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Clinicians recognise nonsteroidal anti-inflammatory drugs (NSAIDs) as valuable first-line agents in the treatment of rheumatic disorders and as dangerous irritants to the gastrointestinal tract. This has led to questions about the economic impact of NSAID-induced gastropathy in populations. This study estimated the 1992 costs of NSAID-associated gastropathy episodes, and calculated an iatrogenic cost factor for NSAID-associated gastropathy among elderly members of a health maintenance organisation (HMO), the Northwest Region of Kaiser Permanente. Using data retrieved from automated databases and from medical records, NSAID and antiulcer drug costs were calculated, and estimates were made of the incidence rates of inpatient and outpatient NSAID-associated gastropathies, the services provided to treat them, and the cost of those services. Kaiser Permanente Northwest spent $US0.35 for each $US1.00 spent on NSAID therapy for the elderly, an iatrogenic cost factor of 1.35. The estimated average treatment per NSAID-associated gastropathy episode was $US2172. The average outpatient pharmacy cost per elderly NSAID user was $US80 and estimated average NSAID-associated treatment cost per elderly NSAID user was $US43. Although the findings were specific to the HMO because of the databases used, the methodology employed and the drug formulary influence on NSAID selection, they show that a substantial amount of resources were used to treat NSAID-induced gastropathies in the elderly, underscoring the risk of prescribing NSAIDs and reinforcing the need for their prudent use in elderly patients.

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Radiologists must consider several factors when asked by a patient to disclose the results of a radiologic examination. This study represents a survey of radiologists' and clinicians' opinions regarding disclosure of information to patients by the radiologist. A clearer understanding of the preferences of radiologists and clinicians may serve to improve communication and enhance cooperation between the two groups, with the ultimate result being improved patient care.

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Biliary leaks are uncommon complications of abdominal surgery. Left untreated, they may result in significant morbidity and mortality. The traditional treatment has been surgical, but several authors have reported successful endoscopic management. We review 77 cases of endoscopically managed postoperative biliary leaks reported in the literature over the past 15 yr. Endoscopic treatment was technically successful in 95% of cases, and resulted in biliary leak healing in 82%. Cystic stump leaks had a better prognosis for healing compared with common bile duct or hepatic duct leaks. We also present two additional cases of postoperative biliary leaks with biloma formation successfully treated with endoscopic stent placement. Our experience lends additional support to endoscopic management as the preferred approach to postoperative biliary leaks.

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Disorders of calcium and parathyroid hormone homeostasis have been reported in subjects with essential hypertension. In many of these studies, dietary intakes of sodium and calcium were not carefully controlled. The present study was designed to compare calcium and parathyroid hormone homeostasis in normal and hypertensive subjects on controlled dietary sodium and calcium intakes and to examine the impact of dietary sodium loading on hemodynamic and metabolic responses to infused calcium. Seven subjects with essential hypertension and seven age-matched and sex-matched controls were studied while consuming a standard diet containing 600 mg of elemental calcium. Each subject was studied while consuming 10, 160, and 510 mEq of sodium per day, before, during, and after a 3-hour calcium infusion (3.75 mg/kg/hr). Before calcium infusion, hypertensive subjects had increased urinary cyclic adenosine 3',5'-monophosphate excretion independent of sodium intake (p less than 0.05). Urinary potassium excretion was greater in normotensive than in hypertensive subjects (p = 0.002). At baseline, dietary sodium intake had no effect on systolic, diastolic, or mean arterial pressure. During calcium infusion, systolic pressure increased in both groups, whereas diastolic pressure increased only when dietary sodium content was high and mean arterial pressure increased only in hypertensive subjects (p = 0.007). Together, these data provide evidence for interactions between dietary sodium intake and the cardiovascular response to calcium. They confirm that hypertensive subjects exhibit enhanced parathyroid gland function even when dietary factors are controlled, and they suggest that these subjects are more sensitive to the cardiovascular effects of short-term calcium infusion.

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The blood pressure of the spontaneously hypertensive rat (SHR) is influenced by the Ca2+ content of its diet. As the SHR's greater dependence on dietary calcium may reflect a defect in intestinal calcium absorption, we measured in vitro unidirectional Ca2+ flux (J) in the duodenum-jejunum (four segments each) of the SHR (n = 6) and the normotensive Wistar-Kyoto rat (WKY; n = 6) by a modified Ussing apparatus. Because of the known and postulated interactions between Ca2+ and Na+ in both intestinal and vascular tissue, we assessed in vivo the influence of a concurrent manipulation of Na+ intake (three levels: 0.25%, 0.45%, and 1.0%) on the blood pressure development of SHRs (n = 35) and WKYs (n = 35), between 6 and 20 wk of age, exposed to three levels of dietary calcium (0.1, 1.0, and 2%). Net calcium flux (Jnet) (mean +/- SEM) was significantly (P less than 0.01) lower in the SHR (-2.8 +/- 6.3 nmol/cm2 X h) than in the WKY (34.6 +/- 8.8 nmol/cm2 X h). The SHR's decreased Jnet resulted from a significantly (P less than 0.03) lower mucosa-to-serosa flux (Jm-s) in the SHR (41.0 +/- 5.6 nmol/cm2 X h) compared with the Jm-s of the WKY (70.1 +/- 9.1 nmol/cm2 X h). Serosa-to-mucosa flux for calcium did not differ between the SHR (43.8 +/- 6.6 nmol/cm2 X h) and the WKY (35.5 +/- 8.0 nmol/cm2 X h). The SHR's decreased (P less than 0.002) Jm-s was confirmed by additional measurements in SHRs and WKYs. Jm-s was 36.2 +/- 3.7 nmol/cm2 X h in the SHRs (n = 11) and 64.4 +/- 6.7 nmol/cm2 X h in the WKYs (n = 9). The provision of an increased dietary Ca2+ (2% by weight) and increased Na+ (1%) to the SHR prevented the emergence of hypertension (P less than 0.001) (mean +/- SEM systolic blood pressure at 20 wk of age; 135 +/- 5 mmHg for the 2% Ca2+, 1% Na+ SHR vs. 164 +/- 2 mmHg for the control diet SHR). Ca2+ (0.1%) and Na+ (0.25%) restriction accelerated the SHR's hypertension (192 +/- 2 mmHg) (P less than 0.001) and was associated with higher pressures in the WKY (146 +/- 4 mmHg in the restricted WKY vs. 134 +/- 4 mmHg in the control WKY). In a parallel group of 24 SHRs and 24 WKYs fed one of three diets (2% Ca2+/1% Na+; 1% Ca2+/0.45% Na+; or 0.1% Ca2+/0.25% Na+), the heart (P < 0.05) and kidney (P = 0.08) weight of the SHRs varied depending on the diet at 20 wk of age. Low Ca2+ and Na+ intake was associated with increased heart weight (1.6+/-0.9 g) compared with the normal diet for SHR (1.51+/-0.07 g). Increased Ca2+ and Na+ intake was associated with a significantly (P = 0.05) lower heart weight in the SHR (1.37+/-0.03 g) and in the WKY (1.35+/-0.06 g) compared with their normal diet controls. These findings show one mechanism for the SHR's depressor response to supplemental dietary Ca2+ and, in part, explain the sodium dependence of calcium's cardiovascular protective effect.

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