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Biomedical subjects

N E Hansen

Publications and source records attributed to N E Hansen.

At least 73 records · Page 4Linked to original sources
PubMed1986

Serum ferritin as indicator of iron responsive anaemia in patients with rheumatoid arthritis.

In order to test the hypothesis that serum ferritin below 60 micrograms/l is a good indicator of iron deficiency in patients with rheumatoid arthritis peroral iron was given to 67 patients with active rheumatoid arthritis over a three month period. A rise in haemoglobin concentration was taken as evidence of iron responsive anaemia. In anaemic patients serum ferritin below 60 micrograms/l was a good indicator of iron responsive anaemia, with a predictive value of 83%. Although high plasma transferrin and low mean cell volume showed similar predictive values, more patients with iron deficiency anaemia could be diagnosed by serum ferritin measurements than by other conventional blood tests. In contrast, the predictive value of serum ferritin above 60 micrograms/l was low (50%). The test was of no predictive value in non-anaemic patients. In patients with anaemia and active rheumatoid arthritis serum ferritin is the best blood test currently available for the prediction of iron responsive anaemia.

Adult↗
PubMed1985

Immunological markers in acute leukaemia.

61 acute leukaemias were classified by both immunological and morphological criteria. In 58 (95%) of the cases correlation was found between the immunological and morphological diagnosis. In 3 (5%) cases, no correlation was found between the immunological subclasses and the FAB-subgroups in ALL. Neither was a correlation found between FAB-subclasses in AML and reaction with myeloid antibodies other than MY-7 which did preferentially react with M4 and M5 leukaemia.

Adult↗
PubMed1985

Hypercalcaemia in the accelerated phase of chronic myelogenous leukaemia: no relationship to the phenotype of the blast cells.

2 patients with chronic myelogenous leukaemia developed hypercalcaemia and severe myelofibrosis in the terminal phases of their disease. Hormonal studies excluded the hypercalcaemia being caused by primary hyperparathyroidism or ectopic parathyroid hormone secretion. Its development was unrelated to the phenotype of the blast cells, as assessed by conventional cytochemistry and immunological surface typing. The finding of increased urinary cAMP excretion in 1 of the patients suggests a circulating, nonparathyroid humoral bone resorbing factor with partial biological PTH-activity to be one of the pathogenetic mechanisms responsible for the occurrence of hypercalcaemia in patients with chronic myelogenous leukaemia.

Adult↗
PubMed1984

Lactoferrin receptors in normal and leukaemic human blood cells.

The binding of 125I-lactoferrin to a variety of peripheral blood cells was examined. In the concentration range from 10(-9) mol/l to 10(-6) mol/l a receptor-like binding of lactoferrin was observed in monocytes as well as in polymorphonuclear leucocytes. At the low concentrations of lactoferrin in plasma (about 10(-9) mol/l) the cellular binding to monocytes was about 10 times higher than the binding to polymorphonuclear leucocytes and lymphocytes. A major result from a kinetic analysis was a lower apparent binding affinity to polymorphonuclear leucocytes (KD about 2 X 10(-7) mol/l) than to lymphocytes and monocytes (KD about 2 X 10(-8) mol/l). Studies in leukaemic cells showed that lymphocytes from patients with chronic lymphocytic leukaemia bound lactoferrin to the same small extent as normal lymphocytes. In contrast, a larger component of binding with high affinity (KD about 2 X 10(-8) mol/l) could be demonstrated to lymphoblasts as well as to myeloblasts.

Binding Sites↗
PubMed1983

Receptor binding of lactoferrin by human monocytes.

The binding of iron-saturated 125I-lactoferrin to human monocytes was studied at pH 7.4 and 37 degrees C. Monocytes in suspension bound 125I-lactoferrin by a reversible, saturable and specific binding indicating the presence of a receptor. The dissociation constant (KD) of the binding was estimated at about 4.5 x 10(-9) M and the number of receptors was about 1.6 x 10(6) per monocyte. The affinity of native lactoferrin (20% iron saturated) was only slightly below that of iron-saturated lactoferrin (KD about 7.9 x 10(-9) M). Human transferrin, horse cytochrome c and human immunoglobulin G were without inhibitory effect on the binding of 125I-lactoferrin. The majority of cell-bound 125I-lactoferrin was dissociable. The dissociation rate was not affected by addition of unlabelled lactoferrin to the dissociation medium. The binding of 125I-lactoferrin to adherent mononuclear blood cells showed an about 100-fold lower affinity (KD about 2.5 x 10(-7) M) than to cells in suspension, but the specificity of the binding was the same. These results are compatible with the idea that lactoferrin exerts a biological effect mediated by an interaction with cells of the monocyte/macrophage lineage.

Adult↗
PubMed1983

Serum ferritin and the assessment of iron deficiency in rheumatoid arthritis.

In order to evaluate the diagnostic and pathogenetic importance of s-ferritin and p-lactoferrin in the anemia of rheumatoid arthritis (RA), 38 patients were examined. Twenty-one out of 38 randomly selected anemic patients with classical or definite RA had iron deficiency, as estimated from the iron content in stained bone marrow aspiration. S-ferritin concentrations below 60 micrograms per litre had sensitivity and a specificity for iron deficiency of 86% and 88%, respectively, which was much better than such commonly used variables as s-iron, p-transferrin, MCV, and MCHC. Although this cut-off level is higher than in patients without inflammatory disease, s-ferritin was not correlated to disease activity. In 7 out of 8 patients, the s-ferritin level rose during iron therapy. P-lactoferrin values were within the normal range and did not vary with the anemia or with disease activity. Thus p-lactoferrin appears to be of no pathogenetic importance in the anemia of RA.

Adult↗
PubMed1983

Trends in the incidence of leukemia in Denmark, 1943-77: an epidemiologic study of 14,000 patients.

An epidemiologic study of the total population of patients with leukemia in Denmark during 1943-77 was performed with special emphasis on time trends. The material stemmed from the national Danish Cancer Registry and was believed to be virtually complete. Of the 13,813 patients, 40% had acute leukemia; 40%, chronic lymphocytic leukemia; patients, 40% had acute leukemia; 40%, chronic lymphocytic leukemia; and 20%, chronic myeloid leukemia. Over the 35-year period, the incidence of acute leukemia increased threefold in the age groups 0-9 and 50-70+ years; whereas the increase in the age group 0-9 years climaxed in the 5-year period 1968-72, and the increase in the age group 50-70+ years was sustained. The incidence of chronic lymphocytic and chronic myeloid leukemia remained unchanged. No geographic pattern was discernible.

Acute Disease↗
PubMed1982

Neutrophil and lymphocyte function in patients with diabetes mellitus.

Neutrophil granulocyte chemotaxis and intraneutrophilic and plasma levels of lysozyme as well as the number of T and B lymphocytes and lymphocyte transformation in vitro on stimulation with mitogens and microbial antigens were studied in four groups of patients with diabetes mellitus (DM). Twelve patients with insulin-dependent diabetes mellitus (IDDM) and ketoacidosis and 4 patients with non-insulin-dependent diabetes mellitus were studied at the time of diagnosis and before and after start of treatment. Ten patients with IDDM of less than 10 years' duration which had been difficult to regulate well and 10 patients with IDDM well regulated for more than 20 years were studied at their regular outpatient visits. Apart from a slight increase in plasma lysozyme in group 1 from the first to the second examination, we found no differences between diabetics and healthy control persons. It is concluded that if patients with DM are more susceptible to infections, it is probably caused by elements of neutrophil or lymphocyte function not examined in this study or by factors unrelated to immunity.

Adolescent↗
PubMed1981

Tissue and plasma lysozyme in Hodgkin's disease.

Lysozyme positivity in lymph nodes from 33 patients with Hodgkin's disease was examined with an immunoperoxidase technique. Positive reactive histiocytes were found in 18 cases; in 7 cases lysozyme was found also in mononuclear Hodgkin cells and in 3 cases in both reactive histiocytes, mononuclear Hodgkin cells and Reed-Sternberg cells. There was no clear-cut correlation between cellular lysozyme positivity and such feature as histological type, clinical stage and plasma lysozyme. The findings support the theory that the malignant cell in Hodgkin's disease is derived from a lysozyme producing macrophage. The finding that lysozyme positivity was an inconstant feature may reflect both varying functional status of the macrophages and varying differentiation of Hodgkin cells. Increased plasma lysozyme in Hodgkin's disease may stem from both reactive histiocytes, mononuclear Hodgkin cells and Reed-Sternberg cells, but the major part is probably contributed by reactive histiocytes.

Adolescent↗
PubMed1979

Development of acute myeloid leukaemia in a patient with psoriasis treated with oral 8-methoxypsoralen and longwave ultraviolet light.

Acute myeloid leukaemia developed in a patient with psoriasis treated with oral 8-methoxypsoralen and longwave ultraviolet light (PUVA) 2 years earlier. Attention is called to the possibility that the effect of PUVA on DNA synthesis may not be limited to the areas of the skin being treated but - through damage to circulating multipotential stem cells - may also lead to haematological malignancies.

Aged↗
PubMed1979

Elevated plasma lysozyme in Hodgkin's disease. An indicator of increased macrophage activity?

Plasma lysozyme levels were studied in 42 patients with Hodgkin's disease and were found significantly increased. Plasma lysozyme varied with the stage of the disease and with symptoms, but did not correlate with the histological subtype or with blood neutrophil and monocyte counts. Serial measurements in four patients on MOPP treatment showed a rapid decrease following treatment. The increased plasma lysozyme in Hodgkin's disease stems most likely from the macrophage system, either because the macrophages are hyperactive and/or because the malignant cell in Hodgkin's disease is of macrophage origin.

Adolescent↗
PubMed1979

Turnover of human lactoferrin in the rabbit.

Lactoferrin turnover was studied in the rabbit with 125I- and 131I-labelled human lactoferrin. Plasma lactoferrin activity showed a rapid decrease during the first 24 h, followed by a 'final slope' with a T1/2 of about 25 h. Turnover studies after transfer of plasma from one rabbit (A) 3 h after injection to another rabbit (B), showed a recovery of 100% compared to 30% in A rabbits but otherwise a similar disappearance curve. The rapid turnover was confirmed in whole body studies. Concomitantly with the initial dissapearance from the plasma, there was a marked accumulation of proteinbound activity only in the liver in both A and B rabbits. From these results, the rate of synthesis in normal man can be estimated at around 25 mg per d. The disappearance pattern and hepatic uptake are discussed in relation to knowledge about lactoferrin receptors in macrophages, asialo elimination, and fucose group recognition. Concerning the significance of lactoferrin turnover for iron metabolism it is concluded that the plasma turnover results are insufficient to explain the disturbance in iron kinetics seen in the anaemia of chronic disorders; however, it is likely that lactoferrin plays a role in iron metabolism within the extravascular space.

Animals↗