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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the first phase of treatment of acute lymphatic leukemia in children (ALL) with aggresive cytostatic protocols, the doctor is, in some patients, forced to modify the antitumor therapy over a certain period of time because of bone marrow depression. The authors attempted to pull patients with ALL through this critical phase of the disease - by administering "profilactically" Lithium Carbonate (Li2CO3) ( in order to stimulate granulopoiesis) or, if anaemia, leukopenia and thrombocytopenia had already occurred, by administering concentrates of erythrocytes, leukocytes and platelets - without discontinuing the administration of cytostatics. The results of these attempts are reported.
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PMID:[Treatment of bone marrow aplasia in phase I of acute lymphatic leukemia treatment in children]. 12 57

1. Patterns of carbon dioxide excretion were investigated in rainbow trout (Salmo gairdneri). 2. The loss of erythrocytic carbonic anhydrase caused by severe anaemia does not affect acid/base regulation or the ability of fish to excrete CO2. 3. Bicarbonate excretion across the saline-perfused gills of trout is significant even though residence time for the saline in the gills is only 1--3 s. CO2 excretion across these saline-perfused gills is blocked by the carbonic anhydrase inhibitor, diamox. 4. The excretion of CO2 in fish is via the movement of plasma bicarbonate into the gill epithelium where branchial carbonic anhydrase catalyses the production of CO2. Fish can adjust pH by regulating bicarbonate movement across the gills. 5. The erythrocytic carbonic anhydrase is not necessary for CO2 excretion in the gills but is involved in facilitating Bohr and Root shifts to augment O2 delivery in the tissues.
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PMID:The pattern of carbon dioxide excretion in the rainbow trout Salmo gairdneri. 41 5

It has been established that in conditions of intraoperative blood and plasma loss base deficiency is determined not only by hypocarbonatemia, but also by hypoproteinemia, hypophosphatemia and HCO3 metabolism disturbances caused by anemia. Correction of metabolic acidosis in such patients should include infusions of NaHCO3, protein preparations, blood, phosphates. Mellemgaard and Astrup's technique presupposes correction of the deficiency of all buffer bases only with NaHCO3, which dramatically increases its dosage. Thus, it is evident that the technique should be revised. The comparison of the results of metabolic acidosis correction using a conventional and adapted techniques (hydrocarbonate dose in mmol or ml of a 8.4% solution is 24-SB.body weight.0.2%) in statistically homogeneous groups has shown that differentiated "polybuffer" correction of metabolic acidosis with adapted NaHCO3 dose 1.7 times more frequently normalized acid-base balance parameters, reducing the risk of the onset of post-correction metabolic alkalosis to minimum.
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PMID:[Characteristics of the dosage of sodium hydrocarbonate for correction of metabolic acidosis in surgical patients]. 133 43

Control of phosphorus accumulation in chronic renal insufficiency is crucial to the prevention of secondary hyperparathyroidism and metastatic calcification. In early renal failure, calcitriol levels are normal and parathyroid hormone levels are elevated. The phosphorus levels are maintained in the normal range by the phosphaturia induced by hyperparathyroidism. In this situation, dietary phosphorus restriction increases calcitriol levels and suppresses parathyroid hormone secretion. As renal failure progresses into late stages, hyperphosphatemia is evident along with low levels of calcitriol and worsening hyperparathyroidism. Phosphorus restriction will not affect calcitriol concentrations, yet parathyroid levels may decline. During long-term dialysis, urinary excretion of phosphorus is usually minimal. Therefore, phosphorus balance is determined primarily by the net amount absorbed by the bowel and the quantity removed during dialytic therapy. Given an adequate diet, no form of conventional dialysis is able to fully compensate for the gastrointestinal absorption of phosphorus. Hence, compounds that bind phosphorus in the bowel are often necessary. With the realization that the use of phosphorus binders containing aluminum leads to aluminum accumulation and its sequelae: osteomalacia, dementia, myopathy, and anemia, other phosphorus binders have been evaluated. Calcium carbonate has been investigated the most thoroughly and is in wide use. It is inexpensive and contains a high percent of elemental calcium. However, it is only modestly potent in the binding of phosphorus, and large doses are often necessary to attain satisfactory control of phosphorus. This may lead to hypercalcemia. One approach to this problem is to decrease the concentration of calcium in the dialysate. Alternatively, a more effective phosphorus binder may be used. Calcium acetate has been shown in acute studies to have twice the binding capacity of phosphorus per calcium absorbed than calcium carbonate. Whether use of this compound decreases the incidence of hypercalcemia is unproven. Calcium citrate increases the gastrointestinal absorption of aluminum and offers no advantage over calcium carbonate. Other compounds, such as calcium ketoacids and calcium alginate, have not been extensively studied and are not generally available. The use of phosphorus binders containing magnesium in conjunction with a dialysate low in magnesium may be efficacious. Large doses of magnesium will cause diarrhea and thus limit its use as a single agent. Reasons for failure to control hyperphosphatemia include poor compliance, improper prescription of binders, poor dissolution rates seen with some generic brands of calcium carbonate, and the presence of severe hyperparathyroidism. Optimal control of serum phosphorus in dialysis patients should always be viewed in the context of adequate nutrition and protein intake.
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PMID:Hyperphosphatemia: its consequences and treatment in patients with chronic renal disease. 156 18

In the following study, normal blood values were performed on 58 Friesian calves (30 males and 28 females) under preexisting Moroccan management conditions. The following parameters were evaluated: pH-value, p.CO2, actual HCO3, BE, BB, RBC, WBC, PCV, Hb, MCV, MCHC, Glucose, lactate, urea, creatinine, total protein, total bilirubin, enzyme activities of AST and GGT and electrolyte-values (Na, K, Cl). The values of all parameters varied significantly with age with the exception of MCV, MCHC and K. The female calves presented higher values of act. HCO3, BE, BB, Hb, PCV and MCV than the male calves (p less than 0.01). The calves were born in mixed acidosis stage which was largely restored 24 hours later. At the weaning, the calves showed a slight metabolic acidosis with a partial respiratory compensation. The metabolic acidosis was accompanied with an increase of lactate level in blood plasma. During the first month of life, the development of an anaemia (PCV decreased) was observed. The mean values of glucose and total protein increased after colostrum intake, whereas the electrolyte values in blood plasma decreased. In general, the mean values of lactate, creatinine, urea, total bilirubin and the activities of AST and GGT decreased with age, while glucose and total protein remained nearly unchanged. The age and the sex should be taken in consideration judging the above mentioned parameters in a new born calf from birth to weaning (here: two months).
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PMID:[Hemocytological and hemobiochemical studies in black pied, clinically healthy breeding calves in Morocco]. 204 72

To evaluate objectively the effects of recombinant human erythropoietin (rHuEPO) administration on nutritional status in stable dialyzed patients, we used urea kinetic modeling (UKM) analysis and dietary protein intake evaluation by dietary assessment. Fifteen patients (9 females, 6 males; mean age 46.9 +/- 15.6 years) dialyzed for 9.4 +/- 6.3 years were studied longitudinally for 18 months, consisting of a control period (6 months) and an rHuEPO treatment period (12 months). Treatment modalities based on 3 weekly sessions were hemodialysis in 12 patients (6 cuprophane, 3 cellulose acetate and 3 highly permeable membranes), hemodiafiltration in 2 patients and postdilutional hemofiltration in 1 patient. Bicarbonate buffered dialysate was used in 9 patients and acetate in 6 patients. Urea kinetic modeling using a single-pool model was performed monthly over 1-3 cycles. rHuEPO was administered intravenously at the end of dialysis according to a two-phase protocol: (1) correction of anemia by stepwise increment of rHuEPO dose, and (2) maintenance dose to keep hemoglobin at 10-11 g/dl. rHuEPO administration corrected anemia in all patients, improving their general clinical condition. Dialysis efficacy was significantly reduced (15%) after the 3rd month of rHuEPO therapy. Clearnces were restored by increasing dialysis time and/or improving dialyzer performances, and adequacy of dialysis was maintained in all patients. During the 12 months of rHuEPO therapy, the protein catabolic rate remained stable at 1.2 g/kg/24 h in spite of an increase in appetite. At the same time, dry body weight increased significantly after 9 months, and the ratio dietary protein intake/protein catabolic rate a gross estimation of nitrogen balance, increased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Erythropoietin-induced changes in protein nutrition: quantitative assessment by urea kinetic modeling analysis. 209 90

Besides anemia, coagulopathies, and hypertension, electrolyte disturbances are among the most significant features of end-stage renal disease. Although plasma potassium represents only 1.5%-2% of the whole-body content, hyperkalemia has definite effects on cardiac pacemaker cells and myocardial conduction. The typical ECG findings and therapeutic management will be discussed. Case report. A 64-year-old man with chronic renal failure due to phenacetin abuse was scheduled for transplantation of a 41-h-old cadaver kidney. The preoperative laboratory check revealed BUN 51 mg% and creatinine 11.5 mg%; serum sodium and potassium were within normal limits (sodium 141 mmol/l, potassium 5.11 mmol/l). A central-venous blood gas sample after induction of anesthesia and intubation revealed pH of 7.32, pCO2 43 mmHg, HCO3 22.1 mmol/l, base excess - 3.4 mmol/l, and venous oxygen saturation 84%. Plasma potassium (5.22 mmol/l) was within the normal range. As an endarterectomy of the left common and external iliac arteries had to be performed, the arterial cross-clamping time was longer than normal (73 min). After declamping an ECG pattern (modified V5 lead) typical of hyperkalemia (atrial arrest, idioventricular rhythm, right bundle-branch block-like QRS, AV dissociation, AV block I) was observed. Plasma potassium had increased to 6.77 mmol/l (+1.55 mmol/l). Immediate treatment was started with a bolus injection of 20 ml 10% calcium gluconate, rapid infusion of 200 ml 8.4% sodium bicarbonate, and glucose-insulin infusion (glucose 33 1/3%, 15 U regular insulin). After 25 min sinus rhythm was restored and potassium levels decreased to normal. Despite the observed ECG changes the cardiovascular status remained stable.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Atrial arrest and intraventricular conduction disorders due to accidental hyperkalemia during kidney transplantation]. 267 72

Blood, pH and bicarbonate were examined in 40 normal subjects and in 53 patients with anemia. Included were 28 patients with thalassemia, 18 with aplastic anemia and seven with iron deficiency anemia. Mean increases in pH of 0-0.04 and decreases in HCO3 of 2.3-3.5 mEq/L were observed. Changes were not significantly affected by the degree of erythropoiesis or by the severity of the anemia and were essentially the same in the three groups of patients studied. Typical changes of a mild, uncompensated alkalosis were also produced on four occasions in one transfused thalassemic patient.
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PMID:A mild uncompensated alkalosis in anemia. 312 64

Megakaryocytic hypoplasia or aplasia causing thrombocytopenia was diagnosed in a 3-year-old Miniature Poodle with scleral hemorrhage, melena, ecchymoses, and blood-loss anemia. Immunosuppressive, cytotoxic, and lithium carbonate therapy resulted in successful correction of the dog's disease. It is important to recognize megakaryocytic hypoplasia or aplasia as the cause of thrombocytopenia, since the response to therapy will be slower when there is stem cell injury.
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PMID:Suspected immune-mediated megakaryocytic hypoplasia or aplasia in a dog. 401 93

Lithium is an agent capable of influencing many aspects of blood cell production, in particular, the formation of granulocytes. Because of this property, lithium has been demonstrated to be an effective agent whenever granulocyte production is either faulty or inadequate. The anti-viral drug zidovudine (AZT) has used been extensively in the treatment of acquired immune deficiency syndrome (AIDS). However, its effectiveness is limited because of the myelosuppression and bone marrow toxicity associated with its use. We have previously demonstrated that lithium, when combined with AZT in vitro with normal bone marrow cells or when administered in vivo to mice receiving dose-escalation AZT, reduced the myelosuppression and marrow toxicity of AZT significantly. We report here further studies designed to evaluate the extent of lithium's capacity to modulate AZT toxicity by investigating the ability of lithium to influence blood cell production when administered to normal mice during an initial exposure to AZT. C57BL6 were administered dose-escalation AZT (1.0 mg/ml and 2.5 mg/ml) for a period of 4-weeks in the presence or absence of lithium carbonate (1 mM). This was followed by an additional 4-week period during which mice received only AZT. Animals were analyzed on a weekly basis for their peripheral blood indices. Animals receiving dose-escalation AZT demonstrated anemia, thrombocytopenia, and neutropenia which was dose-related. During the period when animals received combination lithium/AZT, there was significantly less anemia, thrombocytopenia, and neutropenia as compared to the AZT controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lithium and anti-viral drug toxicity: II. Further studies on the ability of lithium to modulate the hematopoietic toxicity associated with the anti-viral drug zidovudine (AZT). 758 37


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