Potassium homeostasis in patients receiving prophylactic dose enoxaparin therapy.
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Biomedical subjects
Publications and source records attributed to A Potti.
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BACKGROUND: The aim of this study was to determine the incidence and role of CD117 (c-KIT) overexpression as a predictive/prognostic marker in extensive-stage small-cell lung carcinoma (ESSCLC). We performed a retrospective study on subjects with a biopsy-proven diagnosis of ESSCLC. PATIENTS AND METHODS: A chart review for demographic and clinical data was performed on patients with ESSCLC diagnosed between 1991 and 2001. CD117 overexpression was evaluated using immunohistochemistry (A4052 polyclonal antibody) performed on archival paraffin-embedded specimens. RESULTS: Two hundred and twenty-three patients with ESSCLC were identified, of whom 193 (84 females, 109 males) with a mean age of 68.5 years (range 42-90) had adequate tissue specimens available for CD117 testing. The most commonly presenting symptom was weight loss, seen in 61 patients (31.6%). Of the 193 specimens, 54 (27.9%) showed CD117 overexpression. The median length of survival for CD117-positive patients was 9 months as compared with the CD117-negative population, in whom the survival was 6 months (P = 0.025, Cox proportional hazard method). CONCLUSIONS: CD117 overexpression detected using immunohistochemistry is observed in about a third of patients with ESSCLC and does not have statistically significant prognostic value. However, CD117 may be a potential target for site-specific immunotherapy in ESSCLC. Our findings suggest a role for clinical trials assessing the role of selective tyrosine kinase inhibitor STI-571 (alone or in combination with conventional therapy) in patients with ESSCLC.
Abciximab (c7E3 Fab) inhibits platelet aggregation and is used to prevent complications of percutaneous coronary intervention. Thrombocytopenia is an often-cited complication of abciximab. Pseudothrombocytopenia is due to ethylenediaminetetraacetate (EDTA)-activated platelet agglutination, resulting in a spuriously low platelet count. We have looked at both "true" and pseudothrombocytopenia after infusion of abciximab. Sixty-six patients receiving their first exposure to abciximab after an unstable coronary event/revascularization were eligible. All the patients received a bolus of c7E3 Fab followed by a continuous infusion. Platelets were monitored in all patients at 2, 4, 12, 24, and 48 h, and more frequently if required. The incidence of thrombocytopenia and acute severe thrombocytopenia (platelet count < or =20,000/microl) was evaluated. A peripheral blood smear was performed on all patients showing thrombocytopenia to evaluate for pseudothrombocytopenia. Seventeen (25.6%) developed thrombocytopenia and nine (13.6%) developed acute severe thrombocytopenia. However, 18 of these patients had pseudothrombocytopenia. The onset of true thrombocytopenia was at 4 h after the infusion, while pseudothrombocytopenia occurred at anytime during the first 24 h. Only two (3.03%) patients required platelet transfusions. No life-threatening hemorrhagic complications were recognized. Five of six subjects with true thrombocytopenia had positive laboratory findings of disseminated intravascular coagulation; however, none had an adverse outcome. Acute severe thrombocytopenia was noted to be a relatively benign adverse effect of abciximab. There is an increasing incidence of pseudothrombocytopenia in this subgroup of patients. It would be worthwhile examining a peripheral blood smear or collecting blood for platelet counts in a heparin-coated tube in order to exclude this phenomenon and thereby prevent inappropriate discontinuation of this drug.
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Interleukin-2 (IL-2) acts by increasing the efficiency of the immune system to exert a tumoricidal effect. Although it is well known that immune stimulation with IL-2 plays a role in unmasking autoimmune phenomena such as autoimmune thyroiditis, hematological effects such as anemia and thrombocytopenia are more frequently due to toxic non-immune mechanisms. We describe a patient who developed severe Evans's syndrome [autoimmune hemolytic anemia (AHA) and immune thrombocytopenic purpura (ITP)] secondary to IL-2 therapy. ITP was refractory to multiple treatment modalities including steroids and splenectomy. ITP and AHA were initially managed with intravenous gamma globulin therapy and frequent blood transfusions, respectively. Ultimately, immunosuppressive therapy with cyclophosphamide and chimeric monoclonal anti-CD20 antibody (rituximab) were successful in inducing complete remission of Evans's syndrome.
Patients with CLL have an excess risk of developing second primary malignancies. The etiology of this excess risk is unclear, and has been thought to be related to smoking. HER-2/neu overexpression has evolved as a prognostic/predictive factor in some solid tumors. We reviewed our experience with non-smokers who had CLL and subsequently developed lung carcinoma, in an effort to better understand the clinical course of these patients, and to evaluate the role of HER-2/neu overexpression. We reviewed the records of all patients who had a diagnosis of both CLL and lung carcinoma between 1986 and 2000. HER-2/neu overexpression was estimated by immunohistochemistry (IHC) using the Hercep test (DAKO). An IHC score of 2+ or greater was considered positive. Overall survival was calculated from the date of diagnosis of lung carcinoma by the Kaplan-Meier product limit method. Fourteen non-smokers in whom a diagnosis of CLL was made at least 6 months prior to the diagnosis of lung carcinoma were identified. The median age for diagnosis of CLL in this group was 67 years while that for lung carcinoma was 70 years. The lung carcinomas included 10 non-small cell (NSCLC) and four small cell (SCLC) carcinomas. Nine specimens (six NSCLC and three SCLC) showed HER-2/neu overexpression. Interestingly, 90% of patients with advanced stage cancer (stage IIIB/IV NSCLC or extensive SCLC) overexpressed HER-2/neu. The presence of CLL did not alter outcome in patients with early stage lung cancer. However, after adjustment for age and performance status, patients with advanced stage NSCLC and CLL had a worse than expected outcome. HER-2/neu overexpression (independent of smoking) may be involved in the development/progression of lung cancer in patients with CLL, and has an associated worse outcome. It is appropriate to consider heightened surveillance of CLL patients for lung carcinoma.
OBJECTIVE: To present a case of fluconazole-associated torsade de pointes (TDP) and discuss fluconazole's role in causing TDP. CASE SUMMARY: A 68-year-old white woman with Candida glabrata isolated from a presacral abscess developed TDP eight days after commencing oral fluconazole The patient had no other risk factors for TDP, including coronary artery disease, cardiomyopathy, congestive heart failure, and electrolyte abnormalities There was a temporal association between the initiation of fluconazole and TDP. The TDP resolved when fluconazole was discontinued; however, the patient continued to have premature ventricular contractions and nonsustained ventricular tachycardia (NSVT) until six days after drug cessation DISCUSSION: Use of the Naranjo probability scale indicates a probable relationship between the use of fluconazole and the development of TDP. The possible mechanism is depression of rapidly activating delayed rectifier potassium currents. In our patient, there was no other etiology identified that could explain QT prolongation or TDP The complete disappearance of NSVT and premature ventricular contractions followed by normalization of QT interval after the drug was stopped strongly suggests fluconazole as the etiology. CONCLUSIONS: Clinicians should be aware that fluconazole, even at low doses, may cause prolongation of the QT interval, leading to TDP. Serial electrocardiographic monitoring may be considered when fluconazole is administered in patients who are at risk for ventricular arrhythmias.
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Complex regional pain syndrome (CRPS) type-1 (previously termed reflex sympathetic dystrophy syndrome) may be manifested as sympathetically mediated pain and swelling in an extremity. Among the numerous causes of reflex sympathetic dystrophy, the most common is trauma. We describe a 71-year-old diabetic man with endstage renal disease who presented with CRPS type-1 of the left hand one month after construction of a PTFE (polytetrafluroethylene) arteriovenous graft. The symptoms of CRPS improved greatly with stellate ganglion blocks and physical therapy.
A 60-year-old white man sustained a rupture of the renal artery 6 weeks after a cadaveric kidney transplantation. The bleeding site was repaired, and culture of the hematoma showed an isolated growth of Candida albicans. Blood and urine cultures were negative. Systemic antifungal therapy was initiated. Bleeding from the renal artery recurred, eventually requiring removal of the transplanted kidney. Histopathology of the resected specimen showed budding yeast in the wall of the renal artery, but no evidence of fungal invasion of the kidney. The patient received 6 weeks of amphotericin B therapy and currently remains on hemodialysis therapy.
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