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Biomedical subjects

Paul L Fine

Publications and source records attributed to Paul L Fine.

5 recordsLinked to original sources
PubMed2005

Do physicians know when their diagnoses are correct? Implications for decision support and error reduction.

OBJECTIVE: This study explores the alignment between physicians' confidence in their diagnoses and the "correctness" of these diagnoses, as a function of clinical experience, and whether subjects were prone to over-or underconfidence. DESIGN: Prospective, counterbalanced experimental design. SETTING: Laboratory study conducted under controlled conditions at three academic medical centers. PARTICIPANTS: Seventy-two senior medical students, 72 senior medical residents, and 72 faculty internists. INTERVENTION: We created highly detailed, 2-to 4-page synopses of 36 diagnostically challenging medical cases, each with a definitive correct diagnosis. Subjects generated a differential diagnosis for each of 9 assigned cases, and indicated their level of confidence in each diagnosis. MEASUREMENTS AND MAIN RESULTS: A differential was considered "correct" if the clinically true diagnosis was listed in that subject's hypothesis list. To assess confidence, subjects rated the likelihood that they would, at the time they generated the differential, seek assistance in reaching a diagnosis. Subjects' confidence and correctness were "mildly" aligned (kappa=.314 for all subjects, .285 for faculty, .227 for residents, and .349 for students). Residents were overconfident in 41% of cases where their confidence and correctness were not aligned, whereas faculty were overconfident in 36% of such cases and students in 25%. CONCLUSIONS: Even experienced clinicians may be unaware of the correctness of their diagnoses at the time they make them. Medical decision support systems, and other interventions designed to reduce medical errors, cannot rely exclusively on clinicians' perceptions of their needs for such support.

Clinical Competence↗
PubMed2003

Toxic acute tubular necrosis following treatment with zoledronate (Zometa).

BACKGROUND: Renal failure and toxic acute tubular necrosis (ATN) may be seen following exposure to a variety of therapeutic agents. Zoledronate (Zometa) is a new, highly potent bisphosphonate used in the treatment of hypercalcemia of malignancy. We report the first clinical-pathologic study of nephrotoxicity associated with this agent. METHODS: A cohort of six patients (four males and two females) with a mean age of 69.2 years received bisphosphonate therapy for multiple myeloma (five patients) or Paget's disease (one patient). In all patients, zoledronate was administered at a dose of 4 mg intravenously monthly, infused over at least 15 minutes, and the duration of therapy was mean 4.7 months (range, 3 to 9 months). RESULTS: All patients developed renal failure with a rise in serum creatinine from a mean baseline level of 1.4 mg/dL to 3.4 mg/dL. Renal biopsy revealed toxic ATN, characterized by tubular cell degeneration, loss of brush border, and apoptosis. Immunohistochemical staining revealed a marked increase in cell cycle-engaged cells (Ki-67 positive) and derangement in tubular Na+,K+-ATPase expression. Importantly, although all patients had been treated with pamidronate prior to zoledronate, no biopsy exhibited the characteristic pattern of collapsing focal segmental glomerulosclerosis observed in pamidronate nephrotoxicity. Following renal biopsy, treatment with zoledronate was discontinued and all six patients had a subsequent improvement in renal function (mean final serum creatinine, 2.3 mg/dL at 1 to 4 months of follow-up). CONCLUSION: The close temporal relationship between zoledronate administration and the onset of renal failure and the partial recovery of renal function following drug withdrawal strongly implicate this important and widely used agent in the development of toxic ATN.

Aged↗
PubMed2002

Exploring the boundaries of plausibility: empirical study of a key problem in the design of computer-based clinical simulations.

All clinical simulation designers face the problem of identifying the plausible diagnostic and management options to include in their simulation models. This study explores the number of plausible diagnoses that exist for a given case, and how many subjects must work up a case before all plausible diagnoses are identified. Data derive from 144 residents and faculty physicians from 3 medical centers, each of whom worked 9 diagnostically challenging cases selected from a set of 36. Each subject generated up to 6 diagnostic hypotheses for each case, and each hypothesis was rated for plausibility by a clinician panel. Of the 2091 diagnoses generated, 399 (19.1%), an average of 11 per case, were considered plausible by study criteria. The distribution of plausibility ratings was found to be statistically case dependent. Averaged across cases, the final plausible diagnosis was generated by the 28th clinician (sd = 8) who worked the case. The results illustrate the richness and diversity of human cognition and the challenges these pose for creation of realistic simulations in biomedical domains.

Computer Simulation↗
PubMed2001

Collapsing focal segmental glomerulosclerosis following treatment with high-dose pamidronate.

Collapsing focal segmental glomerulosclerosis (FSGS) is a distinct clinicopathologic entity seen most commonly in young African American patients who present with renal insufficiency and nephrotic syndrome. The only epidemiologic factor previously linked to collapsing FSGS is HIV infection. Here clinicopathologic findings are reported for a distinctive population of seven patients, who were older, Caucasian, and HIV negative and developed collapsing FSGS during active treatment of malignancy (multiple myeloma in six patients and metastatic breast carcinoma in one). Although oncologic treatment regimens included vincristine for four patients, doxorubicin for five patients, cisplatin for two patients, and total-body irradiation for one patient, the only agent common to all patients was pamidronate (Aredia). All patients had normal renal function before the administration of pamidronate. Patients began therapy with pamidronate at or below the recommended dose of 90 mg, intravenously, monthly, which was increased to 180 mg monthly in two patients and 360 mg monthly in three patients. Patients received pamidronate for 15 to 48 mo before presentation with renal insufficiency (mean serum creatinine, 3.6 mg/dl) and full nephrotic syndrome (mean 24-h urinary protein excretion, 12.4 g/d). Pamidronate, which is a member of the class of bisphosphonates, is widely used in the treatment of hypercalcemia of malignancy and osteolytic metastases. At the recommended dose of 90 mg, intravenously, monthly, renal toxicity is infrequent; however, higher doses have produced nephrotoxicity in animal models. The temporal association between pamidronate therapy and the development of renal insufficiency, the use of escalating doses that exceed recommended levels, and the distinctive pattern of glomerular and tubular injury strongly suggest a mechanism of drug-associated podocyte and tubular toxicity. These data provide the first association of collapsing FSGS with toxicity to a therapeutic agent.

Aged↗