred to as high output heart failure. However, the term is a misnomer because the heart in these conditions is normal, capable of generating very high cardiac output. The underlying problem in high output failure is a decrease in the systemic vascular resistance that threatens the arterial blood pressure and causes activation of neurohormones, resulting in an increase in salt and water retention by the kidney. Many of the high output states are curable conditions, and because they are associated with decreased peripheral vascular resistance, the use of vasodilator therapy for treatment of congestion may aggravate the problem. There are other clinically important issues in high output failure that have received little attention in the current medical literature. This article reviews the available data on high output cardiac failure with particular emphasis on the underlying mechanisms and treatment.
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PMID:High Output Cardiac Failure. 1124 61

Aluminium (Al.) is an ubiquitous element found in every food product. The sources of Al. are especially corn, yellow cheese, salt, herbs, spices, tea and tap water. In household Al.-made ware is a major source of the element. Al. may cause diseases in humans, especially hampers many metabolic processes especially turnover of calcium, phosphorus and iron. Salts of Al. may bind to DNA, RNA, inhibit such enzymes as hexokinase, acid and alkaline phosphatases, phosphodiesterase and phosphooxydase. Al. salts are especially harmful to nervous, hematopoietic systems and to skeleton. Al. gets to organism with food, water, cosmetics, from aluminium ware and containers. Toxicity comes from substitution of Mg and Fe ions effecting in disturbances in intracellular signaling, excretory functions and cellular growth. Neurotoxic action of Al. probably comes from substitution of Mg ions in ATP, what finally influences function of every ATP using-enzymes. There are observations in experimental models proving Al. salts are responsible for Alzheimer disease development. Toxicity of Al. to skeletal system results in diminished resistance thus tendencies to breaking, and comes from lower collagen synthesis and slowing down of mineralisation. Low erythropoietin production, inhibition of hem-synthesing enzymes and binding of Al. to transferrin, effects in anaemia. Carcinogenic effects of Al. were nor proved nor denied, but high concentrations of Al. were found in many neoplastic cells. In conclusion, we should introduce prophylactic measures effecting in less Al. intake esp. avoiding use of Al.-made ware nad controlling food for Al. content.
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PMID:[Aluminum--occurrence and toxicity for organisms]. 1129 16

Under the supervision of the central and local health authorities, a pilot project was conducted in four villages in the Luangprabang Province, Lao PDR. The objective of the project was to test different regimes to supplement females with oral iron preparations to reduce iron deficient anemia (IDA) and control iodine deficiency disorders (IDD) in school children. Compared with iron sulphate tablets, iron fumerate tablets were well accepted and good compliance results were achieved. Hemoglobin concentration improved only in the group of females taking iron fumerate tablets. The goiter rate decreased from approximately 90% to about 45% for school children, regardless of whether iodine salt were used by their families or whether iodine capsules were used to treat the children. The latter attempt was hampered by the fact that also in the control village iodine fortified salt was used. This was due to a governmental attempt to control IDD nation-wide. Therefore, also in the control village a significant decrease in the goiter rate was observed.
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PMID:Community based intervention of iron deficiency anemia in females and iodine deficiency disorders in school children in Lao PDR. 1148 44

Fortification of salt with iron has been developed by the National Institute of Nutrition (NIN) as a strategy for the control of iron deficiency anaemia (IDA) in India, similar to iodization of salt for control of iodine deficiency disorders (IDD). Stability of the iron fortified salt (IFS), its bioavailability and organoleptic evaluation of food items containing the IFS have been demonstrated. Acceptability and effectiveness of the IFS in school children and in multicentric community trials have been demonstrated. With the introduction of universal iodization of salt as a national policy in 1988, NIN has developed a formulation for double fortification (DFS) of salt with iodine and iron. The stability of the nutrients under laboratory conditions along with their bioavailability were found to be good but varying with the quality of salt used. The DFS has been evaluated in controlled trials in tribal communities and in residential school children. The findings of these studies are discussed. Overall, in these trials, DFS effectively controlled iodine deficiency but a clear impact on reducing anaemia was not demonstrated. In residential schoolchildren, increased urinary excretion of iodine as well as reduced anaemia were observed. The quality of salt has been found to be an important determinant of the stability of iodine in DFS. Further evaluation of this potentially important intervention is in progress.
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PMID:Prospects of fortification of salt with iron and iodine. 1150 6

The association of the angiotensinogen (AGT) gene variation at codon 235, the T235 variant, with hypertension induced by erythropoietin (Epo) was investigated in patients with progressive renal disease requiring treatment for renal anemia with Epo. The subjects for the study were patients with renal diseases with serum creatinine concentration exceeding 2 mg/dl and a hematocrit (Ht) of less than 30%. During the run-in period, blood pressure was well controlled with an appropriate salt restricted diet and/or antihypertensive treatment. The patients were then given 6,000 IU of Epo once a week until the Ht rose by 5%. For the overall patient group, AGT gene polymorphism analysis revealed T235T (T/T) in 31 cases (61%), M235T (M/T) in 19 cases (37%), and M235M (M/M) in 1 case (2%). In response to treatment with Epo, hypertension (defined as an increase in mean blood pressure greater than 10 mmHg) was found in 11 cases (22%), all of who carried the homozygous T allele (T/T). On the other hand, the frequency of T/T in patients who did not develop hypertension was 50% (T/T:T/M=20:19 cases), indicating a significant difference (p=0.003 by Chi-square). Variables estimated to be associated with Epo-induced hypertension were the T allele, gender (male), and the degree of increase in Ht, in descending order. Our preliminary research indicates that individuals who carry two copies of the T allele, i.e., who are homozygous for T, are highly susceptible to development of hypertension when subjected to Epo. These results suggest that the AGT T235 variant may be the primary gene responsible for the development of Epo-induced hypertension.
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PMID:Association of angiotensinogen gene polymorphism with erythropoietin-induced hypertension: a preliminary report. 1167 43


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