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At least 19 recordsLinked to original sources
PubMed1975

Intestinal iron absorption under the influence of available storage iron and erythroblastic hyperplasia. Comparative studies in children with hereditary spherocytosis, nonspherocytic enzymopenic hemolytic anemia, acquired hemolytic anemia, vitamin B12 deficiency induced megaloblastic anemia, erythroblastic hypoplasia and aplastic anemia.

A high negative correlation (coefficient similar to 0.9) between increased 59Fe absorption from a diagnostic 0.56 mg 59Fe2+ dose and the depletion of available storage iron was observed in menstruating and pregnant women, fullterm and premature infants, blood donors, patients with infections, inflammations, tumors, hepatic cirrhosis, gastric surgery, increased urogenital or gastrointestinal blood loss. The increased diagnostic 59Fe2+ absorption is a reliable and sensitive indicator of at least depleted iron stores or prelatent iron deficiency as caused by iron malnutrition or maldigestion, increased iron requirement in pregnancy, infancy, urogenital or gastrointestinal blood loss. Although the messenger system which signalyzes the depletion of iron stores to the iron absorbing enterocytes of the duodenal and jejunal mucosa is not yet known available storage iron seems to control intestinal iron absorption under normal and the great majority o pathological condition in humans. Anemia per se or high erythropoietin levels in blood do not influence iron absorption since patients with even severe erythroblastic hypoplasia, aplastic anemia and megaloblastic anemia due to vitamin B12 deficiency absorb iron according to their iron stores. An only mild hyperplasia of the erythropoietic system in the bone marrow does also not effect iron absorption which was still under the control of available storage iron in patients with hereditary spherocytosis, nonspherocytic congenital hemolytic anemia due to glucose-6-phosphate dehydrogenase deficiency, acquired hemolytic anemia and vitamin B12 deficiency induced megaloblastic anemia..

Adolescent↗
PubMed1997

Analysis of 65 Turkish patients with congenital aplastic anemia (Fanconi anemia and non-Fanconi anemia): Hacettepe experience.

During the last 14 years, 65 unrelated patients were diagnosed as having constitutional aplastic anemia (CAA). In 52 of 65 patients the diepoxybutane (DEB) test was positive. Comparison of several hematological and clinical parameters in Fanconi anemia (FA) (DEB+) and non-Fanconi anemia (non-FA)(DEB ) patients disclosed no statistically significant differences. The study indicated that in Turkey there were no peculiarities in associated congenital abnormalities in FA and non-FA. The rate of consanguinity was 78% in FA and 46% in non-FA, suggesting that also among the non-FA group recessively inherited disorders are hidden. The mean age at diagnosis in FA was 7.7+/-4.4 (1.8-12) and in non-FA 7.8+/-3.8 (2-15) years. Nine out of 52 FA and five out of 13 non-FA patients died during the follow-up period. Five of the 52 FA patients developed malignancies, three of them had acute myeloblastic leukemia (AML), one a squamous cell carcinoma of the gingiva, and another a hepatocellular carcinoma. Peliosis hepatica occurred in three of the FA and one of the non-FA patients. A total of seven patients stayed in remission without any medication. The remaining 58 patients were given 2-5 mg/kg of oxymetholone and 5 mg prednisolone treatment. Because of sustained remission, oxymetholone therapy was terminated in four of the 45 FA and two of the 13 non-FA patients. Detailed examination of the pedigrees of all of patients indicated the presence of multiple congenital anomalies. In seven of 52 FA and one of 13 non-FA patients there was increased risk for AML and/or other cancers among family members.

Abnormalities, Multiple↗
PubMed2000

[Cytogenetic Diagnosis of Fanconi's Anemia-Distinguishing Fanconi's Anemia from Aplastic Anemia]

Fanconi's anemia (FA) is an autosomal recessive disease featuring a great diversity of clinical symptoms, including congenital malformation, growth retardation and bone marrow failure. Cells obtained from FA patients show a specific hypersensitivity to crosslinking agents such as mitomycin C (MMC). In this study, MMC-induced chromosome breakage tests have been done on 27 healthy controls and 51 patients with bone marrow failure [including 48 patients with aplastic anemia (AA) and 3 patients with FA before cytogenetic analysis]. The results showed that: (1) Diagnosis of 4 FA cases was confirmed, and one of them was the correction of clinical misdiagnosis; bone marrow failure combined with congenital malformation was observed in a few of non-FA aplastic anemia patients, while 1 FA patient lacked congenital abnormality and underdiagnosed before cytogenetic analysis. The data confirmed that misdiagnosis or underdiagnosis of FA could be caused without cytogenetic study. (2) Spontaneous chromosome breakages observed in FA patients were the same as those in AA patients and healthy controls. MMC-induced chromosome breakages observed in FA patient cells were much higher than those in AA patients and healthy controls, especially, metaphases containing more than 5 breakages were easily found in FA lymphocytes treated with 50 ng MMC. (3) Mosaic was found in one of the 4 FA patients. MMC-induced chromosome breakage test at different MMC concentrations could help to dignosis of FA mosaic patient.

Journal Article↗
PubMed1983

Cytogenetic differentiation of Fanconi anemia, "idiopathic" aplastic anemia, and Fanconi anemia heterozygotes.

We have analyzed chromosome breaks in 8 patients with Fanconi anemia (FA), 42 with "idiopathic" aplastic anema (AA), 15 first-degree relatives of FA patients, and 13 controls. Their lymphocytes were treated in culture with three concentrations of mitomycin-C (MMC). A 60-fold increase in breaks was observed in FA patients as compared to AA patients, regardless of severity of clinical signs. The MMC-stress test was standardized to clearly differentiate FA from other pancytopenias in doubtful cases. Also, the effect of storage of MMC in solution was investigated. The data on SCEs of 12 subjects tested, 10 mo apart, showed an inverse relationship between length of storage of MMC and chromosome damage. The 10-month-old solution induced only one half as many SCEs as it induced at 4 months. Further, the usefulness and power of diepoxybutane (DEB) in detection of FA heterozygotes was investigated in 12 first-degree relatives of patients with Fanconi anemia and 12 healthy controls. The mean number of chromosome breaks per mitosis by DEB stress in obligate heterozygotes was 0.08 in comparison to 0.06 in controls. Four of twelve control subjects showed proportions of breaks almost identical to or higher than those of FA heterozygotes, ie, 0.12, 0.10, 0.10, and 0.11 breaks per mitosis. The responses of healthy controls to DEB could be separated into two groups: one with mean chromosome breaks of 0.11 per mitosis, and a second with mean breaks of 0.04 per mitosis. Thus, it appears that heterozygote detection by DEB stress of cultured lymphocytes is not unequivocal.

Adolescent↗
PubMed1998

Significance of p53 overexpression in bone marrow biopsies from patients with bone marrow failure: aplastic anemia, hypocellular refractory anemia, and hypercellular refractory anemia.

Among patients with bone marrow failure, differentiating acquired aplastic anemia (AA) from hypocellular refractory anemia (hypo RA) can be a difficult and challenging task. Morphological, cytochemical, immunocytochemical, and cytogenetic studies may provide tools for discriminating between both entities. In addition, differences in the pattern of proliferation and apoptosis of bone marrow cells in AA and in the myelodysplastic syndrome have been reported. Because of the correlation between p53 and apoptosis, we examined the overexpression of p53 on bone marrow biopsies in RA and AA. Our study included 14 patients with hypo RA, 14 patients with hypercellular (hyper) RA, ten patients with classic acquired AA, and 37 hematologically normal individuals. p53 was overexpressed in eight (57%) hypo RA patients and 11 (79%) hyper RA patients. All normal individuals and patients with AA showed no overexpression of p53 in their marrow. These results were statistically significant:p < 0.01 (AA vs hypo RA), p<0.001 (AA vs hyper RA), while the difference between hypo RA and hyper RA was not statistically significant. We conclude that p53 overexpression in bone marrow biopsies is a valuable tool for studying bone marrow failure and may provide additional information to help differentiate hypo RA from acquired AA.

Adolescent↗
PubMed1987

Factors influencing nonleukemic death in refractory anemia, refractory anemia with ring sideroblasts, and refractory anemia with excess of blasts.

The association between nonleukemic death and various features recorded at presentation in patients with refractory anemia (RA), RA with ring sideroblasts, and RA with excess of blasts was analyzed in 251 patients using the proportional hazards model. Features associated with higher nonleukemic death rates were: 1% or more metamyelocytes in peripheral blood (PB); lower 59Fe incorporation rate; 1% or more blasts in PB; lower hematocrit or hemoglobin; presence of giant platelets; 1 microgram/liter or higher serum vitamin B12 levels; higher periodic acid-Schiff positive erythroblasts; and 1% or higher promyelocytes in PB. Multivariate analysis was also performed using the following predictor variables: metamyelocytes in PB, micromegakaryocytes, hemoglobin, giant platelets, presence or absence of RA with excess of blasts, and mononuclear large megakaryocytes. Patients were divided arbitrarily into low (hazard ratio, less than 0.55), intermediate (hazard ratio, 0.55-1.5), and high (hazard ratio, greater than 1.5) risk groups. The cumulative nonleukemic death rates in the high and intermediate risk groups reached a median at 602 and 1984 days from presentation, respectively, while the rate reached a plateau level of 49.4% after 2644 days in the low risk group. The risk factors for leukemic transformation and nonleukemic death were found to be different and to need separate consideration.

Anemia, Refractory↗
PubMed2005

Angiotensin-converting enzyme inhibitor as a risk factor for the development of anemia, and the impact of incident anemia on mortality in patients with left ventricular dysfunction.

OBJECTIVES: We aimed to investigate the impact of angiotensin-converting enzyme inhibitors (ACEIs) on hematocrit values in those with heart failure, and the relationship between incident anemia and mortality. BACKGROUND: Prevalent anemia is an independent risk factor for morbidity and mortality in those with heart failure. Studies in patients with polycythemia have demonstrated that ACEIs are effective in lowering hematocrit values. METHODS: We used the Studies Of Left Ventricular Dysfunction (SOLVD) database to compare the odds of developing new anemia at one year in patients who were not anemic at entry and who were randomized to enalapril or placebo. Cox proportional hazards models were utilized to determine the impact of incident and prevalent anemia on subsequent mortality. RESULTS: Enalapril increased the odds of incident anemia (hematocrit < or =39% in men or < or =36% in women) at one year by 48% (odds ratio [OR] 1.48, 95% confidence interval [CI] 1.20 to 1.82) in unadjusted and 56% (OR 1.56, 95% CI 1.26 to 1.93) in adjusted models. With multivariate analysis, prevalent anemia at randomization was associated with a 44% (hazard ratio [HR] 1.44, 95% CI 1.31 to 1.66) increase in all-cause mortality, whereas incident anemia after randomization was associated with a 108% increase (HR 2.08, 95% CI 1.82 to 2.38). After adjusting for incident and prevalent anemia, use of enalapril was associated with a survival benefit. CONCLUSIONS: Enalapril was associated with increased odds of developing anemia at one year. Those with periods of time with incident anemia had the poorest survival, followed by those with prevalent anemia, then those without anemia. Enalapril was protective of overall mortality after adjusting for incident anemia and in those with prevalent anemia.

Aged↗
PubMed1996

Severe aplastic anemia including Fanconi's anemia and dyskeratosis congenita.

The primary pathophysiology in the majority of cases of acquired aplastic anemia remains unknown ("idiopathic"). In contrast, there have been major advances in Fanconi's anemia, the commonest of the familial aplastic anemias. The key has been complementation analysis that provides evidence for at least five complementation groups (FA-A, FA-B, FA-C, FA-D, and FA-E) and therefore five genes for Fanconi's anemia; only the FAC gene has been cloned to date. The FAC gene has an important role in normal hematopoiesis, and expression of the mutant FAC allele is associated with increased apoptosis. Increased apoptosis is also seen in patients with idiopathic aplastic anemia. Furthermore, patients with Fanconi's anemia or dyskeratosis congenita, another familial form of aplastic anemia, have a high incidence of hematopoietic clonal disorders, as do patients with idiopathic aplastic anemia. Therefore, the familial aplastic anemias are good in vivo models for studying aplastic anemia in general; some of the idiopathic aplastic anemias could prove to be due to mutations in genes characterized originally in familial aplastic anemias. Thus identification of these genes may provide insights into the pathophysiology of idiopathic aplastic anemia and suggest new treatment options, because treatment remains unsatisfactory for patients who lack HLA-identical siblings who can serve as bone marrow donors. The recent mapping of the FA-A (16q24.3), FA-D (3p22-26), and dyskeratosis congenita (Xq28) genes suggests this goal is achievable.

Dyskeratosis Congenita↗
PubMed2004

Prevalence of anemia in persons 65 years and older in the United States: evidence for a high rate of unexplained anemia.

Clinicians frequently identify anemia in their older patients, but national data on the prevalence and causes of anemia in this population in the United States have been unavailable. Data presented here are from the noninstitutionalized US population assessed in the third National Health and Nutrition Examination Survey (1988-1994). Anemia was defined by World Health Organization criteria; causes of anemia included iron, folate, and B(12) deficiencies, renal insufficiency, anemia of chronic inflammation (ACI), formerly termed anemia of chronic disease, and unexplained anemia (UA). ACI by definition required normal iron stores with low circulating iron (less than 60 microg/dL). After age 50 years, anemia prevalence rates rose rapidly, to a rate greater than 20% at age 85 and older. Overall, 11.0% of men and 10.2% of women 65 years and older were anemic. Of older persons with anemia, evidence of nutrient deficiency was present in one third, ACI or chronic renal disease or both was present in one third, and UA was present in one third. Most occurrences of anemia were mild; 2.8% of women and 1.6% of men had hemoglobin levels lower than 110 g/L (11 g/dL). Therefore, anemia is common, albeit not severe, in the older population, and a substantial proportion of anemia is of indeterminate cause. The impact of anemia on quality of life, recovery from illness, and functional abilities must be further investigated in older persons.

Age Factors↗