“What concerns me is…” Expression of emotion by advanced cancer patients during outpatient visits

OBJECTIVE: Cancer patients have high levels of distress, yet oncologists often do not recognize patients' concerns. We sought to describe how patients with advanced cancer verbally express negative emotion to their oncologists. MATERIALS AND METHODS: As part of the Studying Communication in Oncologist-Patient Encounters Trial, we audio-recorded 415 visits that 281 patients with advanced cancer made to their oncologists at three US cancer centers. Using qualitative methodology, we coded for verbal expressions of negative emotion, identified words patients used to express emotion, and categorized emotions by type and content. RESULTS: Patients verbally expressed negative emotion in 17% of the visits. The most commonly used words were: "concern," "scared," "worried," "depressed," and "nervous." Types of emotion expressed were: anxiety (46%), fear (25%), depression (12%), anger (9%), and other (8%). Topics about which emotion was expressed were: symptoms and functional concerns (66%), medical diagnoses and treatments (54%), social issues (14%), and the health care system (9%). Although all patients had terminal cancer, they expressed negative emotion overtly related to death and dying only 2% of the time. CONCLUSIONS: Patients infrequently expressed negative emotion to their oncologists. When they did, they typically expressed anxiety and fear, indicating concern about the future. When patients use emotionally expressive words such as those we described, oncologists should respond empathically, allowing patients to express their distress and concerns more fully.     

Characterization of CD33 as a new member of the sialoadhesin family of cellular interaction molecules

CD33 is a member of the Ig superfamily that is restricted to cells of the myelomonocytic lineage but whose functions and binding properties are unknown. It shares sequence similarity with sialoadhesin, CD22, and the myelin-associated glycoprotein, which constitute the Sialoadhesin family of sialic acid-dependent cell adhesion molecules. In the present study, we show that CD33 is a fourth member of this family. As a model for sialic acid-dependent binding, human erythrocytes were derivatized with N-acetylneuraminic acid (NeuAc) in different linkages. A recombinant soluble form of CD33, Fc-CD33, bound red blood cells with a specificity similar to that of sialoadhesin, preferring NeuAc alpha 2,3Gal in N- and O-glycans over NeuAc alpha 2,6Gal in N-glycans. Fc- CD33 also bound selectively to the myeloid cell lines HL-60 and U937. However, CD33 was unable to mediate cell binding after transient expression in COS cells, despite high levels of surface expression. Pretreatment of the CD33-transfected cells with sialidase rendered them capable of mediating sialic acid-dependent binding. These results show that CD33 can function as a sialic acid-dependent cell adhesion molecule and that binding can be modulated by endogenous sialoglycoconjugates when CD33 is expressed in a plasma membrane.     

Ancrod in systemic lupus erythematosus with thrombosis. Clinical and fibrinolysis effects

A patient with systemic lupus erythematosus had severe hypertension, rapidly worsening renal failure, and multiple successive thrombotic cerebrovascular and retinal lesions develop. In a kidney biopsy specimen luminal thrombi were demonstrated in arteries and arterioles, without vasculitic or inflammatory changes. The patient's plasma was markedly deficient in both prostacyclin stimulating factor (PSF) and vascular plasminogen activator (VPA), and also contained a potent inhibitor of in vitro urokinase-induced fibrinolysis. Treatment with ancrod resulted in striking reversal of the progressive renal damage and clinical recovery from the thrombotic cerebrovascular and retinal lesions. This clinical improvement was associated with improved renal histologic appearance, correction of the PSF and VPA deficiencies, and disappearance of the urokinase inhibitor. Possible mechanisms of action of ancrod are discussed.     

Novel promoter polymorphism in insulin-like growth factor-binding protein-3: correlation with serum levels and interaction with known regulators

Insulin-like growth factor (IGF)-binding protein-3 (IGFBP-3) is a major determinant of circulating levels of the IGFs and is clinically useful for the evaluation of GH deficiency and for predicting the response to GH treatment. Recent studies provide evidence that the circulating level of IGFBP-3 is inversely related to the risk of several common cancers, and that antiproliferative agents such as antiestrogens and retinoids act in part by up-regulating IGFBP-3 gene (IGFBP3) expression. Although approximately 50% of the substantial interindividual variability in circulating IGFBP-3 levels is known to have a genetic basis, the specific loci involved are unknown. Direct sequencing of genomic DNA specimens from a multiethnic population identified several single nucleotide polymorphisms in the promoter region of IGFBP3. For the most common single nucleotide polymorphism (nucleotide -202) found to be in Hardy-Weinberg equilibrium, genotype was highly correlated to circulating level of IGFBP-3 in 478 men from the Physicians' Health Study. In vitro, we documented significantly higher promoter activity of the A allele at the -202 locus compared with the C allele, consistent with the relationship observed between genotype and circulating IGFBP-3 (AA > AC > CC). A positive correlation was observed between circulating retinol levels and circulating IGFBP-3 levels; subset analysis by genotype showed that this relationship was only present among individuals carrying an A allele at -202 (AA > AC > CC). Tall individuals or individuals with a body mass index of 27 or greater had levels of circulating IGFBP-3 that were significantly higher when they possessed at least one A allele (AA > AC > CC). The IGFBP3 promoter region deserves investigation as a locus where polymorphic variation occurs frequently and may influence GH responsiveness, somatic growth, and possibly cancer risk.     

Discordant Diagnosis of Lower Extremity Peripheral Artery Disease Using American Heart Association Postexercise Guidelines

To determine whether postexercise criteria for peripheral artery disease (PAD) diagnosis recommended by the American Heart Association (AHA) identifies the same group of PAD patients.Diagnosis of PAD is performed using ankle-brachial index at rest (resting-ABI). When resting-ABI is not contributive, an AHA scientific statement recommend to use 1 of 2 following criteria: a postexercise ABI decrease of greater than 20% or a postexercise ankle pressure decrease of greater than 30 mm Hg.Between 1996 and 2012, 31,663 consecutive patients underwent lower-extremity arterial study at Mayo Clinic. Among them, only unique patients who had exercise treadmill testing were analyzed. In this retrospective analysis, resting-ABI, postexercise ABI, and postexercise decrease of ankle pressure measured at 1-minute were measured in each patient. We conducted an analysis of agreement between postexercise criteria expressing the agreement separately for the positive and the negative ratings. Twelve thousand three hundred twelve consecutive patients were studied with a mean age of 67 ± 12 years, 61% male. According to resting-ABI, 4317 (35%) patients had PAD. In the whole population, if a clinician diagnoses “PAD” with 1 postexercise criterion, the probability that other clinicians would also diagnose “PAD” is 74.3%. If a clinician diagnoses “no PAD”, the probability that other clinicians would also diagnose “no PAD” is 82.4%. In the patients to be of potential benefit from treadmill test when the resting-ABI > 0.90, if a clinician diagnoses “PAD” with 1 postexercise criterion, the probability that other clinicians would also diagnose “PAD” is 58.4% whereas if a clinician diagnoses “no PAD,” the probability that other clinicians would also diagnose “no PAD” is 87.5%.Postexercise criteria do not identify the same group of PAD patients. In our opinion, postexercise criteria to define PAD deserve additional study.