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Protein-calorie malnutrition, common among the elderly, often escapes recognition. This article reviews some of the etiologic factors and the clinical manifestations. Ways to assess and prevent protein-calorie malnutrition are also discussed.

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In order to understand better the causes of diminished delayed hypersensitivity in the elderly, we studied lymphocyte function in 10 healthy subjects over 80 years of age. Markedly decreased antigen-stimulated lymphokine production (3 of 30 assays positive versus 24 of 31 in young control subjects) was the most significant finding in the elderly subjects and appeared to be the best explanation for their reduced cutaneous responses to recall antigens. Although mitogen-stimulated lymphocyte transformation in the elderly group was more sensitive to suppression by prostaglandin E2 than that of the young group, direct prostaglandin action did not appear to explain the diminished antigen-stimulated lymphokine responses. The nonspecific mitogen concanavalin A elicited normal lymphokine responses in 9 of 10 elderly subjects, indicating that lymphocytes from the elderly have a normal capacity for lymphokine production when activated by a sufficient stimulus. Therefore, diminished delayed hypersensitivity in aged humans may be related to deficient lymphokine production, which in turn appears to involve a decreased capacity of the lymphocytes producing these mediators to undergo activation by recall antigens.

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Genetically obese hyperglycemic mice (ob/ob) were compared with their nonlittermate lean controls at 4-5 months of age with regard to brain serotonin, pituitary ACTH content, and circulating levels of glucose, glucagon, insulin, TSH, T3, T4, total tryptophan and free tryptophan. Brain serotonin pituitary ACTH content, and plasma insulin, glucose, total tryptophan, and free tryptophan were all significantly higher in obese mice than in the controls. TSH, T3, and T4 were not significantly different in obese mice vs. controls, suggesting that the obese mouse is euthyroid. Fasting improved but failed to normalize the glucose and insulin levels or insulin to glucagon ratios. Since serotonin is an important neurotransmitter with regard to hypothalamic-pituitary function and since its levels in the brain are dependent on the availability of tryptophan, the findings of elevated levels of free tryptophan in the plasma and serotonin in the brain of the obese hyperglycemic mouse may help to explain some of the previously observed abnormalities of pituitary hormone secretion in these animals.

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Of 1,825 subjects with a history of head or neck irradiation, 358 (19.6%) were found to have thyroid abnormalities. One hundred sixty-five (9%) had either single or multiple nodules 153 (8.4%) had diffuse thyromegaly, and 40 (2.2%) had had thyroid surgery. Surgery was performed on 113 subjects with nodules; carcinoma was found in 34 (30.1%). Clinical examination of the neck was the most valuable method of detecting abnormalities. Detection of nodules was not significantly enhanced by routine use of thyroid imaging studies. Measurements of levels of serum thyroid-stimulating hormone, thyroxine, triidothyronine resin uptake, and thyroid antibodies were not useful in screening for nodules or carcinoma.

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A 33 year old man presented with symptoms of one week's duration; he had a serum calcium of 22.5 mg/dl and a markedly hypercellular bone marrow. Despite therapy with saline diuresis, furosemide mithramycin, total parathyroidectomy and corticosteroids, symptomatic hypercalcemia was poorly controlled. Inappropriate serum parathyroid hormone (PTH) levels were found before and after parathyroidectomy whereas assays of the peripheral blood for osteoclast-activating factor and prostaglandin E (PGE2) were negative. An elevated leukocyte alkaline phosphate level, the inability to aspirate marrow, the marked generalized hyperplasia of all hematopoietic marrow elements, the focal accumulations of blastic cells and increasing reticulin fiber formation led to the diagnosis of acute myelofibrosis. A single course of cytosine arabinoside and thioguanine therapy was followed by profound hyperphosphatemia, hypocalcemia and death. The rarity of hypercalcemia with myeloproliferative disorders is documented by a review of the world literature, and the possible mechanism for hypercalcemia in this patient is discussed.

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Plasma from normal human subjects was subjected to a 3-phase methanol extraction. An increase in prolactin release from rat anterior pituitary tissue in vitro obtained with increasing doses of the plasma extract, while no increase in TSH release occurred. Control studies with an extract of simulated plasma using incubation medium with human serum albumin resulted in less release than a comparable plasma extract dose. The plasma extract did not lose activity with heating to 100 degrees C for 10 min, and incubation of normal plasma at 37 degrees C for 4 h prior to methanol extraction resulted in no loss of prolactin releasing activity. The plasma extract was subjected to cascade ultra-filtration through UM-10, UM-2, and UM-0.5 filters with no significant loss of prolactin releasing activity. Finally, the extract contained no TRH immunoreactivity. These results support the existence of a heat stable, ultra-filterable circulating PRF in human plasma. The origin of this material is unknown.

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A rapid radioimmunoassay for TRH with a high degree of specificity and sensitivity is described. The procedure is capable of measuring TRH in amounts less than 15 pg/tube. Such an assay system has enabled us to study the effect of hypoglycemia on hypothalamic TRH content. Forty-eight female, adult Holtzman rats were divided into 8 groups of 6. Regular insulin was injected intraperitoneally into each rat except for the basal group. A separate batch of similar rats was studied in the same fashion except that saline was injected instead of insulin. Each group of rats was decapitated and the trunk blood collected at 0, 15, 30, 45, 60, 90, 120 and 180 min post-injection. Appropriate tissues were rapidly taken and immediately extracted in ice-cold methanol. Hypothalamic TRH, pituitary TSH, serum TSH and serum triiodothyronine (T3) and thyroxine (T4) were serially determined. In the insulin-treated group, a rapid fall in blood sugar was observed reaching a nadir in 15 min. Hypothalamic TRH fell from a basal mean +/- SE value of 3.25 +/- 0.31 ng to 1.54 +/- 0.14 ng/hypothalamus (P less than 0.01). Pituitary TSH decreased from 10.0 +/- 0.9 mug to a low of 2.6 +/- 0,8 mug/pituitary (P less than 0.02) at 30 min postinsulin. Serum TSH increased from a basal level of 42.5 +/- 20.5 muU/mo to a peak of 102.1 +/- 10.0 muU/ml 45 min (P less than 0.05) after insulin administration. The incremental change in serum T3 occurred at 90 min when T3 levels increased from a baseline of 107.5 +/- 53.7 ng/100 ml to a peak of 711.7 +/- 20.2 ng/100 ml (P less than 0.01). No changes in T4 were observed. The control group of rats did not show significant changes in hypothalamic TRH. The results of the study indicate that hypoglycemia can induce depletion (presumably release) of hypothalamic TRH with a consequent cascade stimulation of the pituitary-thyroid axis.

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The effect of insulin-induced hypoglycemia on TSH release was studied in 7 normal subjects (Group I), 5 patients with sellar enlargment, 1 patient with idiopathic panhypopituitarism (Group II-A) and 2 acromegalic patients (Group II-B). Serial measurements of TSH, GH and corrtisol, after a bolus of insulin (0.1 U/kg body weight), were made over a period of 120 min. The peak TSH value of 8.3 plus or minus 0.9 pU/ml (mean plus or minus SEM) did not differ statistically from the basal value of 6.0 plus or minus 1.3 pU/ml in Group I. GH levels, however, increased from 1.0 plus or minus 0.0 ng/ml to 28.1 plus or minus 4.3 ng/ml, which was highly significant (P less than 0.001). In contrast, Group II-A patients had an increase in serum TSH from 4.3 plus or minus 1.4 pU/ml to 28.6 plus or minus5.7 pU/ml (P less than 0.02). The peak GH levels of 4.0 plus or minus 1.7 ng/ml did not differ significantly from the basal value of 1.2 plus or minus ng/ml. In group II-B, the untreated acromegalic patient (G) did not show alterations in TSH levels consonant with the increase in GH from a basal value of 34.9 ng/ml to a peak of 46.9 ng/ml with the induction of hypoglycemia. In the treated acromegalic subject (H), basal GH increased from 7.8 ng/ml to 11.4 ng/ml with no significant changes in TSH. Serum cortisol levels in Groups I, II-A and II-B did not show consistent inverse relationship to circulating TSH. The observations in this study suggest that hypoglycemia may stimulate TSH release in certain pituitary disorders. Through GH release might play an inhibitory role on TSH secretion, the results suggest other unidentified factor(s).

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