Washout of intranasal DDAVP with swimming.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to A L Rosenbloom.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Age, sex, and estimated time of onset of insulin-dependent diabetes were determined for children in Pittsburgh (N = 673), Gainesville (N = 976), Galveston (n = 741), and Melbourne (N = 851). The US cities had a decrease in new cases during the summer and peak incidence in January through April. In Melbourne, monthly trends were reversed: there were more cases during May through August. In US cities, but not in Melbourne, children less than 6 years old showed a greater variation by season than children 6 years old and older. Observations of the same fall and winter onset (in different calendar months) of insulin-dependent diabetes in Australia and the United States, and exaggeration of seasonal differences in young US children, suggest that onset of insulin-dependent diabetes is associated with seasonally varying viral diseases. Mumps and rubella infections do not seem to be responsible for much of the seasonal variation. Seasonal peaks of mumps and rubella are later than those observed for insulin-dependent diabetes, and immunization with live mumps and rubella viruses has not been associated with changes in incidence of insulin-dependent diabetes. An increase in disease incidence in boys over girls below age 6 years and in girls over boys at ages 6 through 11 years was consistently observed but not explained.
During a one-year period, six patients were admitted to the hospital in diabetic ketoacidosis following 12 to 24 hours of illness at home. Urine testing with strips impregnated with sodium nitroprusside had indicated that no ketone bodies were present. Nine of 11 bottles of reagent strips in use for less than three months by these and other patients contained totally unreactive strips. Nitroprusside tablets exposed more than three months continued to give accurate readings.
Previous reports have noted a constant association between the Carpenter syndrome (acrocephalopolysyndactyly, type II) and mental retardation. We report two patients with this condition with normal intelligence. These observations indicate that mental deficiency is not necessarily a component of the Carpenter syndrome and that early surgical correction of the craniosynostoses may improve the chances of normal mentality.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Cultured skin fibroblasts from clinically normal offspring of two parents with non-insulin-dependent diabetes have demonstrated premature senescence as a decreased ability of cells to establish colonies when inoculated at low density (plating efficiency). The present study tested the hypothesis that there is an inherent cellular defect affecting viability of diabetic cells in insulin-dependent diabetes. Four insulin-dependent patients, aged 12 to 19 years, included two with joint contracture, skin changes, and growth failure; one with thyroiditis and past history of nephrosis; and one with a family history of insulin dependency. Ten control subjects, aged 10 to 52 years, had negative family histories and normal oral glucose tolerance tests. Number of cells per confluent dish correlated significantly with donor age (p less than 0.001) at 30 and 40 in-vitro generations. The patients' cells' mean confluent density did not differ from that of five age-matched controls. Plating efficiency correlated with donor age at 30 in-vitro generations ( p less than 0.001); plating efficiency of cells from the youngsters with diabetes was virtually identical to that of control cells at 20, 30, and 40 generations. In this small series of two subjects with in-vivo growth failure, one with associated autoimmune disease and another with familial insulin-dependent disease, cultured fibroblasts demonstrated normal viability and the hypothesis of a cellular growth defect was not confirmed.
Explore the source record for details and available documents.
The prevailing concept of etiologic heterogeneity for the diabetes mellitus syndrome is one of multiple genetic factors interacting with a variety of environmental influences. Variation in expression of the disorder, particularly the need for insulin, does not correlate with known etiologic distinctions. There is much evidence for genetic heterogeneity, as well as phenotypic variation when etiology can be presumed to be identical. The vascular manifestations of diabetes include microangiopathy unique to diabetes and larger vessel disease that differs from that of normal aging only by its prematurity. There is as much evidence for heterogeneity of the vascular expression as there is for glucose intolerance. Approximately 25% of persons with insulin-dependent diabetes may never develop the microvascular disease. The pathogenesis of vascular disease in diabetes may involve a number of abnormalities of plasma, circulating cells, and vascular tissue. Were absolute control of glycemia possible, some of the contributing factors involved in vasculopathy would possibly be alleviated. In the absence of automated physiologic insulin replacement the potential deleterious effect of our current methods of treatment might be reduced by specific inhibition of excess catecholamine, growth hormone and/or glucagon responses.
Confluent fibroblasts were assayed for insulin binding to determine whether there was an inherent abnormality in receptor function to explain the insulin resistance of lipoatrophic diabetes (LD). Cells from three patients and four controls were compared for confluent density, receptor saturation, specific and non-specific binding and the concentration of unlabelled hormone producing 50% competition for binding with labelled ligand. Cells from patients with LD did not differ significantly in any of these characteristics from the controls. These findings indicate that there is not a basic defect in insulin receptors of LD patients. A secondary disruption of binding, e.g. by a circulating factor, remains possible.
A regional diabetes program for children and youth comprising outreach clinics, frequent routine and emergency telephone contact, and a camping program was developed within the State Children's Medical Services (Crippled Children's) Program. The pediatric nurse specialist in diabetes served as the pivotal professional in the education and supervision of patients. Cost benefit was calculated from estimated hospital days prevented based on average length of admissions at diagnosis (14 days) and hospital days in the year prior to referral of those with established diabetes. During the first year 369 hospital days were prevented, for an estimated savings of $65,000; the second year 547 hospital days were avoided, a value of $96,000. Total annual program costs to the state and private patients (including camp fees) were $36,000. Although hospital costs are an apparent and useful reference to justify funding, the main value of the program must be in the prevention of secondary physical and emotional disability. This requires continuous commitment and availability of persons who know the patient and family, who can interpret information related to metabolic control of diabetes, and who are able to influence the family and community to respond appropriately to the youngster's needs.
Explore the source record for details and available documents.
Specific and nonspecific [125I]insulin binding and concentration of unlabeled hormone producing 50 percent competition with 1.0 nanomolar [125I]insulin for specific binding sites correlated positively with age of fibroblast donors. Cells from four children with precocious aging--three with progeria and one with Rothmund syndrome-resembled those from the chronologically old.
Clinical and laboratory evaluations are reported on two patients with congenital goiter and hypothyroidism due to iodide organification defect. In one patient, a 31-year-old white male with severe mental retardation, administration of perchlorate caused discharge of 69% of the radioiodine accumulated in the thyroid gland. Thyroid tissue had negligible peroxidase activity in the tyrosine-iodinase, triliodide, and guaiacol assays. Preincubation of subcellular fractions with hematin restored activity. The restored enzyme was labile to high concentrations of H2O2 (5.6times 10-4 h2o2 produced inhibition in the triiodide assay). Heating of the enzyme for 5 min at 46 degrees C produced 50% inactivation, while higher temperatures were required to half-inactivate normal peroxidases. This case represents a second example of the "peroxidase apoenzyme-prosthetic group defect" causing congenital goiter. The second patient, an example of the "deficient peroxidase defect," was a 10-yr-old girl with 35% discharge of thyroidal radioiodine by perchlorate. Peroxidase activity in the goiter tissue was quantitatively decreased (10%-20% of normal values) but kinetically normal with respect to apparent Km for H2O2. Hematin had little effect on the enzyme. Peroxidase activity had abnormal subcellular distribution, since pellets sedimenting between 39,000 and 105,000 g contained most of the activity. Normal thyroglobulin was observed in the thyroid gland of the patient. Two distinct defects of the peroxidase system can produce congenital goiter by limiting organification of iodide.
Explore the source record for details and available documents.