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Anemia frequently is revealed in the laboratory Work-up of outpatients. This finding reflects an absolute or relative decrease in red blood cell (RBC) mass, which may be a manifestation of [...]

The laboratory discovery of an anemia is common among outpatients. This finding is a manifestation of RBC loss through bleeding, RBC destruction through hemolysis, or inadequate RBC production secondary to [...]

Iron deficiency anemia is the most common form of the blood disease because of its many causes, but thalassemia and anemia of chronic disease are also prevalent. Factors to consider when screening patients for anemia are presented.

Angioimmunoblastic lymphadenopathy with dysproteinemia (AILD) is an uncommon disorder of the lymph glands that is characterized by an increase in the blood levels of proteins called gammaglobulins. Symptoms of AILD include fever, anemia (decreased red blood cell production), abnormal white blood cell production, and the presence of autoantibodies (antibodies that attack the body's own tissues). AILD can affect the liver, spleen, bone marrow and skin. A diagnosis of AILD is usually made by examining samples of lymph node tissue (biopsy). Early in the disease, immune cells (B cells) in the lymph tissue increase in number and make large quantities of antibodies. In some cases this results in the development of malignant (cancerous) lymph node tumors. Most treatments are not effective in treating AILD, and roughly 70 percent of those diagnosed as having AILD die within two years. Most of the patients die as a result of infections. In most cases of AILD the joints are not affected. This article describes the case report of a 61-year-old male patient who developed arthritis several months prior to the onset of AILD. Radiographs (x-rays) of the joints showed signs of swelling, but no cartilage damage or loss. Joint fluid and blood tests for the presence of rheumatoid arthritis were negative. Joint fluid from the wrist contained elevated levels of white blood cells characteristic of AILD. The patient was treated successfully with methylprednisolone and cyclophosphamide. This finding indicates that AILD may affect the joints, and that joint biopsies provide a better method for diagnosing joint involvement than joint fluid sampling. (Consumer Summary produced by Reliance Medical Information, Inc.)

The iron transport function of transferrin from normal subjects and patients with idiopathic hemachromatosis has been studied using the radioisotopes Fe59 and Fe55. It was concluded that transferrin from hemochromatotic patients functions in a normal manner in vivo.

1. By means of phlebotomy to recover and measure accumulated iron and by determining the rate of replenishment of hemoglobin after induction of iron-deficiency anemia, it is possible to compute the rate at which iron is accumulated by absorption from the diet. Normal humans are presumed to be in iron balance and absorb iron only to replace what is lost; under these conditions they accumulate none. During recovery from induced iron deficiency a normal human accumulated iron at the rate of 5 to 6 mg. per day. 2. Patients with hemochromatosis were found to accumulate iron at the rate of 1.5 to 5 mg. per day. With iron deficiency the rate increased to 8 to 10 mg. per day. Because of uncertainty concerning the manner of onset of iron accumulation in hemochromatosis, whether gradual or abrupt, it is not possible by extrapolation to establish the time of onset in these patients. However, at the rates of accumulation established in this study there was an insufficient excess of iron to permit a conclusion that such rates had existed throughout the patient’s life. If the disease began early, the initial or interim rates were less than those found. If the disease began and continued at the rate found, its onset was 10 to 17 years prior to this study. 3. In a patient with hypochromic iron-loading anemia the rate of accumulation was about 2.5 mg. per day. It was not appreciably increased by iron deficiency except when the deficiency was severe and the plasma iron was quite low. While this patient was iron deficient the plasma iron became abnormally high even before the hemoglobin mass was completely reconstituted. 4. A patient with transfusion siderosis who had recovered from his anemia was phlebotomized to remove the accumulated iron. When iron deficiency finally developed the total amount of iron which had been recovered was less than half of the 32.5 Gm. given in the transfusions some years before. It was computed that during those years the patient was losing iron at a rate of about 4.0 mg. per day. The rate of iron accumulation during his recovery from the induced iron deficiency was the same as the normal: 5 to 6 mg. per day. 5. The ability to lose iron which is in excess of requirement is implicit in the demonstration of iron-laden deciduous cells such as the glandular epithelium of the stomach and duodenum and macrophages in the intestinal villi. 6. In hemochromatosis there is a failure of the intestinal mucosal block to prevent absorption of unneeded iron. When absorption exceeds the capacity of the iron excretory mechanisms, iron accumulation occurs. In iron deficiency the excretory mechanisms become less active so that the rate of iron accumulation is further increased.

1. Using Fe59 and whole body counting, various aspects of gastrointestinal absorption of iron salts were studied in normal, iron-loaded, and iron-deficient rats. 2. Following a single intragastric dose of iron, peak small intestinal uptake was observed by 30 to 60 minutes with subsequent gradual loss over 24-hour period. 3. Iron absorption showed two phases, an initial period of rapid absorption lasting up to 2 hours during which 60 to 80 per cent of total absorption into carcass took place. The remainder took place at a slow rate over the subsequent 12 to 20 hours. 4. Depending on the relationship between body iron stores and dose of administered iron, the intestine may take up more iron than is ultimately transferred to plasma. A variable amount of this iron is lost when the epithelial cell is sloughed into the gastrointestinal lumen. 5. Regulation of iron absorption appears to involve two steps, mucosal uptake and transfer to the blood.

Using an in vitro assay for gastric intrinsic factor, it was shown that seventeen of twenty-three patients with treated and untreated tropical sprue have adequate intrinsic factor in their gastric juice.

1. Two Negro brothers with homozygous hemoglobin C disease are reported. In one splenectomy was performed. 2. Intraerythrocytic crystals in smears of peripheral blood were demonstrated only in the patient who had splenectomy. The crystals could not be found in re-examination of bone marrow preparations of this patient that were made prior to splenectomy. 3. Absence of the spleen may be a necessary factor for the formation of these crystals. 4. The presence of homozygous C disease is compatible with a normal life span.

Abnormalities of jejunal histology were compared with clinical and laboratory tests of small bowel absorptive function in 110 symptomatic untreated patients in Puerto Rico, who were referred for evaluation of diarrhea or weight loss and possible intestinal malabsorption (tropical sprue).A spectrum of progressive degrees of abnormality of the jejunal mucosa paralleled, in general, the clinical status and the presence and degree of malabsorption. Sixty-eight of 71 patients (96%) whose biopsies were classified as tropical sprue had steatorrhea and d-xylose malabsorption. Among the 15 patients with borderline biopsy changes, 67% had steatorrhea, and 60% had abnormal d-xylose tests. Serum carotene levels were low in only 26%. In the 25 patients with a biopsy reading of nonspecific jejunitis, only one-fourth had malabsorption of fat or d-xylose.The criteria used in this study for categorizing jejunal biopsy abnormalities are useful in predicting the presence of malabsorption in symptomatic, untreated patients in a tropical area endemic for tropical sprue. The degree of biopsy abnormality correlates, in general, with severity of clinical illness.

Jejunal and ileal biopsies were compared histologically and by dissecting microscopy in 27 patients with tropical sprue. Fifteen of the patients were previously untreated, whereas 12 were treated with either tetracycline or folic acid or vitamin B12, or both. By dissecting microscopy the jejunum was judged to be more abnormal than the ileum in 15 of 27 patients. However, by histologic criteria, the mucosal abnormalities in 20 of the 27 pairs of biopsies were considered to be of equal severity. We conclude that in tropical sprue the ileum and jejunum are usually equally affected by the injurious process.

Long-term response to corticosteroid therapy and splenectomy was evaluated in 66 adults with idiopathic thrombocytopenic purpura (ITP). In 75% of 57 patients, a rise in platelet count was observed during administration of corticosteroids. In 49% of the 57, platelet counts of greater than 50,000/cu mm were documented four months after cessation of treatment, and in 37% a sustained remission throughout follow-up periods of 1 to 18 years was seen. Splenectomy produced good or excellent responses in 83% of 35 patients evaluated four months after operation and in all but two patients remission has been sustained during follow-up periods of 1 to 25 years. Prognosis based upon response to the initial course of corticosteroid treatment appears to be more reliable than that based upon duration of symptoms prior to treatment.