Bone marrow involvement in small cell lung cancer: Prognostic significance and correlation with hematological and biochemical parameters

The more metastatic sites and bone marrow metastasis in small cell lung cancer (SCLC), the worse the prognosis. Diagnosing the bone marrow invasion at the beginning of the therapy is important for determining of the prognosis and planning the treatment. Abnormalities of some blood parameters may help to estimate the extent of bone marrow invasion by cancer cells. In this retrospective review, the changes in routine laboratory tests that may indicate bone marrow invasion, the predictive values of these tests, and the prognostic importance of bone marrow invasion were evaluated in SCLC patients who were being followed up according to a protocol. One hundred and forty‐four patients with SCLC were enrolled in this study. Retrospectively, it was evaluated that 25 (17.4%) of the patients had bone marrow metastasis. According to univariate analysis, there was a significant difference between hemoglobin, white blood cell count, platelet count, lactate dehydrogenase, alkaline phosphatase and uric acid of the patients with and without bone marrow involvement. Among the biochemical parameters, the elevated LDH and AP had the highest sensitivity and specificity as indicators of bone marrow invasion (0.80–0.82 and 0.84–0.78, respectively). The median overall survival of extensive‐stage disease with and without bone marrow metastasis were 4.0 ± 1.0 months (95% CI 2.2–5.7) and 7.0 ± 1.2 months (95% CI 4.7–9.3), respectively (P = 0.03). Bone marrow metastasis was found to be an indicator of a bad prognosis. Bone marrow biopsy, that is an invasive procedure, can be performed on selected patients who have changes of routine laboratory tests suggesting bone marrow invasion.     

Paroxysmal Bundle Branch Block of Supraventricular Origin: A Possible Source of Misdiagnosis in Detecting Ventricular Tachycardia Using Time Domain Analyses of Intraventricular Electrograms

Current implantable antitachycardia devices use several methods for differentiating sinus rhythm (SR) from supraventricular tachycardia (SVT) or ventricular tachycardia (VT). These methods include sustained high rate, the rate of onset, changes in cycle length, and sudden onset. Additional methods for detecting VT include techniques based upon ventricular electrogram morphology. The morphological approach is based on the assumption that the direction of cardiac activation, as sensed by a bipolar electrode in the ventricle, is different when the patient is in SR as compared to VT. Whether paroxysmal bundle branch block of supraventricular origin (BBB) can be differentiated from VT has not been determined. In this study, we compared the morphology of the ventricular electrogram during sinus rhythm with a normal QRS (SRNIQRS) or SVT with a normal QRS (SVTNIQRS) with the morphologies of BBB and VT in 30 patients undergoing cardiac electrophysiology studies. Changes in ventricular electrogram morphology were determined using three previously proposed time domain methods for VT detection: Correlation Waveform Analysis (CWA), Area of Difference (AD), and Amplitude Distribution Analysis (ADA). CWA, AD, and ADA distinguished VT from SRNIQRS or SVTNIQRS in 16/17 (94%), 14/17 (82%), and 12/17 (71%) patients, and BBB from SRNIQRS or SVTNIQRS in 15/15 (100%), 13/15 (87%), and 6/15 (40%) patients, respectively. However, the ranges of values during BBB using these methods overlapped with ranges of values during VT in all cases for CWA, AD, and ADA. Hence, BBB may be a source of misdiagnosis in detecting VT when these time domain methods are used for ventricular electrogram analysis.     

Potentiation of fibroblast DNA synthesis by a phenytoin-induced mononuclear cell derived factor in vitro

Abstract – Human mononuclear cells purified by Lymphoprep flotation were incubated with phenytoin (PHT) (20 μg/ml) or its metabolite p-HPPH (2 μg/ml) in the presence of Concanaval-in A (10 μg/ml) in vitro. The results indicate that phenytoin and its metabolite p-HPPH induce the release of a mononuclear cell factor(s) that activates quiescent human gingival fibroblast to synthesize DNA.