Hospitalisation and morbidity due to adverse drug reactions in elderly patients: a single-centre study.

BACKGROUND: Adverse drug reaction (ADR) is a leading but under-recognised cause of illness, particularly in frail subjects with multiple comorbidities. AIM: To investigate the frequency, patterns and outcomes of ADR as a cause of hospitalisation in elderly patients admitted to an internal medicine ward. METHODS: We performed a retrospective observational study including every patient aged over 65 years who was admitted to our department during a 12-month period. Patients admitted to short-stay (<24 h) observation unit were excluded. RESULTS: ADR accounted for 106 of total 1750 recorded admissions, which constituted a proportion of 6.1% (95% confidence interval 5.0-7.3%). The median age of patients was 83.5 (78.0-87.0) years and 56.6% were on polypharmacy. A total of 170 ADR was recorded with 45.3% of subjects experiencing concomitantly more than one ADR from a single molecule. Diuretics were the most commonly imputed molecules (30 events, 17.6%), followed by antithrombotics (25 events, 14.7%) and central nervous system-active drugs (16 events, 9.4%). Interactions were judged responsible for 39 cases of ADR (36.8%). An unfavourable outcome was observed in about one-third of patients (37.7%). Among those subjects, 11 (10.4%) died and 29 (27.4%) had residual disability. CONCLUSION: ADR are a common cause of hospital admission in elderly patients and are often associated with adverse outcomes. Our data underline the need of appropriate strategies aimed at identifying high-risk patients and avoiding potentially preventable drug toxicities.

Glucoreceptors located in the brain mediate NPY release induced by hypoglycemia in normal men.

The NPY secretory pattern after an insulin tolerance test (ITT) (0.15 IU/kg body weight) was evaluated in 8 normal men. They were infused with normal saline (control test), glucose or fructose. Insulin-induced hypoglycemia produced a significant increment in serum NPY in the control test. The infusion of fructose was unable to change the NPY secretory pattern during insulin-induced hypoglycemia. In contrast, the NPY increase during ITT was completely abolished when the concomitant infusion of glucose prevented insulin-induced hypoglycemia. These results exclude a direct role of hyperinsulinemia in the mechanism underlying the stimulation of NPY secretion during ITT. Furthermore, since glucose but not fructose crosses the blood-brain-barrier (BBB), the NPY increase during ITT appears to be generated by low glucose concentrations at the level of glucosensitive areas located inside the brain.

Naloxone decreases the inhibitory effect of somatostatin on GH release induced by cigarette smoking in man.

To establish whether somatostatin (SRIH) exerts its inhibitory effect on the nicotine-induced release of GH by interacting with an opioid pathway, normal volunteers were treated with naloxone during (2 no-filter) cigarettes smoking and with SRIH. Nicotine significantly increased serum GH levels about 3.5 fold. Naloxone alone did not change GH rise induced by cigarette smoking. The stimulatory effect of GH by nicotine was completely blocked by SRIH. In the presence of both SRIH and naloxone, GH levels rose 1.5 fold in response to nicotine. Since naloxone only partially reversed the inhibiting action of SRIH, only a partial involvement of opioid peptides in SRIH action might be supposed. Alternatively, SRIH and naloxone-sensitive opiates might produce this inhibiting effect on GH rise in response to cigarette smoking through independent pathways.

Marked sinus bradycardia and QT prolongation in a diabetic patient with severe hypoglycemia.

We report an uncommon case of an insulin-treated diabetic patient, presenting severe hypoglycemia, coma, marked sinus bradycardia and QT prolongation. Intravenous administration of glucose and atropine awaked the patient and increased heart rate but did not affect QT prolongation. Basal and exercise electrocardiogram excluded primary diseases associated with QT prolongation. Pathophysiologic aspects of electrocardiographic and clinical findings occurring in the hypoglycemic patients are briefly discussed.

Estradiol and metabolic syndrome in older italian men: The InCHIANTI Study.

The increasing prevalence of metabolic syndrome (MS) with age in older men has been linked with decreasing testosterone levels. Interestingly, while testosterone levels decline with age, estradiol (E2) levels remain relatively stable, resulting in a decreased testosterone:E2 ratio. Because E2 levels tend to be elevated in morbid obesity, insulin resistance, and diabetes, it is reasonable to hypothesize that high E2 levels are associated with MS in older men. We studied the relationship of total and free E2 with MS after adjustment for multiple confounders, including age, BMI, smoking, alcohol consumption, physical activity, interleukin-6 (IL-6), fasting insulin, and testosterone. Men 65 years or older (age range, 65-96; n = 452) had complete data on E2, testosterone, fasting insulin, sex hormone-binding globulin, IL-6, and albumin. Concentrations of free E2 and free testosterone were calculated using the mass action equations. MS was defined according to Adult Treatment Panel III (ATP-III). Participants with MS had significantly higher serum free and total E2 (P < .001) (P = .003). After adjusting for confounders, including age, smoking, alcohol consumption, physical activity, log(IL-6), and log(insulin), participants with higher log(total E2) (odds ratio [OR], 2.31; 95% confidence interval [95% CI], 1.39-4.70; P = .02) and higher log(free E2) (OR, 2.69; 1.38-5.24; P < .001) had an increased risk of having MS. Log(free E2) (P = .04) maintained significant correlation with MS, even after further adjustment for BMI. In older men, high E2 is independently associated with MS. Whether confirmed in other studies, assessment of E2 should be also considered in older men. Whether changes in this hormonal pattern play a role in the development of MS should be further tested in longitudinal studies.