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W J Riley

Publications and source records attributed to W J Riley.

At least 91 records · Page 5Linked to original sources
PubMed1984

Pancreatic alpha cell autoantibodies and glucagon response to arginine.

The frequency and significance of cytoplasmic pancreatic alpha cell autoantibodies (ACA) were investigated in 2102 healthy controls, 879 patients with insulin-dependent diabetes mellitus (IDDM) who were negative for islet cell autoantibodies (ICA), and 1567 relatives of IDDM patients. ACA were found in approximately 1 in 200 people of all ages and were not significantly associated with IDDM, the IDDM-associated HLA phenotypes DR3 and DR4, or thyrogastric or adrenal autoantibodies. Of 11 ACA-positive patients studied by arginine stimulation tests, none had frank glucagon deficiency. Thus, ACA do not appear to be associated with defective alpha cell function or with IDDM.

Adrenal Glands↗
PubMed1984

Intestinal absorption of thiamin in man compared with folate and pyridoxal and its subsequent urinary excretion.

off intestinal absorption of thiamin was compared with that of folate and pyridoxal in six healthy volunteers using an oral dose of each vitamin equivalent to ten times the recommended daily allowance. Folate and pyridoxal were rapidly absorbed and following the oral dose, serum concentrations rose from a mean basal level of 10.9 micrograms/liter and 17.5 micrograms/liter to 174.8 micrograms/liter and 315.2 micrograms/liter respectively--an increases of 1,500% for folate and 1,701% for pyridoxal. The mean serum level of thiamin rose only marginally from 5.1 micrograms/liter to 7.2 micrograms/liter, an increase of 42%. One hour following the oral test dose of thiamin, the vitamin was actively excreted in the urine of all volunteers, with a mean creatinine/thiamin renal clearance ratio of 2.4. Active excretion continued for up to six hours. In contrast, folate was only actively cleared for a short period in two volunteers. Thiamin absorption appeared to be controlled and limited, and modest increases in the serum concentration were accompanied by active renal clearance.

Administration, Oral↗
PubMed1984

Clinical significance and partial biochemical characterization of lactate dehydrogenase isoenzyme 6.

We report nine patients with a sixth band, migrating cathodic to lactate dehydrogenase 5, appearing on routine electrophoresis for serum lactate dehydrogenase (LD, EC 1.1.1.27). Eight of these patients died during their hospitalization. Acidosis, hypotension, and sepsis were the common clinical conditions preceding the band's appearance. In several cases the band appeared transiently. We examined tissue samples from two of the cases, finding LD-6 in liver and skeletal muscle but not in heart. In randomly selected autopsy tissues, LD-6 was detected consistently in liver and skeletal muscle, sometimes in spleen, kidney, and adrenal tissue, but never in heart. Biochemical studies indicate that the LD-6 isoenzyme is not an artifact or an immunoglobulin complex, is larger than the other LD isoenzymes, contains an M-subunit but not an H-subunit, has an isoelectric point in the pH range of 9.0-9.6, and is more heat stable than LD-5.

Adolescent↗
PubMed1983

Coincident presence of thyro-gastric autoimmunity at onset of type 1 (insulin-dependent) diabetes.

We have determined thyroid microsomal and gastric parietal cell autoantibodies in 972 patients with onset of Type 1 (insulin-dependent) diabetes before age 20 years. In a cross sectional study, the frequencies of these autoantibodies did not change significantly over the ensuing 20 years following diagnosis of diabetes. In a longitudinal study of 424 patients with Type 1 diabetes followed up to 5.3 years, few new patients with thyro-gastric autoantibodies were identified. Whereas the frequencies of these autoantibodies among the diabetic patients were more than fivefold greater than for age, sex and race matched controls, they resembled those seen in the non-diabetic general population (n = 1524) for the over 60 year age group. We conclude that in patients with thyro-gastric autoantibodies and Type 1 diabetes, the onset of autoimmune processes affecting the thyroid, gastric mucosa and pancreatic islets tend to be simultaneous, although the resultant diseases have different natural histories.

Autoantibodies↗
PubMed1983

Autosomal dominant hypoparathyroidism with variable, age-dependent severity.

Hypoparathyroidism (hypocalcemia, hyperphosphatemia, mild hypomagnesemia, and inappropriately low serum C-terminal parathyroid hormone concentration) was found in six members of a family representing three successive generations. No patient had aortic arch or conotruncal malformations, lymphopenia, or features of type I or type II autoimmune polyglandular syndromes. Two individuals had transient neonatal seizures without further difficulties despite persistent hypocalcemia. None of the four affected adults has had major complications of hypoparathyroidism (mental retardation, cataracts, or seizures). We believe that persistence of hypoparathyroidism after resolution of neonatal hypocalcemic seizures should prompt a survey of the family for hypoparathyroidism.

Adult↗
PubMed1983

Autoimmune diatheses and T lymphocyte immunoincompetences in BB rats.

BB rats were found to have autoantibodies to gastric parietal cells, thyroid colloid antigens, smooth muscle, and thymocytes. No autoantibodies reactive with pancreatic islet cells (cytoplasmic), thyroid epithelial cells, adrenal cortex, testes, or anterior pituitary sections were identified. BB rats with gastric parietal autoantibodies had modest degrees of lymphocytic gastritis, but none developed iron or vitamin B12 deficiencies. These results suggest that BB rats have an underlying autoimmune diathesis. In addition, reports of peripheral T lymphopenia in such rats were confirmed, and markedly reduced helper T cell and cytotoxic-suppressor T cell subsets were demonstrated. Histological studies also revealed depletions of the T cell areas of spleen and lymph nodes. Furthermore, BB rats exhibited a profound inability to reject skin grafts across major and minor histocompatibility barriers. This was confirmed by mixed lymphocyte culture studies in vitro. BB-rat lymphocytes from either spleen or peripheral blood also showed profoundly reduced responses to T cell mitogens. Although BB-rat lymphocytes could produce normal levels of interleukin-2, they were unable to respond to this T cell growth factor. However, examination of thymuses from BB rats showed largely normal histologies, normal numbers of thymocyte subsets, and good mitogenic responses to con A. Thus, it appears that BB rats may have a thymic or post thymic defect in T lymphocyte maturation. The relevance of the immunologic lesion to the etiology of IDD in BB rats remains to be shown.

Animals↗
PubMed1983

Steroid-induced diabetes in pediatric renal transplant recipients.

Seven patients in a series of 79 children receiving 101 kidney transplants developed steroid-induced diabetes. Black children, recipients of cadaveric allografts, and patients receiving higher average daily prednisone dosage were more likely to develop hyperglycemia. The diabetes was transient and easily controlled. No patient developed permanent insulin dependence. No patients exhibited is let cell autoantibodies or an HLA haplotype associated with diabetes. Oral glucose tolerance testing demonstrated significant hyperglycemia with an inadequate insulin response. Three patients also exhibited unusual complications; two had cerebral vascular accidents (CVA) and one developed aspergillosis in a native kidney. Pediatric patients exhibiting steroid-induced diabetes following kidney transplantation may constitute a group at greater risk for complications.

Adolescent↗
PubMed1982

Limited joint mobility in diabetes mellitus of childhood: natural history and relationship to growth impairment.

We report a prospective study of the recently recognized complication of limited joint mobility in childhood diabetes, summarizing data collected over the seven years after the initial description of this sign. Of 309 patients, ranging in age from 1 to 28 years, 30% had limited joint mobility. No race or sex influence on expression of limited joint mobility was found; its appearance was temporally more influenced by age than by duration of diabetes. Of 142 patients with diabetes onset before puberty and of longer than three years' duration, 74 had limited joint mobility. Disproportionate distribution of height percentiles for age characterized this entire group, but those with limited joint mobility had four times the skewing of those without (74 vs 37% below the twenty-fifth percentile). The presence or absence of thyroid microsome or islet cell antibodies did not relate significantly to limited joint mobility. Diabetes control, assessed subjectively by clinical estimation and objectively by hemoglobin A1 levels, was generally unrelated to the joint findings. For patients with diabetes duration less than five years, there was a significant association between hemoglobin A1 and limited joint mobility, but the variability in values explained by this association was small (11%).

Adolescent↗
PubMed1982

Metabolic and underlying causes of diabetes mellitus.

It is emphasized that animal models should be used to study specific genotypic or phenotypic expressions associated with diabetes rather than assuming a single animal model can reflect diverse forms of the human disease. Diabetic and normal animals are reviewed on the basis of their usefulness as models of genetic, viral, and chemically induced diabetes, including the often associated immune phenomena. Characteristics of spontaneously diabetic animals with and without obesity are also described with an emphasis on both genetics and metabolic derangements. Recommendations for future animal experimentation include: more longitudinal studies evaluating the role of sex, prenatal environment, diet, and viral or chemical attack on B-cell function; characterization of the immune phenomena associated with B-cell lesions (and insulitis) in diabetic and immunologically incompetent lines; clarification of relationships between obesity and islet-cell function with emphasis on the role of fuel metabolism, vitamins, and minerals; and, finally, the development of new models with specific genetic aberrations placed in normal or diabetic lines.

Alloxan↗
PubMed1982

Predictive value of gastric parietal cell autoantibodies as a marker for gastric and hematologic abnormalities associated with insulin-dependent diabetes.

The frequency and significance of gastric parietal cell autoimmunity was assessed in 771 patients with insulin-dependent diabetes (IDD) of onset before 30 yr of age. Gastric parietal autoantibodies (PCA) were found 4 times more frequently in the patients with IDD (9%) than among 600 matched nondiabetic controls (2%). Caucasian female patients with IDD had PCA twice as frequently as male patients. Thyroid microsomal autoantibodies were more frequent in patients with IDD and PCA, than in those with IDD alone (Caucasian 46% versus 18%, black 25% versus 2.5%). A history of pernicious anemia and/or PCA was found in 25 or 40 families of IDD probands with PCA. Achlorhydria was demonstrated in 6 of 11 patients (54%) with PCA but in none of seven IDD patients without PCA. The six patients with achlorhydria had significantly lower uptakes of oral radiolabeled cobalamin, lower serum cobalamin levels, lower intrinsic factor-R protein ratios in their gastric aspirates, and lower plasma ferritin levels than patients with IDD but without PCA. None of the study group had IF antibodies in their serum or gastric juice. Overt pernicious anemia and neuropathy were found in one patient with PCA. Young patients with IDD at risk for atrophic gastritis and cobalamin deficiency can initially be identified by screening for PCA. Many of these young patients with PCA already have achlorhydria and evidence of decreased absorption of cobalamin. These patients can then be followed with cobalamin levels and/or with complete blood counts to identify those requiring therapy.

Achlorhydria↗
PubMed1981

Non-enzymatically glycosylated serum protein in diabetes mellitus: an index of short-term glycaemia.

We measured non-enzymatically-glycosylated serum protein by a colorimetric assay in 107 diabetic and 82 control subjects. The mean level in diabetics was more than twice that in controls. Cross sectional and longitudinal studies in diabetic patients showed that glycosylated serum protein levels correlated with both fasting serum glucose and glycosylated haemoglobin levels. The correlation between glycosylated serum protein and fasting serum glucose was closer in Type 2 than in Type 1 diabetes. Treatment aimed at improving control in eight poorly controlled diabetic patients resulted in a 37% mean fall in glycosylated serum protein within one week, whereas glycosylated haemoglobin decreased only 8%. These studies confirm that non-enzymatic glycosylation of serum proteins is enhanced in diabetes. Measurement of glycosylated serum protein appears to provide an index of glycaemia over the preceding several days. It has the advantage of detecting improvements in glycaemic control much sooner than does glycosylated haemoglobin measurement.

Adult↗
PubMed1981

Human leukocyte interferon treatment of two children with insulin dependent diabetes.

Two patients with newly diagnosed insulin dependent diabetes mellitus were treated with human leukocyte interferon based on the hypothesis that the diabetes was induced by an active viral infection in the pancreatic islets and could be arrested. High peak levels of serum interferon were achieved (100-200 U/ml) with minimal systemic side effects. There was no sustained therapeutic benefit as measured by increased production of endogenous insulin, or of C-peptide, or by a lower requirement for exogenous insulin. Further trials with interferon treatment should be undertaken only if evidence of active viral infection (culture, antigen detection) can be associated with insulin dependent diabetes onset and these markers followed during treatment.

Blood Glucose↗
PubMed1981

Thyroid autoimmunity in insulin-dependent diabetes mellitus: the case for routine screening.

Of 771 young diabetic patients, thyroid microsomal autoantibodies occurred in 136 (17.6%) at a female/male ratio of nearly 2:1 and with a predominance of white patients (20.1%) over black patients (5.5%) (P less than 0.001). Thus, one in every four white female patients with insulin-dependent diabetes mellitus had TMA. Thyroglobulin autoantibodies were no more common in patients with IDDM than among controls. Of the 117 patients (out of the 136) with serologic evidence of chronic thyroiditis who could be studied, eight (7%) had hyperthyroidism and 45 (38%) were hypothyroid. Hyperthyroidism usually preceded or coincided with the appearance of IDDM, whereas hypothyroidism occurred with or following the onset of IDDM. Hypothyroidism appeared irreversible in most patients, but in three, periods of hypothyroidism were followed by euthyroidism, presumably explained by a compensatory hyperplasia of the thyroid gland. In the 136 patients with TMA, gastric and adrenocortical autoantibodies also occurred at relatively high frequencies (16.8% and 5.1%, respectively). On the basis of these studies, we urge that all patients with IDDM be screened for TMA and that those with positive results undergo annual thyroid function tests as well as determinations of gastric parietal and adrenocortical autoantibodies.

Adolescent↗
PubMed1981

Impaired glucose tolerance and growth hormone in chronic liver disease.

Of 30 patients with chronic liver disease 16 showed some degree of impairment of glucose tolerance, and 16 patients had lack of suppression of raised fasting growth hormone levels or showed an anomalous rise after oral glucose. No relationship, however, existed between the state of glucose tolerance and the presence of abnormal growth hormone levels. Plasma glucose in those with normal growth hormone response at 0, 1/2, 1, 1-1/2, and 2 hours, after 50 g glucose were 5.55 +/- 0.41 mmol/l, 8.71 +/- 0.59, 10.66 +/- 0.99, 10.28 +/- 1.37, 8.90 +/- 1.40 (mean +/- SEM; n = 14). Under the same conditions those with abnormal growth hormone responses showed values of 5.32 +/- 0.59, 7.83 +/- 0.81, 9.41 +/- 0.95, 9.46 +/- 0.99, 8.69 +/- 0.98. At no time were the differences significantly different as judged by Student's t test. Measurement of serum insulin indicated a relative deficiency in patients with impaired tolerance. It is concluded that the abnormal growth hormone is not directly responsible for the impaired glucose tolerance.

Blood Glucose↗