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

Dapsone has been used in various dermatological disorders and in leprosy. One of the main side effects of dapsone therapy is anemia, mostly hemolytic. We aimed at finding the effect of dapsone therapy on serum haptoglobin levels which could be an indirect evidence for intravascular hemolysis, supported by secondary investigations such as liver functions (serum lactic dehydrogenase, alkaline phosphatase, bilirubin), blood hemoglobin levels, urinary excretion of urobilinogen, and erythrocytes. As in other infectious conditions, haptoglobins were raised in untreated lepromatous cases, compared to controls (p less than 0.05). Dapsone treatment of 100 mg daily for 14 days brought down the haptoglobin level significantly as compared to the untreated cases and the controls (p less than 0.05). An elevated alkaline phosphatase and lactate dehydrogenase indicate some liver dysfunction following dapsone therapy. A significant drop in blood hemoglobin level and a concomitant increase in serum bilirubin, urinary excretion of urobilinogen, and a significant fall in the serum hemoglobin binding capacity (haptoglobin level) following treatment with dapsone are quite suggestive of mild intravascular hemolysis.
 ...
PMID:Dapsone induced hypohaptoglobinemia in lepromatous leprosy patients. 719 20

Systemic iron deficiency was found in 63 (56%) of 113 joggers and competition runners (33 women and 80 men). Thirteen women and ten men had latent anemia. A majority of the women were fertile with iron loss from menstruation; the men were runners training long distances. The average transferrin iron-binding capacity was 80 mu mol/l serum in the women and 77 (iron-binding groups) in the men. The haptoglobin and iron concentrations in serum were remarkably low (most often below 10 and 20 mu mol/l, respectively). Three of the long-distance runners ran 25 km daily. They returned with so much free hemoglobin in their plasma that an accompanying iron loss (integrated over months), if not balanced by diet, would lead to iron deficiency and anemia. Oral iron therapy (200 mg ferrous sulphate per day) normalized the hemoglobin concentration and improved the transferrin saturation fraction in 61 persons. The competition runners reported personal records.
 ...
PMID:Runner's anemia and iron deficiency. 723 8

The haptoglobin (Hp) status of the population of Keneba, The Gambia was investigated. Of the 825 persons examined 22.9% were ahaptoglobinaemic (HpO). The incidence of HpO was higher in the 209 persons showing malaria parasites in their blood (38.8%) than in non-parasitaemic individuals (17.5%). Children less than two years old had low incidences of HpO except in the first two months of life. After two years the incidence rose with little tendency to change in older age groups. No correlations were seen between HpO and sex, anaemia or sickle cell trait. However, a positive correlation was found with malariometric indices in all age groups except the two to four years. The Hp of individuals was found to be unstable suggesting that in Africans it is a poor genetic marker. These results indicate that Hp is utilized in removing free haemoglobin liberated intravascularly, during malaria infections and that although this is a major cause of the high incidence of HpO in The Gambia, other factors are also important.
 ...
PMID:Haptoglobin polymorphism and its relationship to malaria infections in The Gambia. 730 32

A 79 year-old Japanese man was admitted because of brownish urine and Raynaud phenomenon. Laboratory data showed mild anemia with reticulocytosis, positive direct Coombs test against anti-C3, elevated level of lactate dehydrogenase, undetectable level of serum haptoglobin and low titer of cold agglutinin (1:256 at 4 degrees C), the immunoglobulin subclass of which was IgM. Cold agglutinin disease is usually associated with very high levels of cold agglutinins, the specificity of which is anti-I. This case had low titer cold agglutinin disease due to anti-HI cold agglutinin.
 ...
PMID:[Low titer cold agglutinin disease due to anti-HI antibody and a review of this disease in Japan]. 754 Feb 24

Initial studies have shown that recombinant human interleukin-6 (rhIL-6) induces anemia. Until now, the pathophysiologic mechanism of this induced anemia has been unknown. To unravel the underlying mechanism, we examined 15 cancer patients receiving rhIL-6 as an antitumor immunotherapy in a phase II study. rhIL-6 was administered subcutaneously at 150 micrograms once daily for 6 consecutive weeks. Various hematologic and biochemical parameters were measured weekly during rhIL-6 treatment and 4 weeks after rhIL-6 discontinuation. To determine plasma volume and red blood cell (RBC) volume, radioisotope dilution assays with labeled autologous RBCs and with human serum albumin were performed before rhIL-6 administration and on day 8 of rhIL-6 therapy. Hemoglobin levels decreased (mean change +/- SE) 7% +/- 1.5% within 3 days after the start of rhIL-6 therapy (P < .0001) and 19% +/- 2% at week 4. Levels had normalized at follow-up. The plasma volume increased 18% +/- 5% during the first week of rhIL-6 administration (P < .003), whereas RBC volume remained unaffected. The mean RBC corpuscular volume remained unchanged for 2 weeks and then began to decrease slowly, reaching its nadir at week 6 (5% +/- 1%; P < .01). Serum iron levels decreased 65% +/- 12% at week 4 (P < .002) and then returned to initial baseline values. Erythropoietin levels increased rapidly up to 68% at week 3 (P < .0001) and had normalized 4 weeks after rhIL-6 therapy. Levels of serum albumin, prealbumin, and transferrin decreased (P < .0001, P < .003, and P < .0001, respectively), whereas levels of serum amyloid A (P < .003), C-reactive protein, haptoglobin, and alpha-1-antitrypsin (P < .0001) increased during rhIL-6 treatment. All levels returned to pretreatment values after discontinuation of rhIL-6. No alterations in reticulocyte counts, serum lactic dehydrogenase levels, and bilirubin levels were observed. A 6-week regimen of subcutaneous rhIL-6 results in a rapid dilution anemia, caused by an acute and significant increase in plasma volume and followed by hypoferremia. This anemia is reversible after the cessation of rhIL-6 treatment.
 ...
PMID:Recombinant human interleukin-6 induces a rapid and reversible anemia in cancer patients. 754 2

Recombinant human interleukin-6 (rhIL-6) is a pluripotent cytokine with proinflammatory, antitumor, and growth factor effects. Clinical investigations of rhIL-6 either alone as immunotherapy or as a colony-stimulating factor in conjunction with chemotherapy have shown a dose-dependent, rapid onset, and largely reversible decrease in venous hematocrit levels. In an effort to determine the mechanism for the rhIL-6-associated anemia, we measured red blood cell volume serially in patients receiving rhIL-6 at either 30 micrograms/kg/day as a 120-hour continuous intravenous infusion (renal cell carcinoma) or 100 micrograms/kg/d intravenously over 1 hour for 5 days (melanoma) as part of two separate phase II trials. Radioisotope dilution assays with 51Cr-labeled autologous red blood cells and hemolysis screens were performed on day 1 before the initiation of therapy and on day 5 shortly before the end of therapy. In the 6 patients studied, the mean decrease in hemoglobin concentration was 1.9 +/- 0.94 g/dL. The mean decrease in the hematocrit level was 6% +/- 2% and the mean increase in total blood volume was 731 +/- 337 mL. These changes were explained by a mean decrease in red blood mass of 106 +/- 109 mL and a mean increase in plasma volume of 743 +/- 289 mL. The decrease in red blood cell mass was largely explained by phlebotomy during the hospitalization, but was not statistically significant (paired t-test, P = .06). All other changes were statistically significant (P < .05). Simple regression analysis indicated that the decrease in hematocrit level and increase in plasma volume were related (y = -1.78 - .0066X; R = -.74). Measurements of lactate dehydrogenase, bilirubin, haptoglobin, and reticulocyte counts and serial stool hemoccults did not indicate hemolysis or blood loss. We conclude that the anemia caused by IL-6 is caused by an increase in plasma volume.
 ...
PMID:Interleukin-6-associated anemia: determination of the underlying mechanism. 763 34

Endurance training can lead to what has been termed 'sports anaemia'. Although under normal conditions, red blood cells (RBCs) have a lifespan of about 120 days, the rate of aging may increase during intensive training. However, RBC deficiency is rare in athletes, and sports anaemia is probably due to an expanded plasma volume. Cycling, running and swimming have been shown to cause RBC damage. While most investigators measure indices of haemolysis (for example, plasma haemoglobin or haptoglobin), RBC removal is normally an extravascular process that does not involve haemolysis. Attention is now turning to cellular indices (such as antioxidant depletion, or protein or lipid damage) that may be more indicative of exercise-induced damage. RBCs are vulnerable to oxidative damage because of their continuous exposure to oxygen and their high concentrations of polyunsaturated fatty acids and haem iron. As oxidative stress may be proportional to oxygen uptake, it is not surprising that antioxidants in muscle, liver and RBCs can be depleted during exercise. Oxidative damage to RBCs can also perturb ionic homeostasis and facilitate cellular dehydration. These changes impair RBC deformability which can, in turn, impede the passage of RBCs through the microcirculation. This may lead to hypoxia in working muscle during single episodes of exercise and possibly an increased rate of RBC destruction with long term exercise. Providing RBC destruction does not exceed the rate of RBC production, no detrimental effect to athletic performance should occur. An increased rate of RBC turnover may be advantageous because young cells are more efficient in transporting oxygen. Because most techniques examine the RBC population as a whole, more sophisticated methods which analyse cells individually are required to determine the mechanisms involved in exercise-induced damage of RBCs.
 ...
PMID:Exercise, training and red blood cell turnover. 774 Feb 49

The main biological sign of inflammation is an increase in erythrocyte sedimentation rate (ESR). However it can be falsely normal (polyglobulia, cryoglobulinemia, hemoglobinopathy) or spuriously high in the absence of inflammation (anemia, hypergammaglobulinemia). In cases of doubt, the acute phase reactants (APR) should be measured: C reactive protein (CRP), fibrinogen, haptoglobin, alpha 1 acid glycoprotein. They have different kinetics of variation and various degrees of increase (some--the so called "negative" proteins--actually decrease). Several pitfalls can be avoided if it is remembered that the APR themselves can be modified by causes other than inflammation: low fibrinogen in intravascular coagulation, very low haptoglobin in hemolysis, raised orosomucoide in renal insufficiency and elevated transferrin in iron deficiency. Furthermore liver insufficiency or leakage through the kidney or gut lesions can lower them. In some patients, the observed levels of APR are thus the result of opposite trends. In complex cases, these pathological mechanisms are more apparent on profiles which express the concomitant blood levels of several APR in a normalized or comparative manner. In medical practice, ESR serves first and foremost to detect an inflammatory syndrome. CRP is prominent among the APR because its changes show a great sensitivity, are independant of those of ESR and have a time course fitting closely that of the inflammatory processes. Profiles yield detailed information but rarely provide major evidence in the quest of a diagnosis or the choice of a treatment. Because of their cost they are to be used only in difficult cases.
 ...
PMID:[From sedimentation rate to inflammation profile]. 784 87

From 1980 to 1987 ileoanal pouches were made in 83 patients. Specimen for a set of laboratory analyses were taken preoperatively, during the ileostomy and loop ileostomy periods and repeatedly during 36 months of follow-up. Cobalamine absorption and 14C-triolein breath tests were performed preoperatively in electively operated patients and postoperatively in all patients at 12 and 36 months. Low S-Ca was most pronounced preoperatively in patients who were to undergo acute colectomy (53%). Decreased S-Mg was detected in 16-36% at all stations. None had signs or symptoms of hypomagnesemia. Low S-albumin was rarely seen except for preoperatively in acute patients. Increased IgM was found in 40% of the patients during the loop ileostomy phase compared to 6-10% preoperatively. Substantially increased orosomucoid and/or haptoglobin were seen in patients during the functional periods but these increased values could not be correlated to episodes with acute pouchitis. High values of S-ALAT and ALP were much more frequent during the loop ileostomy periods than it was preoperatively and during pouch function. Low S-haemoglobin and/or iron were noticed during the functional period in 3-8% and 10-16%, respectively. Severe anaemia, due to iron deficiency developed in one patient after 2.5 years of pouch function. Preoperatively, slight decreases of S-B12 were found in 13% and impaired cobalamine absorption was revealed in 38% of the electively operated patients. The corresponding figures were 3% and 31% after 12 months and 5% and 36% after 36 months of follow-up, respectively. B12 substitution was given to in all 8 patients during the follow-ups. Lipid absorption was disturbed in 38% preoperatively and in 35% and 41% at 12 and 36 months, postoperatively.
 ...
PMID:Biochemical laboratory data in patients before and after restorative proctocolectomy. A study on 83 patients with a follow-up of 36 months. 784 1

Some unsolved problems--late onset of anemia and growth retardation (at age 7 years), healthy siblings showing very low transferrin (TF) level, and unexplained mode of inheritance--were found in family members of a congenital atransferrinemia already reported in 1972. The long-term clinical, laboratory, and developmental observations revealed that after 5 years of apo-TF supplementary therapy the patient's anemia gradually disappeared, and he started to grow again without further therapy. Immunoelectrophoretic study disclosed a severe deficiency of both TF and haptoglobin in the patient. The recovery from his anemia and the resumption of his physical development were dependent only on his TF level: that is, from a negligible level it increased to 10-20 mg/dl (normal, 205-370 mg/dl), a level similar to that of his TF-deficient siblings, who had been in good health since birth. The TF analysis of the patient and his family suggests that the minimum TF requisite in this family may be close to 10-20 mg/dl; subjects with more than 20 mg/dl are apparently healthy; with less than 10 mg/dl they may develop severe growth retardation and anemia, and extreme deficiency may be lethal. Also, coexisting haptoglobin deficiency might alleviate hemosiderosis. Further, the isoelectric focusing study disclosed that there was only a small amount of TF variant in these siblings including the patient. The study of the family confirmed that this variant was produced by an allelic gene derived from their father. So, the original diagnosis of congenital atransferrinemia should be revised as familial hypotransferrinemia transmitted with autosomal recessive mode, and the subjects with a recessive character may be compound heterozygotes of the "variant" allele and the "null" allele.
 ...
PMID:Studies on familial hypotransferrinemia: unique clinical course and molecular pathology. 831 85


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>