HL-A Antigens in Leprosy

HL—A phenotype frequencies were studied in 30 patients with leprosy and in 149 healthy controls. Leprosy patients had a significantly higher frequency of HL—A14. In addition, a majority of the HL—A14 patients gave a negative response to leproma antigen using the Mitsuda test.     

CALCITONIN GENE-RELATED PEPTIDE II, SUBSTANCE P AND VASOACTIVE INTESTINAL PEPTIDE IN PLASMA AND SYNOVIAL FLUID FROM PATIENTS WITH INFLAMMATORY JOINT DISEASE

Immunoreactive plasma and synovial fluid concentrations of calcitoningene-related peptide II (CGRP II), substance P and vasoactiveintestinal peptide (VIP) were measured in patients with osteoarthritis,gout and rheumatoid arthritis. Significantly higher levels ofCGRP II and substance P and VIP-like immunoreactivity levelsin synovial fluid were found in gout as well as CGRP II, substanceP and VIP-like immunoreactivities in rheumatoid arthritis whencompared to those in osteoarthritis. Plasma CGRP II, substanceP and VIP-like immunoreactivity levels showed no significantdifferences among patients in the three different groups ofarthritis. Our results suggest that these neuropeptides releasedfrom peripheral nerve endings into the synovial cavity probablyplay a pathogenic role in human joint inflammation. KEY WORDS: Rheumatoid arthritis, Gout, Calcitonin gene-related peptide II, Substance P, Vasoactive intestinal peptide, Synovial fluid     

Hookworm Anemia: Iron Metabolism and Erythrokinetics

Iron metabolism, balance of red cell production and destruction and ironabsorption from hemoglobin were determined in 11 patients with heavy hookworm infection and severe anemia.

The plasma iron, total iron binding capacity, bone marrow hemosiderinand plasma Fe⁵⁹ clearance are in agreement with the idea that the anemia associated with hookworm infection is of the iron deficiency type.

The rate of red cell production measured by the E/M ratio, absolute reticulocyte count and plasma iron turnover showed an increase to about twicenormal, while the rate of destruction estimated by the T erythrocytesurvival showed a destruction about 5 times normal. This unbalance betweenproduction and destruction could explain the severity of the anemia.

The increase of fecal urobilinogen output to twice normal was interpretedas due to the metabolism of the hemoglobin lost into the intestine rather than toan increase of hemolysis.

The estimation of fecal blood loss in the patients whose red cells weretagged with Cr⁵¹ and Fe⁵⁹, showed that the radioactivity counted with Fe⁵⁹was only about 63 per cent of the radioactivity counted with Cr⁵¹. This difference was interpreted as due to iron absorption from the hemoglobin lostinto the intestine.

The mean daily fecal excretion of iron reaches 4.7 mg. Since the ironmetabolism in these patients is in equilibrium, we have concluded that theiron loss is replaced by the iron from food; this is in addition to the 3 mg.hemoglobin iron which is reabsorbed from the blood lost into the gut.

Submitted on January 9, 1961 Accepted on April 2, 1961