Citations

AbstractThe collective term “pancreatic cancer” should be replaced by more specific terminology indicating the histological subtype, e.g., pancreatic ductal adenocarcinoma, ampullary adenocarcinoma, duodenal carcinoma, pancreatic cystadenocarcinoma, cholangiocarcinoma, and malignant islet cell carcinoma. Each of these tumors has its own inherent prognostic and therapeutic characteristics‐95% of ampullary lesions being resectable in contrast to ±10% of pancreatic ductal malignancies and comparable 5‐year survival figures for these two subtypes are 40% and 5%, respectively.Since the results of adjuvant therapy (chemo‐ and/or radiotherapy) have been dismal, the only chance of cure remains resective therapy, either by the performance of a total or subtotal pancreatectomy (Whipple procedure). The operative mortality rate for these procedures at our institution has been 12% and 4%, respectively, with corresponding 5‐year survival rates of 2% and 4%. Despite earlier promise that total pancreatectomy only would be a superior procedure (elimination of the pancreatojejunal anastomosis, wider lymphadenectomy, irradication of multicentric disease), the operation has thus far not fulfilled these expectations.The Whipple procedure remains the resective procedure of choice at our institution—total pancreatectomy being performed principally in those patients in whom a safe pancreatojejunal anastomosis cannot be constructed.Value of early diagnosis in patients with ductal adenocarcinoma does not appear to imply improved prognosis. Energies should be diverted toward etiological identification of this lethal malignancy which is steadily increasing in incidence.

AbstractUltrasound and computed tomography have had an enormous impact on the imaging procedures used in the detection of tumors of the parathyroids, pancreas, and adrenals. Ultrasound is now the examination of choice in localizing parathyroid adenomas in the neck prior to cervical exploration or after unsuccessful exploration. Its role as a screening test in patients without biochemical confirmation of hyperparathyroidism awaits further study. Computed tomography is useful in identifying mediastinal parathyroid adenomas in patients who have had unsuccessful neck explorations and islet‐cell tumors of the pancreas if they are sufficiently large (greater than 2 cm). Angiography remains the most accurate method of localizing insulinomas prior to surgery. Computed tomography scanning has become the procedure of choice in localizing adrenal tumors and has sufficient sensitivity to be used as a screening test in patients without biochemical confirmation of an adrenal abnormality.

AbstractSymptomatic hypercalcemia is a medical emergency. Knowledge of the alteration in the factors that control normal calcium homeostasis permits selection of a plan of treatment, which includes general supportive measures along with therapeutic agents directed at the specific alteration in calcium homeostasis. The rationale for the selection of various modes of treatment and treatment schedules and the untoward side effects of the therapeutic agents are reviewed.Acutely developing hypocalcemia often requires emergency treatment. Relief of symptoms can be achieved with intravenous calcium preparations. Knowledge of the underlying cause permits selection of appropriate medications when long‐term treatment is required. When vitamin D is needed, measurement of serum calcium and phosphate at regular intervals is essential. Hypoparathyroidism may be temporary after thyroid or parathyroid surgery, and efforts should be made 6 to 12 months after operation to determine whether the abnormality is permanent.

AbstractSuccessful therapy for pituitary apoplexy depends on prompt recognition of the clinical syndrome, accurate anatomic evaluation of the lesion with the CT scan, intensive steroid replacement therapy, and effective transphenoidal decompression of the tumor. Successful long‐term management of patients who have suffered pituitary apoplexy requires recognition by the complex interrelationships of the pituitary with adrenal, thyroid, gonadal, pancreatic, and gut physiology. Such patients often require multiple medications for replacement therapy. Surgical treatment is often supplemented with radiation therapy, and prolactin‐ and growth hormone‐secreting adenomas may require long‐term management with bromocriptine. Careful follow‐up evaluations and appropriate post‐surgical therapy enable most of these patients to live normal lives.

Abstract The ability to differentiate benign from malignant Hürthle cell thyroid neoplasms has provoked considerable controversy. This has significant therapeutic implications, since some have advocated total thyroidectomy for all of these lesions. The principal objectives of this study were: (a) to determine whether the histologic diagnosis of Hürthle cell adenoma could be reliably made, (b) to quantitate the risk of inappropriately labelling a Hürthle cell cancer as an adenoma, and (c) to ascertain whether the type of operative procedure affected the clinical course . We reviewed 272 patients who had undergone thyroid resection for benign Hürthle cell neoplasms at the Mayo Clinic from 1960 to 1980. All pathologic sections were rereviewed. Postoperative follow‐up was available on 233 patients (86%), with a mean of 8.9 years. A minimum of 5 years of follow‐up was obtained on 10% of the patients. Nodules ranged in size from 0.3 to 11 cm; 195 (55%) were 2 cm or larger. Surgical resection was limited to one side in 137 (50%) patients and involved both sides in 135 patients. No total thyroidectomies were performed. Evidence of malignancy—a local recurrence—developed in only 1 patient, and she died of unrelated causes. None of the 272 patients died of thyroid cancer, and none showed evidence of metastases. Our data is in agreement with most published reports, with only 6 (0.9%) of 642 reported patients being diagnosed incorrectly. These tumors can be accurately separated into benign and malignant. Routine total thyroidectomy for Hürthle cell adenomas is not justified .

Healthy older men manifest concomitant hypoandrogenemia and attenuation of LH pulse size. Because exogenous GnRH remains effective, a plausible intuition is that aging reduces hypothalamic GnRH secretion, thus mediating relative hypogonadotropic hypogonadism. To assess the impact of age on central GnRH outflow indirectly, we quantitated graded suppression of pulsatile LH secretion by saline and escalating doses of a potent and selective GnRH-receptor antagonist, ganirelix, in 18 healthy men ages 23–72 yr. The rationale is that ganirelix should reduce the amplitude of LH pulses in proportion to both drug concentration and endogenous GnRH feedforward. To this end, blood was sampled every 10 min for 2 h before and 16 h after sc administration of saline or ganirelix and for 3 additional hours after iv injection of a fixed dose of GnRH (100 ng/kg); concentrations of LH and ganirelix were measured by immunochemiluminometry and RIA, respectively; and pulsatile LH secretion was quantitated by a deconvolution procedure. Log-linear regression analysis was used to estimate the sensitivity of pulsatile LH secretion to inhibition by a unit increase in serum ganirelix concentrations in each subject. Statistical analyses revealed that increasing age markedly attenuated the capability of ganirelix to decrease LH pulse size (viz., r = −0.648; P = 0.004). In contrast, age did not modify the competitive interaction between injected GnRH and ganirelix. These joint outcomes support the clinical hypothesis that age diminishes hypothalamic GnRH outflow without impairing GnRH action in healthy men.

The present study tests the clinical postulate that elevated testosterone (Te) and estradiol (E2) concentrations modulate the effects of constant iv infusion of saline vs. recombinant human IGF-I on free IGF-I, IGF binding protein (IGFBP)-1, and dimeric IGF-I/IGFBP-1 concentrations in healthy aging adults. To this end, comparisons were made after administration of placebo (Pl) vs. Te in eight older men (aged 61 ± 4 yr) and after Pl vs. E2 in eight postmenopausal women (62 ± 3 yr). In the saline session, E2 lowered and Te increased total IGF-I; E2 specifically elevated IGFBP-1 by 1.5-fold and suppressed free IGF-I by 34%; and E2 increased binary IGF-I/IGFBP-1 by 5-fold more than Te. During IGF-I infusion, the following were found: 1) total and free IGF-I rose 1.4- to 2.0-fold (Pl) and 2.1–2.5-fold (Te) more rapidly in men than women; 2) binary IGF-I/IGFBP-1 increased 3.4-fold more rapidly in men (Te) than women (E2); and 3) end-infusion free IGF-I was 1.6-fold higher in men than women. In summary, E2, compared with Te supplementation, lowers concentrations of total and ultrafiltratably free IGF-I and elevates those of IGFBP-1 and binary IGF-I/IGFBP-1, thus putatively limiting IGF-I bioavailability. If free IGF-I mediates certain biological actions, then exogenous Te and E2 may modulate the tissue effects of total IGF-I concentrations unequally.