Comparison of oral glucose tolerance tests and mixed meals in patients with apparent idiopathic postabsorptive hypoglycemia: absence of hypoglycemia after meals.

The relationship between symptoms of idiopathic postabsorptive hypoglycemia and glucose homeostasis was evaluated by giving oral glucose tolerance tests (OGTT) and mixed meals to 18 patients and 16 controls. Chemical hypoglycemia after OGTT occurred as often in patients referred because of possible hypoglycemia symptoms, 18 out of 80 (23%), as in controls, 4 out of 16 (25%). After glucose, patients showed both clinical and chemical hypoglycemia (mean +/- SE plasma glucose, 48 +/- 3 mg/dl), but insulin, glucagon, and growth hormone responses were similar to controls. After mixed meals, no chemical hypoglycemia occurred in patients (mean plasma glucose, 79 +/- 3 mg/dl), yet 14 out of 18 (78%) had symptoms and/or signs consistent with hypoglycemia. No abnormality of glucose homeostasis was observed after meals that could account for symptoms or signs experienced by patients with idiopathic postabsorptive hypoglycemia. Since factors other than hypoglycemia appear to be involved, the disorder should be termed the idiopathic postprandial syndrome to avoid the connotation of chemical hypoglycemia.

Radioiodine-induced thyroid storm. Case report and literature review.

Thyroid storm developed following radioiodine therapy in a 43-year-old man with Graves' disease, weight loss, myopathy, severe thyrotoxic hypercalcemia, and a pituitary adenoma. The hypercalcemia may have been a significant, and previously unreported, predisposing factor for the radioiodine-associated thyroid storm. This case and 15 other well-documented cases of radioiodine-associated storm found in the literature are reviewed, as are several other cases of less severe exacerbations of thyrotoxicosis associated with radioiodine therapy. Although not often seen, these complications are often fatal. High-risk patients, such as the elderly, those with severe thyrotoxicosis, and those with significant underlying diseases, may benefit from preventive measures such as the judicious use of thyrostatic medications during the periods before and after isotope administration.

Serum thyroglobulin levels predict total body iodine scan findings in patients with treated well-differentiated thyroid carcinoma.

Forty-eight consecutive patients with treated thyroid carcinoma were studied with 131-I total body scans and serum thyroglobulin (hTg) levels. Serum hTg levels during thyroxine treatment accurately predicted scan results (chi square = 18.6, p < 0.001). All patients with negative scans (24 patients) had serum hTg levels (< 7 ng/ml whereas in patients with metastatic thyroid cancer (eight patients) they ranged from 11 to 690 ng/ml. In patients with iodine uptake confined to the thyroid bed (16 patients) serum hTg values ranged from 2 to 17 ng/ml. Serum hTg levels rose in patients with negative scans during hypothyroidism or after exogenous TSH suggesting that hTg levels are more sensitive than iodine scans in detecting residual thyroid tissue. Serum hTg levels could replace total body iodine scans in many patients with treated thyroid carcinoma.

Hyperthyroidism following hypothyroidism.

Two patients are presented who developed autonomous thyrotoxicosis following a diagnosis of primary hypothyroidism. In one of these patients, antibodies to the TSH receptor were typical of Graves' disease when measured as thyrotropin binding inhibitor immunoglobulins (TBII) and as human thyroid adenylate cyclase stimulating (HTACS) activity, while a needle biopsy of the thyroid gland was consistent with lymphocytic thyroiditis. Twenty-one other reported cases of this unusual sequence found in the literature are reviewed. This occurrence is more common than is generally appreciated.

Immune islet killing mechanisms associated with insulin-dependent diabetes: in vitro expression of cellular and antibody-mediated islet cell cytotoxicity in humans.

Because immune mechanisms are associated with insulin-dependent diabetes, multiple organ specific and xenogeneic cytotoxicity assays were developed. Human cellular and antibody effector systems were incubated with 51Cr-labeled dispersed normal rat islet target cells. In eight of 11 diabetic patients, nonenriched mononuclear cells incubated with islet target cells were more cytotoxic than cells from age- and sex-matched controls (p less than 0.01). When non-T cell-enriched mononuclear cells were used at diabetes onset, seven of 11 patients' cells showed excessive islet cytotoxicity (p less than 0.05). In four patients showing elevated cytotoxicity at diabetes onset, cytotoxicity decreased to control levels during diabetes remission. Islet specificity was suggested in that mononuclear cells derived from diabetic subjects did not mediate cytotoxicity against rat spleen or macrophage target cells. Three cytotoxic antibody mechanisms were also evaluated. C-dependent antibody-mediated cytotoxicity with the use of patient serum-coated islet target cells was elevated above control levels in four of 14 patients. Antibody-dependent cellular cytotoxicity exceeded control values in only two of 16 patients, although four assay systems were evaluated. C-augmented antibody-dependent cellular cytotoxicity was elevated in three of 14 patients. No differences were observed for antibody-mediated mechanisms in four patients evaluated at both diabetes onset and remission. Cytotoxic antibody was present in only about one-half of the patients showing increased cellular cytotoxicity, whereas most patients expressing increased cytotoxic antibody had cellular cytotoxicity. Islet cell cytotoxicity assays with the use of effector systems from patients with recent onset insulin-dependent diabetes suggest that direct cellular cytotoxicity is more active than antibody-mediated cytotoxic mechanisms, and that cellular cytotoxicity can correlate with disease activity.

Mechanisms of rat pancreatic islet allograft rejection.

Since the mechanisms of rat islet allograft rejection are unknown, metabolic, histologic, and immunologic parameters were characterized during rejection. Syngeneic intraportal islet transplants in diabetic Lewis rats normalize glucose values without islet cellular infiltrates; after Wistar-Furth allografts, glucose values rapidly return to diabetic levels and infiltration of islets by mononuclear cells occurs. Using lymphocyte proliferative assays, allogeneic islets induce a 3-fold stimulation of lymphocytes derived from nondiabetic allograft recipients. Using cytotoxicity assays, cell-mediated cytotoxicity of allogeneic islet target cells although inefficient is 2-fold greater in diabetic allograft recipients than in syngeneic recipients. Antibody-dependent cellular cytotoxicity is not observed, whereas 14 days after allotransplantation, complement-dependent antibody-mediated cytotoxicity is elevated. These data suggest that islet allograft rejection using metabolic, histopathologic and immunologic methods is associated primarily with cell-mediated cytotoxicity related to histocompatibility antigens.