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R Lendrum

Publications and source records attributed to R Lendrum.

28 records · Page 2Linked to original sources
PubMed1976

Separate autoantibodies to human pancreatic glucagon and somatostatin cells.

Autoantibodies reacting with discrete populations of cells in normal human pancreatic islets were found by immunofluorescence in 17 out of 1279 sera. A double immunofluorescence technique, with antisera to pancreatic glucagon, insulin, somatostatin, and human pancreatic polypeptide was used to show that 13 of the sera contained anitbodies reacting specifically with glucagon cells, while the other 4 reacted with somatostatin cells. These antibodies were directed against intracellular components and not against the hormones themselves. Both types of antibody occurred independently of the islet-cell antibodies which have been described in diabetes mellitus. These findings suggest selective damage to individual cell types in the pancreatic islets and raise the possibility of corresponding hormone deficiency syndromes.

Adolescent↗
PubMed1976

HLA-linked genes and islet-cell antibodies in diabetes mellitus.

In a random series of 139 insulin-dependent diabetics aged 30 or under at the onset of disease islet-cell antibody (ICA) was detected in 33 cases (24%). In 27 patients who had had diabetes for less than one year 16 (59%) had ICA. Only one out of 51 patients with maturity onset diabetes who were not dependent on insulin were positive for ICA. Four out of 19 patients with late onset insulin-dependent diabetes had ICA. There was no association between the presence of ICA and any particular HLA phenotype. Within families containing two or more HLA haploidentical siblings with juvenile onset diabetes ICA was a variable finding both in its occurrence and in its relation to the duration of disease. A possible mode of action for the HLA-linked gene may be to permit a rapid immunological destructive process, possibly associated with viral infection.

Adult↗
PubMed1976

Islet-cell, thyroid, and gastric autoantibodies in diabetic identical twins.

Sera from 54 pairs of identical twins, 29 discordant and 25 concordant for insulin-dependent diabetes, and 11 pairs of concordant non-insulin dependent identical twins were examined for pancreatic islet-cell antibodies (ICAs). ICAs were found in 10 of the 29 diabetic discordant and eight of the 50 concordant twins (difference not significant P greater than 0-05). Six out of nine twins tested within one year of onset of diabetes were positive, whereas nine out of 29 tested after one to 10 years and three out of 41 tested after 10 years were positive. Only one of the 22 non-insulin-dependent twins had ICAs. Repeat ICA testing in five pair of insulin-dependent twins and in the siblings of one pair showed that ICAs may be present in people with normal glucose tolerance' may precede clinical diabetes by several years; and may decline in titre or disappear with increasing duration of disease. Thyroid or gastric autoantibodies, or both, were found in 36 out of 108 insulin-dependent twins and three out of 22 non-insulin dependent twins (difference not significant P less than 0-05). Only four twins had both ICAs and thyrogastric antibodies. There were no significant associations between autoantibodies and HLA histocompatibility types. As ICAs are more common in the diabetic than the non-diabetic twins of the discordant pairs they must be associated with juvenile onset diabetes. ICAs may appear some years before the onset of diabetes, but their prevalence declines with increasing duration of diabetes. The factors determining the production of ICA differ from those for thyroid and gastric autoantibodies.

Adolescent↗
PubMed1975

Islet-cell antibodies in juvenile diabetes mellitus of recent onset.

Antibodies reacting with human pancreatic islet cells were found by immunofluorescence in the sera of 51 of 105 children with diabetes mellitus of recent onset. These antibodies were of IgG class, and several of them fixed complement and reacted with pancreatic islets of other species. Thyroid microsomal and/or gastric-parietal-cell antibodies were found in only 10 of the patients with islet-cell antibodies, and none of them had adrenal antibodies. These findings contrast with previous reports which have stressed the rarity of islet-cell antibodies in adult diabetics and their occurrence only in patients with other evidence of autoimmune disease.

Adolescent↗
PubMed1975

Viral antibody studies in pancreatic disease.

Viral studies were performed on sera from 54 patients with recent acute pancreatitis, 10 with recurrent acute pancreatitis, seven with chronic pancreatitis, and 10 with pancreatic carcinoma, and on sera from 81 age- and sex-matched controls. In 29 of the acute pancreatitis patients from whom paired sera were obtained no convincing evidence of recent viral infection was found. A higher incidence of raised antibody titres against Coxsackie B3 and B4 was observed in the group of acute pancreatitis patients compared with their controls. The possible signficance of these observations and their relationship to the aetiology of the pancreatitis and to other immunological findings are discussed.

Acute Disease↗
PubMed1975

Serum antibodies in human pancreatic disease.

An immunofluorescent study of sera from patients with various pancreatic diseases and from controls was carried out using human pancreas as substrate. A reproducible pattern of immunofluorscence, consisting of a coarse granular appearance in the cytoplasm of acinar cells of the pancreas and independent of the ABO blood group system was found. This occurred in 21 of 61 patients with acute pancreatitis; it was not found in other pancreatic diseases, and occurred in only four of 170 control subjects consisting of mixed hospital patients and healthy adults. Preliminary absorption experiments suggest that the antigen is located in the microsomal fraction of pancreatic homogenates and may be organ-specific. The relationship of positive antibody tests to aetiological factors is discussed.

ABO Blood-Group System↗
PubMed1974

Effects of sulphasalazine (Salazopyrin) on faecal flora in patients with inflammatory bowel disease.

The faecal flora of 21 patients with proctocolitis and five patients with Crohn's disease of the large bowel was examined both while sulphasalazine was being administered and during control periods. Patients with proctocolitis and Crohn's disease who were not receiving sulphasalazine had a similar flora which did not differ in any way from the normal. The effect of sulphasalazine was to decrease the numbers of opalescent-negative clostridia, enterobacteria, and total non-sporing anaerobes. It is suggested that this antibacterial effect of sulphasalazine, which has not been previously demonstrated, may be related to the beneficial effects of this drug in proctocolitis and should be investigated further.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Immunolocalization of pS2, a putative growth factor, in pancreatic carcinoma.

pS2 is a 60 amino acid secretory polypeptide which belongs to a newly described family of trefoil-shaped growth factors. It is widely distributed throughout the gastrointestinal tract, particularly adjacent to damaged mucosa, and is also expressed by some epithelial tumours such as breast carcinoma. The aim of this study was to examine the expression of pS2 in pancreatic cancer. The presence of pS2 was analysed immunohistochemically using two antibodies, a polyclonal (pNR-2) and a monoclonal (pS2TM) in 42 cases of pancreatic adenocarcinoma and 10 cases of ampullary carcinoma. The findings were compared with chronic pancreatitis and normal pancreas. No immunostaining was seen in normal pancreas, with the exception of one area of ductular proliferation, and although 8/10 cases of chronic pancreatitis expressed pS2, it was focal and confined to the occasional duct. In contrast, a significant proportion of malignant cells in 23/42 (55%) of pancreatic adenocarcinoma and 8/10 (80%) of ampullary tumours expressed immunoreactive pS2. The finding of pS2 expression in more than 50% of pancreatic and ampullary carcinomas in contrast to the findings seen in chronic pancreatitis and normal pancreas suggests that pS2 may play an important role in the growth of these highly malignant tumours.

Adenocarcinoma↗