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Biomedical subjects

H J Hodgson

Publications and source records attributed to H J Hodgson.

14 recordsLinked to original sources
PubMed1979

Immunodeficiency, malabsorption and secretory diarrhea. A new syndrome.

Described here is a patient with severe watery diarrhea associated with common variable immunodeficiency. Malabsorption for fat, bile acids, vitamin B12 and xylose was demonstrated, but the patient failed to respond to all the usual therapeutic maneuvers. The diarrhea responded only to high dose steroid therapy. Intestinal perfusion studies showed a hitherto undescribed, presumably acquired, glucose-stimulated water, sodium and chloride secretion in the jejunum and ileum, whereas normal fluid and electrolyte transport occurred from bicarbonate and mannitol solutions. Glucose absorption itself was normal and no hormonal, morphologic or biochemical defect was demonstrated to account for the phenomenon. The patient was also interesting when compared with other patients with common variable immunodeficiency in having normal plasma cells in the intestinal mucosa and an extensive family involvement.

Adult↗
PubMed1979

Chronic immune colitis in rabbits.

A chronic colitis has been induced in rabbits having many of the histological features of human ulcerative colitis. Animals were first immunised with the common enterobacterial antigen of Kunin and haemagglutinating antibodies demonstrated in high titre. An immune complex colitis was then established by the injection of soluble immune complexes following mild irritation of the rectum with dilute formalin as previously described. The rabbits developed an acute colitis within the first week but, in contrast with unsensitised rabbits, the inflammation persisted and was still present at six months as assessed by proctoscopy and rectal biopsy. Kunin-sensitised rabbits receiving intravenous saline, antigen, or antibody alone did not develop a chronic colitis. It is suggested that hypersensitivity to colonic bacterial antigens may be one mechanism whereby an acute colitis becomes chronic.

Animals↗
PubMed1979

Clq metabolism in ulcerative colitis and Crohn's disease.

The metabolism of pure radioiodine labelled Clq has been observed in five patients with ulcerative colitis, five patients with Crohn's disease, and in five control subjects. Both the fractional catabolic rate and the synthesis rate of Clq were increased in the five patients with Crohn's disease and in four of the five patients with ulcerative colitis. The fifth patient was in remission and had a normal synthesis rate. These results support the hypothesis that complement activation plays a role in the pathogenesis of these disease states and that the increased complement activation is primarily via the classical pathway.

Adult↗
PubMed1978

The humoral immune system in inflammatory bowel disease. II. Immunologlobulin levels.

As there have been reports of differences in mean levels of serum immunoglobulins between patients with ulcerative colitis and Crohn's disease, serum IgG, IgA, and IgM were estimated in 158 patients with inflammatory bowel disease and the results correlated with the clinical features of the patients. Although a higher mean IgG level in ulcerative colitis compared to Crohn's disease was confirmed, no difference was found when the comparison was limited to patients with colonic Crohn's disease. Patients with either disease had higher mean IgM levels than controls, and the IgM levels were higher on treatment with corticosteroids and showed a tendency to rise in remission. IgG and IgM levels were also higher in both diseases if extraintestinal manifestations were present. It is concluded that if clinical features, particularly disease site, are taken into account, the overall immunoglobulin responses in these two diseases show no differences.

Antibody Formation↗
PubMed1978

Alteration in suppressor cell activity in chronic active hepatitis.

We have studied peripheral blood mononuclear cells obtained from 24 patients with acute or chronic active hepatitis to determine if there was an abnormality in concanavalin A-induced suppressor cell activity compared to control subjects. Suppressor cells were generated by preincubation of the mononuclear cells with a mitogenic concentration of concanavalin A (6 mug/ml) for 48 hr followed by treatment with mitomycin C and alpha-methyl mannoside. Suppressor cell activity was assessed in second cultures by inhibition of concanavalin A-stimulated blast transformation of fresh allogeneic lymphocytes. Concanavalin A-stimulated suppressor activity was not elicited in mononuclear cells from the majority of patients with chronic active hepatitis in contrast to patients with acute hepatitis or acute inflammatory diseases and controls (P < 0.001). This finding was demonstrable in chronic active hepatitis patients in remission and relapse, both on and off prednisone therapy, and varied considerably during the course of the disease. The extent of liver injury was not related to the measured suppressor cell activity. These studies suggest that in chronic active hepatitis, a disease in which the host immune response may be involved, there appears to be a defect in concanavalin A-stimulated suppressor cells.

Acute Disease↗
PubMed1978

Immune-complex mediated colitis in rabbits. An experimental model.

An experimental colitis in rabbits is described, following the intravenous injection of preformed immune complexes of human serum albumin (HSA) and anti-HSA into non-sensitised rabbits. Tissue damage was localised to the colon by the Auer technique of inducing local non-specific inflammation, by the rectal instillation of dilute formalin. Formalin alone gave transient changes that reverted to normal within 24 hours. In rabbits given intravenous immune complexes formed in antigen-excess, a severe colitis was initiated, with histological features including mucosal ulceration, mixed inflammatory cell infiltration in the lamina propria, and crypt abscess formation. It is possible that immune-complex damage may be one of the pathogenic mechanisms involved in human ulcerative colitis.

Animals↗
PubMed1978

Decreased suppressor cell activity in inflammatory bowel disease.

Studies were performed on eleven patients with inflammatory bowel disease to determine if there was an alteration in concanavalin A (Con A) induced suppressor cell activity. Similar investigations were also performed on twenty-one control subjects and five patients with other inflammatory conditions. Supressor cells were generated by pre-incubation of peripheral blood mononuclear cells with a mitogenic concentration of Con A, followed by treatment with mitomycin C and alpha-methyl mannoside. Under these conditions, cells obtained from normal individuals are then capable of suppressing the Con A-stimulated blast transformation responses of fresh allogeneic lymphocytes in new cultures. We found that in twenty out of twenty-one control subjects, and all five patients with other inflammatory disorders, Con A-stimulated suppressor cell activity was demonstrable. Four patients with inflammatory bowel disease, whose disease was mildly active or was in clinical remission, had elicitable suppressor cell activity which fell within the normal range. In contrast, suppressor cell activity was markedly diminished or absent in seven patients with severe and active inflammatory bowel disease. These studies suggest that an alternation in Con A-stimulated suppressor cells exists in patients with active inflammatory bowel disease, which may contribute, in part, to the persistent inflammation in the gastrointestinal tract.

Adolescent↗
PubMed1977

Selective IgA deficiency and Crohn's disease: report of two cases.

Two patients are described with Crohn's disease and selective IgA deficiency. Serum IgA was undetectable in each case, and immunoperoxidase studies of the lamina propria showed a gross diminution of IgA-bearing plasma cells. Peripheral blood lymphocytes, however, showed normal numbers of IgA-bearing lymphocytes. The typical clinical course and histology in these two patients suggest that IgA-mediated responses in the mucosa are not involved in the pathogenesis of Crohn's disease.

Adult↗
PubMed1977

Humoral immune system in inflammatory bowel disease: I. Complement levels.

Serum levels of complement components Clq, C4, C3, and Properdin factor B, from the classical and alternative pathways of complement activation, have been estimated in patients with ulcerative colitis and Crohn's disease. C3, factor B, and to some extent C4 concentrations all increased when the disease was active. In remission the levels of these components did not differ from hospital control patients. There was no evidence for the preferential consumption of the proteins of either pathway of activation, even in those patients with evidence of circulating immune complexes.

Colitis, Ulcerative↗
PubMed1977

C3 metabolism in ulcerative colitis and Crohn's disease.

The metabolism of the third component of complement (C3) has been investigated in four patients with ulcerative colitis, three patients with Crohn's disease and seven control subjects, using radioiodinated C3 prepared from fresh human plasma. Both the fractional catabolic rate and synthesis rate of C3 were increased in the patients with inflammatory bowel disease, although the serum-C3 levels were normal or raised. The results suggest that complement activation may play a role in the pathogenesis of mucosal inflammation in these diseases.

Adolescent↗
PubMed1977

Immune complexes in ulcerative colitis and Crohn's disease.

Sera from 156 patients with ulcerative colitis and Crohn's disease were tested for the presence of immune complexes, by the detection of anti-complementary activity and 125I-labelled Clq precipitation. Using aggregated IgG, a comparison between the two tests indicated that the anti-complementary test was most sensitive to aggregates of 11S in size, while the 125I-labelled Clq test detected aggregates over 20S in size. Excess anti-complementary activity was common in patients with active bowel disease, and in those with extra-intestinal manifestations, particularly acute arthritis, ankylosing spondylitis and liver disease. Large complexes were only common in patients with liver disease. Immune complexes in the gut mucosa may play a role in the pathogenesis of these diseases, and the deposition of circulatory immune complexes may explain at least some of the extra-intestinal manifestations.

Antigen-Antibody Complex↗
PubMed1976

Cirrhosis in South London.

Alcoholism was the major aetiological factor in 65% of 78 patients presenting with cirrhosis to a hospital in Central London during 1968-74. It is suggested that in the U.K. the importance of alcoholism in patients with cirrhosis has been underestimated.

Adult↗
PubMed1976

Atopic disorders and adult coeliac disease.

A history of asthma, hay fever, and flexural eczema was significantly more common in patients with adult coeliac disease (A.C.D.) than in normal controls. Autoantibodies were also more common in A.C.D. First-degree relatives of A.C.D. patients were more likely than controls to have atopic disorders. A deficiency of local mucosal immunity due to abnormal IgA responses may underly this association between A.C.D. and atopy.

Adult↗