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PubMed1999

Clinical pallor is useful to detect severe anemia in populations where anemia is prevalent and severe.

Clinical pallor is recommended as a simple way to detect severe anemia, but more data are needed on its accuracy and usefulness when assessed by nonphysicians in diverse settings. We measured hemoglobin and trained non-physician health workers to assess clinical pallor of the conjunctiva, palm and nail beds in five population samples in Nepal and Zanzibar, where severe anemia is common. In total, 5,760 individuals were examined, 3,072 of whom were anemic and 192 of whom had severe anemia (hemoglobin <70 g/L). The prevalence of pallor did not correspond to the prevalence of anemia or severe anemia in the groups studied. However, in all studies, pallor at each anatomical site was associated with a significantly lower hemoglobin concentration. The relative performance of different anatomical sites was not consistent among studies, and we recommend that multiple sites be assessed. Pallor at any of the three sites detected severe anemia with >84% specificity. However, the sensitivity varied from 81% in Nepalese postpartum women to 29% in Zanzibari preschoolers in 1996. Overall estimates for sensitivity and specificity were 50 and 92%, respectively. Although imperfect, use of pallor to screen and treat severe anemia by primary care providers is feasible and worthwhile where severe anemia is common. Usually, the majority of persons with severe anemia will be detected at practically no cost. Many people who are not severely anemic will also receive treatment, but the costs of this error are low compared to the benefits.

Adolescent↗
PubMedDate not supplied

Toxic etiology of aplastic anemia. The Cooperative Study Group for Aplastic and Refractory Anemias.

In this retrospective investigation into the possible causes of aplastic anemia, the charts of 360 patients with primary or secondary aplastic anemia were analyzed for clinical history, proof of diagnosis, possible etiology, and prognostic criteria. During the period of the study, the proportion of cases of aplastic anemia due to chloramphenicol, benzene, butazone, and sulfonamides decreased, whereas the proportion due to gold salts, penicillamine, amidopyrine, and trimethoprim-sulfamethoxazole increased. No case of secondary aplastic anemia in recent years could be attributed with certainty to thiamphenicol; one possible case of thiamphenicol-induced aplastic anemia could have been due to exposure to other chemicals known to cause aplastic anemia. The disease course and mortality rate for secondary aplastic anemia are similar to those for primary aplastic anemia. The results of this study show the need for more careful investigation into the causes of all cases of aplastic anemia attributed to toxic agents or environmental factors.

Actuarial Analysis↗
PubMed2004

The role of anemia in congestive heart failure and chronic kidney insufficiency: the cardio renal anemia syndrome.

Anemia is a major problem in patients with chronic kidney insufficiency. The development of recombinant human erythropoietin has enabled physicians to correct this anemia. Although anemia has not been considered to be a common or important contributor to congestive heart failure, anemia of any cause can lead to cardiac damage and eventually congestive heart failure. Our joint renal-cardiac heart failure team found that anemia was indeed very common in congestive heart failure and was associated with severe, medication-resistant cardiac failure. Correction of the anemia with erythropoietin and intravenous iron led to a marked improvement in patients' functional status and their cardiac function, and to a marked fall in the need for hospitalization and for high-dose diuretics; renal function usually improved or at least stabilized. Subsequent investigations by others have confirmed many of our observations. We call this interrelationship between congestive heart failure, chronic kidney insufficiency, and anemia the Cardio-Renal Anemia syndrome. Treatment of the anemia in congestive heart failure may prove vital in preventing progression of both the heart failure and the associated renal disease.

Anemia↗
PubMed1988

Pernicious anemia. The expected findings of very low serum cobalamin levels, anemia, and macrocytosis are often lacking.

When patients are examined for possible cobalamin deficiency, great stress is often placed on the presence or absence of macrocytosis and anemia and on how low the serum cobalamin level is. The present study, however, shows that only 45 (64%) of 70 consecutively diagnosed patients with pernicious anemia, the most common cause of cobalamin deficiency, had very low cobalamin levels (less than 74 pmol/L [or less than 100 ng/L]). Anemia was absent in 13 (19%) of the patients, and macrocytosis was absent in 23 (33%) of the patients; such absence was particularly common when cobalamin levels were only slightly or moderately low (74 to 184 pmol/L). Coexisting iron deficiency was responsible for the absence of macrocytosis in nine patients. Of the ten patients with neither anemia nor macrocytosis, neurological disturbance was prominent in six, including four whose only noticeable abnormality was cerebral. These observations indicate that macrocytosis and anemia, two classic features of pernicious anemia, may be overstressed in our diagnostic approach. All subnormal serum cobalamin results are best viewed as pathological until proved otherwise. Emphasis on only very low cobalamin levels risks delaying the diagnosis of pernicious anemia in a substantial proportion of cases, particularly in those without anemia or macrocytosis.

Adult↗
PubMed2006

Coexistence of megaloblastic anemia and iron deficiency anemia in a young woman with chronic lymphocytic thyroiditis.

Pernicious anemia is a megaloblastic anemia caused by vitamin B12 deficiency, and is the end-stage of autoimmune gastritis that typically affects persons older than 60 years. It is the most common cause of vitamin B12 deficiency. Pernicious anemia can also be diagnosed concurrently with other autoimmune diseases. We report the occurrence of megaloblastic anemia in a 22-year-old woman with chronic autoimmune thyroiditis for 10.5 years. Recently, she presented with microcytic anemia, and iron deficiency anemia was diagnosed initially. After administration of ferrous sulfate, macrocytic anemia was revealed and vitamin B12 deficiency was detected. Pernicious anemia was highly suspected because of the endoscopic finding of atrophic gastritis, and high titer of antigastric parietal cell antibody, as well as elevated serum gastrin level. After intramuscular injections of hydroxycobalamine 100 microg daily for 10 days, and monthly later, her blood counts returned to normal.

Adult↗
PubMed1983

Prevalences of anemia and iron deficiency anemia in Black and White women in the United States estimated by two methods.

Prevalences of anemia were estimated by two methods for 742 Black and 3,074 White nonpregnant women of childbearing age drawn from a large probability sample of the United States civilian noninstitutionalized population (NHANES I). One method defines the prevalence of anemia as the proportion of women with hemoglobin levels below a 12 g/dl "cut-off". The second method defines the prevalence of anemia as the proportion of women whose hemoglobin values are shifted downwards relative to a distribution of hemoglobin values of non-anemic women. Estimates produced by both methods suggest a higher prevalence of anemia in Black than in White women. Estimates produced by the "cut-off" method, however, are higher than those from the "distribution" method for both racial groups, probably because the "cut-off" method results in large overestimates in populations where anemia prevalence is low. The "distribution" method is further used to estimate the contribution of iron deficiency to anemia. Essentially all anemia in White women and a high proportion of anemia in Black women is associated with iron deficiency in the US civilian noninstitutionalized population. Iron supplementation trials are needed in order to define the magnitude of the problem accurately and plan appropriate public health programs.

Adolescent↗
PubMed2006

Anemia, chronic renal disease and congestive heart failure--the cardio renal anemia syndrome: the need for cooperation between cardiologists and nephrologists.

Many patients with congestive heart failure (CHF) fail to respond to maximal CHF therapy and progress to end stage CHF with many hospitalizations, poor quality of life (QoL), progressive chronic kidney disease (CKD) which can lead to end stage kidney disease (ESKD), or die of cardiovascular complications within a short time. One factor that has generally been ignored in many of these people is the fact that they are often anemic. The anemia in CHF is due mainly to the frequently-associated CKD but also to the inhibitory effects of cytokines on erythropoietin production and on bone marrow activity, as well as to their interference with iron absorption from the gut and their inhibiting effect on the release of iron from iron stores. Anemia itself may further worsen cardiac and renal function and make the patients resistant to standard CHF therapy. Indeed anemia in CHF has been associated with increased severity of CHF, increased hospitalization, worse cardiac function and functional class, the need for higher doses of diuretics, progressive worsening of renal function and reduced QoL. In both controlled and uncontrolled studies of CHF, the correction of the anemia with erythropoietin (EPO) and oral or intravenous (IV) iron has been associated with improvement in many cardiac and renal parameters and an increased QoL. EPO itself may also play a direct role in improving the heart unrelated to the improvement of the anemia--by reducing apoptosis of cardiac and endothelial cells, increasing the number of endothelial progenitor cells, and improving endothelial cell function and neovascularization of the heart. Anemia may also play a role in the worsening of acute myocardial infarction and chronic coronary heart disease (CHD) and in the cardiovascular complications of renal transplantation. Anemia, CHF and CKD interact as a vicious circle so as to cause or worsen each other- the so-called cardio renal anemia syndrome. Only adequate treatment of all three conditions can prevent the CHF and CKD from progressing.

Anemia↗
PubMed2005

Management of cancer-related anemia in patients with breast or gynecologic cancer: new insights based on results from the European Cancer Anemia Survey.

The incidence, prevalence, and treatment of anemia (hemoglobin [Hb] <12 g/dl) in women with breast cancer and gynecologic cancer were evaluated using data from the European Cancer Anemia Survey (ECAS). Adult patients with newly diagnosed treated or untreated disease, persistent/recurrent disease, and disease in remission were enrolled and followed for up to six chemotherapy cycles or six evaluation points within a 6-month period. At enrollment, 30.4% of breast cancer patients and 49.1% of gynecologic cancer patients were anemic. A significant correlation was shown between low Hb level and poor performance status (World Health Organization criteria) at enrollment for both breast cancer and gynecologic cancer patients. In all, 62.4% of breast cancer patients and 81.4% of gynecologic cancer patients were anemic at some time during the survey. The incidence of anemia, determined in a carefully defined population, was 59.8% for breast cancer patients and 74.8% for gynecologic cancer patients. Despite the high prevalence and incidence of anemia, only 26.3% and 42.7% of patients in the respective groups received anemia treatment. In breast cancer patients, the mean Hb trigger was 10 g/dl for epoetin treatment and 8.6 g/dl for transfusion; corresponding values for gynecologic cancer patients were 10.1 g/dl and 9.1 g/dl. Logistic regression analyses in the overall ECAS population identified five factors as significant and suitable predictors of anemia: lower initial Hb, having lung or gynecologic cancer versus gastrointestinal/colorectal cancer, any other cancer versus gastrointestinal/colorectal cancer, treatment with platinum chemotherapy, and being female. The ECAS data highlight the need for greater awareness of the adverse impact of anemia on cancer patients and for optimal anemia management to ensure maximal patient quality of life.

Adult↗
PubMed2003

The cardio renal anemia syndrome: correcting anemia in patients with resistant congestive heart failure can improve both cardiac and renal function and reduce hospitalizations.

Anemia (Hemoglobin of < 12 to 13 g/dl) is frequently encountered in patients with congestive heart failure (CHF). This anemia may be partly due to hemodilution, partly to the associated reduction in renal function, and partly to the use of ACE inhibitors and aspirin. However, there is evidence that CHF alone--through excessive cytokine production may also reduce the bone marrow and cause anemia. In several recent studies anemia has been found to be associated with a more severe degree of CHF, a higher rate of death, renal failure, hospitalization and evidence of malnutrition. In both uncontrolled and controlled studies correction of anemia with erythropoietin with or without the addition of i.v. iron has been attempted. The correction of anemia has been associated with a marked improvement in New York Heart Association (NYHA) functional cardiac class and Left Ventricular Ejection Fraction, a marked reduction in the need for hospitalization and high dose oral and i.v. diuretics, and an improvement in exercise capacity, peak exercise oxygen utilization and quality of life. The serum creatinine, which had been increasing steadily before treatment, stabilized with the correction of anemia. All this suggests that control of anemia in CHF could become a valuable addition to the therapeutic armamentarium of CHF and might also play a major role in the prevention of progressive renal failure.

Anemia↗
PubMed1983

The changing pattern of megaloblastic anemia: megaloblastic anemia in Israel.

The causes of megaloblastic anemia were studied in a survey of patients admitted to six Israeli hospitals over a period of 15 yr. Among the 203 patients identified, 69% had pernicious anemia, 12% had gastrointestinal disease, 9% had primary nutritional deficiency of whom only 1% were associated with pregnancy, and 7% had selective vitamin B12 malabsorption with albuminuria. Comparison with previously published surveys showed, that in contrast with earlier studies where primary nutritional deficiency was the cause of megaloblastic anemia in about 70% of cases and pernicious anemia in only 20%, in more recent studies the proportion of cases with primary nutritional anemia in general and those associated with pregnancy in particular was much lower. This is most probably the result of improved standards of living and a national program of preventive folate supplementation at maternity clinics. A potential hazard of such preventive programs is the aggravation of neurological complications in patients with undiagnosed vitamin B12 deficiency. Early recognition of pernicious anemia and other forms of selective B12 malabsorption is a new challenge created by the changing pattern of megaloblastic anemias.

Adolescent↗
PubMed1979

Macrocytosis, mild anemia, and delay in the diagnosis of pernicious anemia.

Various factors led to delays of several months to several years in the diagnosis of pernicious anemia in 11 patients, occasionally with serious consequences. These cases illustrate that earlier diagnosis is possible with closer attention to abnormal results of common tests. Macrocytosis, detected by high mean corpuscular volume, often preceded anemia but was not investigated, especially when anemia was only slight. Several cases demonstrated that vitamin B12 deficiency may initially produce only a mild macrocytic anemia, which is maintained for a long period before a rapid worsening supervenes; the reason for the latter acceleration of anemia is unknown. Most serious was the evidence that mild anemias are often ignored. Stricter attention to the established limits of normal hemoglobin values is required. These aspects of physician performance have implication for the recognition of all anemias.

Aged↗
PubMed2001

Aplastic anemia in systemic lupus erythematosus: a distinct presentation of acquired aplastic anemia?

Aplastic anemia is a rare but serious complication of systemic lupus erythematosus (SLE) with an often dramatic and unanticipated onset. The peripheral destruction of formed blood elements, which frequently accompanies the syndrome, may obscure or delay the diagnosis of bone marrow suppression, and the number of published cases may be an underestimate of the actual incidence of the disease. Furthermore, the disease course may differ significantly from other forms of acquired aplastic anemia and seems to carry a more favorable prognosis once effectively diagnosed and treated. In addition, aplastic anemia may precede other manifestations of SLE. Therefore, the possibility of bone marrow aplasia should be excluded in all SLE patients with severe pancytopenia, and conversely, the diagnosis of SLE should be explored in cases of aplastic anemia. Two patients with aplastic anemia in SLE, one with aplastic anemia preceding the onset of SLE, are described along with 15 cases reviewed from the English language literature. The presentation, prognosis, treatment, and pathogenesis of aplastic anemia complicating SLE are discussed. Recognition that cytopenias, especially pancytopenia, may occur on the basis of inhibited myelopoesis rather than peripheral destruction as either a harbinger of SLE or as a manifestation of disease flare is important. This knowledge will prompt the astute clinician to obtain screening antinuclear antibodies in the setting of otherwise unexplained bone marrow acellularity or, given the prognosis of SLE associated aplastic anemia, give early consideration to more aggressive immunosuppression.

Journal Article↗
PubMedDate not supplied

Treatment of anemia in patients with HIV Infection--Part 2: guidelines for management of anemia.

The key treatment goal for managing anemia in patients infected with HIV is to maintain an improved or normal hemoglobin level. Whenever possible, the identification and treatment of the underlying cause of anemia is the primary therapeutic strategy. After excluding other etiologies, the Nursing Guidelines Committee for Anemia in Patients With HIV Infection has recommended that patients with mild asymptomatic anemia (hemoglobin level = 1 g/dl below the lower limit of the normal range) receive nutritional support and more frequent screening. Recombinant human erythropoietin (epoetin alfa) therapy is an appropriate treatment option for patients with symptomatic mild anemia or moderate anemia (hemoglobin level = 2 g/dl below the lower limit of the normal range). An immediate blood transfusion may be required under specific instances for patients with severe anemia (hemoglobin level less than or equal to 8 g/dl).

Adult↗
PubMed2002

Blackfan-Diamond anemia and dyserythropoietic anemia presenting with increased nuchal translucency at 12 weeks of gestation.

Blackfan-Diamond anemia is a congenital hypoplastic anemia with a birth prevalence of about 1 in 200,000, usually presenting in the first few months of life and commonly associated with cardiac, urogenital and digital anomalies. Congenital dyserythropoietic anemias are a group of rare congenital anemias characterized by ineffective erythropoiesis. We report on two cases of congenital fetal anemia, one with Blackfan-Diamond anemia and one with dyserythropoietic anemia, presenting with increased nuchal translucency at 12 weeks of gestation.

Adult↗
PubMed2002

Inappropriate expression of hepcidin is associated with iron refractory anemia: implications for the anemia of chronic disease.

The anemia of chronic disease is a prevalent, poorly understood condition that afflicts patients with a wide variety of diseases, including infections, malignancies, and rheumatologic disorders. It is characterized by a blunted erythropoietin response by erythroid precursors, decreased red blood cell survival, and a defect in iron absorption and macrophage iron retention, which interrupts iron delivery to erythroid precursor cells. We noted that patients with large hepatic adenomas had severe iron refractory anemia similar to that observed in anemia of chronic disease. This anemia resolved spontaneously after adenoma resection or liver transplantation. We investigated the role of the adenomas in the pathogenesis of the anemia and found that they produce inappropriately high levels of hepcidin mRNA. Hepcidin is a peptide hormone that has been implicated in controlling the release of iron from cells. We conclude that hepcidin plays a major, causative role in the anemia observed in our subgroup of patients with hepatic adenomas, and we speculate that it is important in the pathogenesis of the anemia of chronic disease in general.

Adenoma, Liver Cell↗