Patients with HIV/AIDS: physicians' knowledge, attitudes, and referral practices.

BACKGROUND: This study investigated Massachusetts family physicians' current care and referral practices with respect to HIV/AIDS patients and examined actors that might influence family physicians in referring these patients to specialists. Educational opportunities for physicians with regard to HIV were also examined. METHODS: In 1994, a 2-page survey was mailed to the 468 members of the Massachusetts Academy of Family Physicians. The survey questionnaire examined such factors as whether the respondents were teaching or nonteaching, rural or urban; number of years since medical school or residency training; and knowledge and attitudes with regard to HIV/AIDS patients. The data were analyzed using Student's t test, chi-square, and correlation analysis. RESULTS: Usable responses were returned by 281 (60%) of the physicians surveyed. Of these, 65% reported having HIV patients in their practice, and 46% reported having AIDS patients was being managed alone by 53% of these physicians, and 11% managed their patients with AIDS. Physicians providing care for HIV/AIDS patients were more likely to be practicing in urban locations, have three or more HIV/AIDS patients in their practice, or recently graduated from residency. Additionally, they were more likely to be involved in residency teaching programs. Those who did not care for HIV/AIDS patients felt less knowledgeable about HIV/AIDS care, and felt that they had no time in their practice to care for this population of patients. Physicians with HIV patients learn more about HIV care from their colleagues than those without HIV patients. CONCLUSIONS: Family physicians are increasingly seeing HIV/AIDS patients in their offices. The majority are continually caring for these patients, either by themselves or co-managing their care with a specialist. Local CME programs relying on colleagues and community resources to discuss management of these patients may be one of the best ways of ensuring that increasing numbers of family physicians obtain the appropriate knowledge to care for these patients within their own communities.

Depression of serum calcium by increased plasma free fatty acids in the rat: a mechanism for hypocalcemia in acute pancreatitis.

Some patients with hypertriglyceridemia and acute pancreatitis have marked hypocalcemia and high levels of plasma free fatty acids (FFAs). This study tests the hypothesis that increased plasma FFAs can significantly reduce the calcium level in vivo, a phenomenon which is different from local formation of calcium soaps due to lipolysis of adipose tissue lipids. Free fatty acid elevation was induced in rats by the administration of heparin and by the infusion of triglycerides. The results show that, compared with controls, induction of elevated FFA (from 1.57 +/- 0.08 mEq/L to 5.64 +/- 0.35, mean +/- SEM) causes the concentration of calcium to fall rapidly (from 9.04 +/- 0.06 mg/dl to 8.42 +/- 0.10, p less than 0.001). There is a significant (p less than 0.001) positive correlation between spontaneous baseline concentration of FFA and the responsiveness of calcium concentration to FFA challenge. At near-normal levels of FFA there is a significant (p less than 0.001) correlation between the magnitude of increased FFA concentration and decreased calcium concentration. Additional studies in vivo and in vitro show that elevated plasma triglycerides per se did not interfere with measurement of calcium concentration; however, FFA-albumin complexes bind calcium and lower its measured value. These findings suggest that (a) changes in the concentration of FFA occurring spontaneously may affect measured serum calcium concentration; (b) the observed depression of serum calcium concentration may be due in part to intravascular sequestration of calcium by FFA, but increased flux of circulating calcium-FFA complexes into extravascular and intracellular sites may also be important; (c) the markedly increased FFA concentration in some patients with acute pancreatitis may contribute significantly to hypocalcemia and calcium flux in these patients. As parathyroid hormone secretion, function, or integrity may be impaired in pancreatitis, the depressant effect of FFA could be even greater in that disease than in this model.

Release of ribonuclease from anoxic pancreas.

Poly-[C]-specific ribonuclease (RNase) is released in large amounts from rat pancreas incubated at 37 degrees C in isotonic saline solution. Pancreatic cell disruption by homogenization releases only 10% of that RNase. The remainder, perhaps membrane-bound, is freed only after further membrane deterioration during anoxic incubation. Other tissues (small intestine, stomach, colon, liver, spleen, kidney, muscle, and skin) do not appear to contain much of this RNase or to release it during anoxic incubation. Relatively little amylase is released from the pancreas under the conditions that release RNase. The findings provide a rational basis for monitoring serum RNase levels in patients with acute pancreatitis for early detection and treatment of pancreatic necrosis in man.