Is chemotherapy associated with cognitive impairment?

Cancer survivors often report difficulties with memory and concentration—sometimes referred to by patients as "chemobrain" or "chemofog". The results from two recent studies suggest that, while chemotherapy itself may not be associated with cognitive impairment, some patients might already be experiencing cognitive difficulties before treatment is even started.     

Is there a role for physical activity in preventing cognitive decline in people with mild cognitive impairment?

Mild cognitive impairment (MCI) is a common clinical syndrome that identifies people at high risk of developing dementia. Although treatments for MCI are currently unavailable, preliminary evidence has identified potential neuro-protective effects of physical activity, which may lead to improved outcomes. However, there is uncertainty regarding the effectiveness, feasibility and acceptability of this treatment strategy. These uncertainties require further investigation before physical activity interventions can be recommended for routine care.     

Is a stable or decreasing prolactin level in a patient with prolactinoma a surrogate marker for lack of tumor growth?

The optimal interval for follow-up imaging of patients with prolactinomas is unclear. We wish to determine the likelihood of tumor enlargement in patients with prolactinomas who have a stable or reduced prolactin (PRL) level over time, whether or not they are treated with a dopamine agonist (DA). We identified 80 patients with prolactinomas (34 men, 46 women) who had at least two paired sets of serum PRL levels and pituitary MRIs, 3 or more months apart. Patients with hyperprolactinemia due to drug or stalk effects were excluded. The median (range) age was 45 (25–77) years. Sixty-three patients (78.8 %) were treated with DA. PRL levels (ng/mL) at the initial and latest sets were 114 (0.3–15,732) and 16 (0.3–1,204), respectively. In patients with identifiable tumors, the maximum tumor diameters (mm) at the initial and latest MRI studies were 12.5 (2–60) and 12.5 (2–39) respectively, with an interval of 2.9 (0.3–9.7) years. Sixty percent of patients (n = 48) had a macroadenoma. Forty-two (52.5 %) patients had either disappearance of the tumor (n = 22) or reduction (n = 20) in tumor size. In the remainder, tumor size was stable in 35 but increased in 3 patients. One of these patients, observed off therapy had a concomitant rise in PRL level. The other 2 had evidence of pituitary hemorrhage with no PRL increase. Tumor growth in prolactinoma patients with a stable or decreasing PRL level, regardless of size, is a rare event. Repetitive pituitary imaging in these patients may not be warranted.     

Is serum cystatin-C a reliable marker for metabolic syndrome?

Purpose

Chronic kidney disease and metabolic syndrome are recognized as major cardiovascular risk factors. It has been shown that cystatin C has a stronger association with mortality risk than creatinine-based estimations of glomerular filtration rate. We measured cystatin values in dyslipidemic patients and looked for correlations between renal function, cystatin, and metabolic syndrome.

Methods

There were 925 dyslipidemic patients prospectively included in this cross-sectional study and evaluated over 10 months. Each visit included clinical and biological assessment.

Results

Most patients exhibited cardiovascular risk factors other than dyslipidemia: hypertension in 34%, diabetes in 11%, and smoking in 18%. Mean triglycerides were 149 ± 136 mg/dL, mean high-density lipoprotein cholesterol 54 ± 14 mg/dL, and low-density lipoprotein 167 ± 48 mg/dL. Metabolic syndrome was present in 238 (26%) patients. Plasma creatinine did not differ between control group and metabolic syndrome patients (80 ± 26 vs 82 ± 20 μmol/L, respectively, P = .2), but creatinine clearance evaluated by abbreviated Modification of Diet in Renal Disease Study formula was lower in the metabolic syndrome group than in the non-metabolic-syndrome group (83.3 ± 18.8 mL/min/1.73m² vs 86.8 ± 16.9 mL/min/1.73m², respectively, P <.007). Cystatin value was significantly higher in metabolic syndrome patients than in others (0.86 ± 0.23 vs 0.79 ± 0.20 mg/L, respectively, P <.0001), independently of serum creatinine level and creatinine clearance. Furthermore, there was a progressive increase in cystatin, as a function of the number of metabolic syndrome components.

Conclusions

Our study shows that cystatin is associated with metabolic syndrome in dyslipidemic patients. Cystatin may be an interesting marker of metabolic syndrome and of increased cardiovascular and renal risk.     

Doppler measurements: a surrogate marker of liver fibrosis?

OBJECTIVE: The potential diagnostic value of performing Doppler measurements of liver vasculature to assess early stages of liver fibrosis has not been established. Due to the potential clinical impact, this study focused on the correlation between Doppler measurements and histologically proven liver fibrosis. METHODS: Forty-three consecutive patients with chronic viral hepatitis (79% hepatitis C) were enrolled. At the time of liver biopsy, two independent investigators measured maximum and mean blood flow velocity, resistance indices, vessel diameter and blood flow volume in the portal vein, hepatic artery and hepatic veins. All measurements were taken in triplicate. The mean values were correlated to the degree of liver fibrosis using the Ludwig score. RESULTS: Sixty-seven per cent of the patients in our study group had no or only mild fibrosis (Ludwig score stage I or II). Thirty-three per cent showed progressive fibrosis or cirrhosis (Ludwig score stage III or IV). There was a large overlap in the Doppler measurements and findings between the various disease stages. No significant changes of Doppler parameters were detected, even between patients with no or mild fibrosis and patients with severe fibrosis (Ludwig score stage III or IV). CONCLUSIONS: Doppler measurements of the portal vein, hepatic artery and hepatic vein(s) are not a valid surrogate marker of liver fibrosis. Nor are Doppler measurements a useful method to estimate the degree of liver fibrosis.     

Is the distal hyperplastic polyp a marker for proximal neoplasia?

CONTEXT: The current literature is unclear about the association between distal hyperplastic polyps and synchronous neoplasia (adenomatous polyps and cancer) in the proximal colon. OBJECTIVE: To estimate the prevalence of proximal neoplasia associated with distal hyperplastic polyps. DATA SOURCES: Database searches (medline and embase from 1966 to 2001) and manual search of the bibliographies of included and excluded studies, case reports, editorials, review articles, and textbooks of Gastroenterology. STUDY SELECTION: Studies describing the prevalence of proximal neoplasia in persons with distal hyperplastic polyps. DATA EXTRACTION: Demographics, clinical variables, study design, and prevalence of proximal neoplasia associated with various distal colorectal findings. DATA SYNTHESIS: Of 18 included studies, 12 involved asymptomatic individuals in which the pooled absolute risk of any proximal neoplasia associated with distal hyperplastic polyps was 25% (95% confidence interval [95% CI], 21% to 29%). In 4 studies where colonoscopy was performed irrespective of distal findings, the absolute risk was 21% (95% CI, 14% to 28%). The relative risk of finding any proximal neoplasia in persons with distal hyperplastic polyps was 1.3 (95% CI, 0.9 to 1.8) compared to those with no distal polyps. Among 6 studies of patients with symptoms or risk factors for neoplasia, the absolute risk of proximal neoplasia was 35% (95% CI, 32% to 39%) in persons with distal hyperplastic polyps. In 2 studies of screening colonoscopy, advanced proximal neoplasia (cancer, or a polyp with villous histology or severe dysplasia, or a tubular adenoma >/=1 cm) was present in 4% to 5% of persons with distal hyperplastic polyps, which was 1.5 to 2.6 times greater than in those with no distal polyps. CONCLUSIONS: In asymptomatic persons, a distal hyperplastic polyp is associated with a 21% to 25% risk for any proximal neoplasia and a 4% to 5% risk of advanced proximal neoplasia, and may justify examination of the proximal colon. Further study is needed to determine the risk of advanced proximal neoplasia associated with size and number of distal hyperplastic polyps.     

Mild cognitive impairment: what's in a name?

BACKGROUND: Nowadays the term mild cognitive impairment (MCI) is used to fill the gap between cognitive changes associated with normal ageing and those associated with dementia. Despite some agreement in general definitions, MCI is still a heterogeneous clinical syndrome for which no DSM-IV criteria have yet been established. Criteria by Petersen et al. are presently the most applied in clinical practice. Moreover, little attention has been paid to the specific relation between MCI and depression. OBJECTIVE: This review highlights some concerns about the concept of MCI and provides guidelines within the field of neuropsychology to solve them. In a second part, the paper focuses on the specific relationship between depression in the elderly and MCI. RESULTS: We hypothesize that certain test instruments can be used to operationalize the criteria proposed by Petersen et al. Moreover, we suggest that cued recall might be of help to differentiate between progressive and non-progressive MCI. Concerning the specific relation between depression and MCI, we assume that elderly depression with concomitant cognitive problems can be seen as an MCI. CONCLUSION: The proposed adjustments and additions (neuropsychological instruments and the incorporation of depressive symptoms) in the diagnostic flowchart of Petersen may serve as useful tools for clinicians when making a diagnosis of MCI.     

Is accelerated idioventricular rhythm a good marker for reperfusion after streptokinase?

BackgroundAccelerated idioventricular rhythm (AIVR) is a common arrhythmia observed in patients with ST segment elevation myocardial infarction (MI). It is not clear how much value AIVR has in predicting successful reperfusion, since there have been conflicting data regarding this in the past. Streptokinase (STK) even today is the commonest thrombolytic agent used in the public health care set-up in India.¹ Most data for the use of STK are from the 1990s, which had showed that at best it is effective in only 50% of patients in restoring adequate flow.² It is probable that with the current dual-antiplatelet loading dose regimen and other newer medications, this figure could be higher. Also, rescue angioplasty for failed thrombolysis is the standard of care now, unlike before. Hence, we need reliable non-invasive markers to judge successful reperfusion in the present era. While ST segment resolution is the standard marker for reperfusion used in thrombolytic trials, in several instances it is not definitive. An additional marker would thus be very useful, especially in such cases.MethodsThis was a prospective observational study carried out at a public teaching hospital. 200 consecutive patients with a diagnosis of acute MI who were given STK within 12 h of index pain were included. The STK dose was 1.5 million units, infused over 30 min; the ECG was again recorded after 90 min of completion of the infusion. Continuous ECG monitoring for the first 24 h of ICCU stay was performed and AIVRs during this period were documented. Early AIVR was defined as that occurring within 2 h of completing the STK infusion. Echocardiography was performed 24 h after presentation. The time course of AIVR was studied vis-a-vis the outcome of thrombolysis.ResultsAIVR was seen in 41% of the patients. Though AIVR was found to have low sensitivity (45%) and specificity (64%) as a predictor of successful thrombolysis, early AIVR was a reliable sign of successful thrombolysis (p < 0.05). The sensitivity (45%) of early AIVR was low; however, the specificity (94%) and positive predictive value (94%) were very good.ConclusionAIVR is a common arrhythmia in the setting of STEMI receiving thrombolytic therapy. Early AIVR is more common with successful thrombolysis, with an excellent positive predictive value. Thus, early AIVR can be used as an additive criterion to ST segment resolution as a non-invasive marker of successful thrombolysis with STK.     

Is C-reactive protein a marker of inflammation?

C-reactive protein (CRP) is the prototype of acute-phase protein which is secreted by the liver in response to a variety of inflammatory cytokines. Levels of CRP can increase up to 1000-fold very rapidly after the onset of inflammation and decrease just as rapidly with the resolution of aggression. CRP is a member of the ancient highly conserved pentraxin family of proteins and it is arranged in a cyclic homopentameric structure. The important role of CRP in innate immunity is largely due to its opsonizing abilities, its capability to activate human complement and to bind to immunoglobulin G receptors. CRP can bind phosphocholine largely present in bacterial membranes, cell membrane and lipoproteins, in addition CRP can recognize nuclear constituent in damaged cells. CRP can activate C3 convertase through the classical pathway but not C5 convertase resulting in generation of opsonic complement fragments. Interactions of CRP with Fc receptors lead to the generation of proinflammatory cytokines and reactive oxygen species by monocyte/macrophage while inhibit neutrophiles functions. Recently, CRP was demonstrated to play an active role in atherogenesis and it has been largely proven that a microinflammatory state as defined by a moderate increase in CRP (up to 3 mg/l), is associated with an increased risk for arterial disease. Moreover it has been postulated that CRP may be a useful tool for monitoring drug therapy.