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To the authors' knowledge, the frequency and clinical impact of errors in the anatomic pathology diagnosis of cancer have been poorly characterized to date.The authors examined errors in patients who underwent anatomic pathology tests to determine the presence or absence of cancer or precancerous lesions in four hospitals. They analyzed 1 year of retrospective errors detected through a standardized cytologic–histologic correlation process (in which patient same‐site cytologic and histologic specimens were compared). Medical record reviews were performed to determine patient outcomes. The authors also measured the institutional frequency, cause (i.e., pathologist interpretation or sampling), and clinical impact of diagnostic cancer errors.The frequency of errors in cancer diagnosis was found to be dependent on the institution (P < 0.001) and ranged from 1.79–9.42% and from 4.87–11.8% of all correlated gynecologic and nongynecologic cases, respectively. A statistically significant association was found between institution and error cause (P < 0.001); the cause of errors resulting from pathologic misinterpretation ranged from 5.0–50.7% (the remainder were due to clinical sampling). A statistically significant association was found between institution and assignment of the clinical impact of error (P < 0.001); the aggregated data demonstrated that for gynecologic and nongynecologic errors, 45% and 39%, respectively, were associated with harm. The pairwise kappa statistic for interobserver agreement on cause of error ranged from 0.118–0.737.Errors in cancer diagnosis are reported to occur in up to 11.8% of all reviewed cytologic‐histologic specimen pairs. To the authors' knowledge, little agreement exists regarding whether pathology errors are secondary to misinterpretation or poor clinical sampling of tissues and whether pathology errors result in serious harm. Cancer 2005. © 2005 American Cancer Society.

Examination of the urine plays a vital role in the diagnosis of kidney diseases. Proteinuria is an important indicator of renal disease, and the types of proteins found in the urine help distinguish glomerular and tubular disorders. The findings of casts and blood cells in the urine provide valuable clues about the causes of the underlying renal pathology. Crystals may be found in the urine of healthy individuals and in patients with urolithiasis, toxic damage, and chronic renal failure.

Thrombotic thrombocytopenic purpura (TTP) is an uncommon disorder characterized by a pentad of microangiopathic hemolytic anemia, thrombocytopenia, renal dysfunction, fever, and a fluctuating neurologic syndrome. Splenectomy is performed for patients who are refractory to plasma therapy and for relapsing TTP. We describe a case of a patient who died due to intramyocardial hemorrhage after undergoing laparoscopic splenectomy for TTP resistant to treatment with plasmapheresis. A 52-year-old woman was admitted with ecchymoses, low platelet count, weakness of left face and upper extremity, and a presumptive diagnosis of TTP. Vital signs were stable. White blood count was 7800μL, hemoglobin 7.9 gdL, and platelet count of 13,000μL. Her basic metabolic panel and liver function tests were normal. Further laboratory workup confirmed the diagnosis of TTP. The patient was initially treated with plasmapheresis and high dose steroid therapy but underwent an emergent laparoscopic splenectomy due to refractory TTP. At the end of the uneventful procedure, the patient suffered a cardiac arrest and died. Autopsy concluded that the death was from myocardial failure due to extensive myocardial hemorrhage secondary to TTP. There are several published case reports of sudden death due to cardiac involvement in TTP. However, intraoperative mortality is not reported. We conclude that TTP-related acute heart failure may represent an extremely important clinical risk in these patients who are undergoing surgery.

The nature of the brain as an mmunologically privileged site is controversial. Using congenic rats, we have demonstrated that grafts that differ from the recipient in the Alocus of the MHC produce sensitization following intracerebral transplantation, thus indicating that the brain is not immunologically privileged. The IC grafts show histologic signs of rejection, which are delayed compared with the changes found in the subsequent orthotopic grafts, suggesting that the immune response is weaker in the brain.

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