The Doctor's Channel - Internal Medicine

Coffee may protect against oral, pharyngeal and esophageal cancer

2009-01-06T16:52:41-05:00

By Megan Rauscher

NEW YORK (Reuters Health) – In the general population of Japan, coffee consumption is related to a lower risk of cancer of the oral cavity, pharynx and esophagus, new research indicates.

Such an association “has been suggested in case-control studies, but few results from prospective studies are available,” Dr. Toru Naganuma of Tohoku University, Sendai and colleagues note in the December 15 issue of the American Journal of Epidemiology.

To investigate further, they turned to the population-based prospective Miyagi Cohort Study in Japan, a country where consumption of coffee is relatively high, as is the incidence of esophageal cancer in men.

Among 38,679 subjects aged 40 to 64 years with no prior history of cancer, 157 cases of oral, pharyngeal and esophageal cancers were identified during 13.6 years follow up in 135 men and 22 women.

The multivariate-adjusted hazard ratio for these cancers for 1 or more cups of coffee consumed per day compared with no coffee consumption was 0.51, Dr. Naganuma and colleagues report.

This inverse association between coffee consumption and oral, pharyngeal and esophageal cancer was consistent across the strata of sex and cancer site and was also observed in populations at high risk for these cancers, namely, those who were current drinkers and/or smokers at baseline, the investigators note.

“Since we conducted this study on the hypothesis that coffee would have preventive effect on oral, pharyngeal, and esophageal cancers, the observed associations were approximately consistent with our expectation,” Dr. Naganuma noted in comments to Reuters Health.

“However, we had not expected that we could observe such a substantial inverse association with coffee consumption and the risk of these cancers, and the inverse association in high-risk groups for these cancers (drinkers and smokers) as well,” the researcher added.

“Although cessation of alcohol consumption and cigarette smoking is currently the best known way to help reduce the risk of developing these cancers, coffee could be a preventive factor in both low-risk and high-risk populations,” Dr. Naganuma and colleagues conclude.

Reference:
Am J Epidemiol 2008;168:1425-1432.

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High systolic pressure a positive sign in chronic heart failure

2009-01-05T18:08:40-05:00

NEW YORK (Reuters Health) – In patients with chronic heart failure, higher systolic blood pressures paradoxically predict better survival, according to researchers in the UK.

Writing in the January issue of Heart, Dr. Claire E. Raphael and colleagues at St. Mary’s Hospital and Imperial College, London note that because “blood pressure is intrinsically related to the heart’s ability to pump….there is a strong case for blood pressure as a marker of prognosis in heart failure.”

The researchers performed a meta-analysis of 10 published reports on the relationship between blood pressure and mortality in chronic heart failure. Altogether, the studies involved 8088 patients and 29,222 person-years of follow-up.

In all 10 papers, a higher systolic blood pressure was a favorable prognostic marker, according to the article.

“The decrease in mortality rates associated with a 10 mm Hg higher systolic blood pressure was 13.0%...in the heart failure population,” the authors report. This effect was not related to etiology or to the use of beta blockers or angiotensin enzyme-converting inhibitors.

Dr. Raphael and her coauthors point out that in patients with cardiac disease but without chronic heart failure affecting systolic function, mean arterial blood pressure is largely determined by peripheral vasoconstriction, and higher systolic pressure indicates poor elasticity of the arteries.

In patients with heart failure, however, systolic pressure reflects the ejection fraction and cardiac output. “Therefore,” the investigators write, “a higher blood pressure is associated with a decreased mortality as it serves as an indirect measure of cardiac function.”

“The potential of this simple variable in outpatient assessment of patients with chronic heart failure should not be neglected,” the authors conclude. In particular, they say, the information could be used to optimize cardiac resynchronization devices.

Reference:
Heart 2009;95:56-62.

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Stem cells preserve cardiac structure and function in porcine model of acute MI

2008-12-24T14:17:40-05:00

NEW YORK (Reuters Health) - German investigators report in Heart that intramyocardial transfer of cord blood-derived stem cells improves left-ventricular function and prevents scar formation in a porcine model of acute MI.

Senior author Dr. Arjang Ruhparwar, at the University of Heidelberg, and colleagues used human cord blood-derived unrestricted somatic stem cells because of their relatively low immunogenicity, their high levels of pluripotency and expansion potential, and their ability to release “a multitude of cytokines.”

Immediately after ligature of the coronary artery of month-old domestic pigs treated with immunosuppressants, the scientists injected cultured cord-blood stem cells in10 animals or culture medium in 8 animals into the free wall of the left ventricle. After 48 hours, there was no difference between groups in apoptosis, recruitment of macrophages, or mitosis;and after 8 weeks, the authors detected no evidence of donor cell engraftment. Thus, they exclude the theory that “functional recovery is simply based on improved neovascularization or modified tissue remodeling.”

Eight weeks post-MI, transesophageal echocardiography showed that the “left ventricular ejection fraction had dramatically improved” in stem cell-treated animals, recovering to 88% of baseline levels, whereas ejection fraction remained severely impaired at 45% of pre-MI levels in control animals.

Left ventricular end diastolic volume significantly increased in the control animals and there was significant scarring in the infarction areas. By contrast, there was no evidence of scarring or ventricular dilation in the pigs treated with stem cells.

Reference:
Heart 2009;95:27-35.

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WBC, serum sodium aid diagnosis of necrotizing soft tissue infection

2008-12-24T14:15:20-05:00

NEW YORK (Reuters Health) - Clinicians report in The American Journal of Surgery that a high white blood cell count or low serum sodium level can help diagnose necrotizing soft tissue infection (NSTI) in suspected cases where classic physical signs are absent.

In an earlier retrospective study, the Dr. Christian de Virgilio from Los Angeles Biomedical Institute at Harbor-UCLA Medical Center and colleagues showed that an admission white blood cell count greater than 15,400/µL and/or serum sodium level below 135 mEq/L could help differentiate NSTI from non-NSTI.

In the current study, the researchers confirmed this earlier finding in 21 consecutive patients with NSTI who were prospectively studied over a 17-month period. Dr. de Virgilio told Reuters Health: “Just based on the classic physical exam findings, necrotizing soft tissue infection was initially only suspected in 9 of the 21 patients and the reason is the physical exam findings were not very dramatic.”

Blood tests showed all 21 patients had either high WBC or low serum sodium, and the surgeon’s suspicion of NSTI significantly increased after being informed of the patients’ WBC and serum sodium values. In this series of NSTI patients, the mean admission WBC count was 31,500 µL and the mean serum sodium level was 127 mEq/L. Suspicion of NSTI increased from 9 patients to 18 patients after considering these laboratory criteria.

Dr. de Virgilio noted: “These abnormal lab values are more useful in their negative predictive value than their positive predictive value. If the sodium isn’t low and the white count isn’t above these criteria then you can be fairly comfortable that it is not this infection.”

Reference
Am J Surg 2008;196:926-930.

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More on Evidence-Based Databases in Medicine

2008-12-23T18:10:21-05:00

Charles Young, MD, Editor, BMJ Clinical Evidence, Editor in Chief of BMJ In Practice, discusses evidence-based information in medicine.

Doctor's Digest single topic reference guides provide physicians with practical how-to solutions from the experts that offer answers to physicians' most-pressing practice management needs - information that is not taught in medical school.

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Lupus affects the brain very early in the disease

2008-12-23T17:24:36-05:00

By Megan Rauscher

NEW YORK (Reuters Health) - Results of an MRI study suggest that the brain may be affected very early in the course of systemic lupus erythematosus (SLE), "even before the clinical diagnosis of SLE is made," researchers report in the December issue of the Journal of Rheumatology.

Among a group of 97 patients (94 female; average age, 38) with newly diagnosed SLE, 25% had anatomic brain abnormalities on MRI. All of the patients were within 9 months of being diagnosed with SLE.

These observations indicate that "lupus affects the brain even in newly diagnosed patients," first author Dr. Michelle Petri of Johns Hopkins University, Baltimore, Maryland, told Reuters Health. "We were shocked actually; we thought it took more time for lupus to involve the brain," she acknowledged.

Cerebral atrophy, the most common abnormality seen on MRI, was present in 18% of patients with newly diagnosed SLE, and focal lesions were present in 8% of study subjects.

Anxiety disorder was more common in patients with cerebral atrophy (p = 0.04). While anxiety disorder has been frequently seen in SLE patients, it was felt to be a nonspecific finding that did not differ from controls, the authors note. "Our study suggests that there may be a relationship between brain volume loss and anxiety," they note.

Patients with focal lesions were more likely to be African American (p = 0.045) and had higher SLE disease activity index scores (p = 0.02) and anti-dsDNA (p = 0.05).

Dr. Petri and colleagues conclude: "Given the high frequency of neuropsychiatric SLE manifestations and structural brain abnormalities, more research is urgently needed to determine the underlying pathophysiology of these changes, in order to develop rational treatment options."

Reference:
J Rheumatol 2008;35:2348-2354.

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Lack of sleep in early middle age tied to coronary artery calcification

2008-12-23T17:20:36-05:00

NEW YORK (Reuters Health) - Objectively measured sleep duration is inversely associated with incident coronary artery calcification in middle-aged adults, independent of traditional risk factors, according to prospective study findings reported in the December 24/31 issue of the Journal of the American Medical Association.

Recent research has tied sleep duration to established risk factors for coronary artery calcification, such as glucose regulation, blood pressure, and body mass index, study director Dr. Diane S. Lauderdale and her team point out. In their current work, they looked for evidence of a direct association between sleep and the incidence of calcification during 5 years’ follow-up.

Their analysis included 495 healthy participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study. Sleep duration was determined by wrist actigraphy at baseline in 2000-2001, when subjects were 35 to 47 years of age. Electron beam computed tomography was used to measure coronary artery calcification at baseline and again in 2005-2006.

Results showed that longer measured sleep was associated with lower incidence of calcification. According to a JAMA statement, the incidence ranged from 6% among subjects who slept more than 7 hours/night, to 11% among those who slept between 5 and 7 hours nightly, and 27% of those who sleep less than 5 hours.

After adjusting for demographics and cardiovascular risk factors, actigraphy-measured sleep per hour was associated with an odds ratio of 0.66 per hour (p = 0.01) for incident coronary calcification.

“The modeled effect of 1 additional hour of sleep on the odds of incident calcification was equal to the modeled effect of a 16.5 mm Hg decrease in systolic blood pressure,” Dr. Lauderdale’s group points out.

“Although this single study does not prove that short sleep leads to coronary artery disease, it is safe to recommend at least six hours of sleep a night,” Dr. Lauderdale remarked.

Reference:
JAMA 2008;300:2859-2866.

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Abnormal ECG findings seen in psoriatic arthritis patients

2008-12-23T12:41:51-05:00

NEW YORK (Reuters Health) – Results of a case-control study suggest that psoriatic arthritis patients may have “subtle” cardiac conduction disturbances.

“In surveying the literature, scant data were found regarding cardiac arrhythmias in psoriatic arthritis patients,” the study team notes in the December issue of the Journal of Rheumatology.

Therefore, Dr. Devy Zisman from Carmel Medical Center, Haifa, Israel and colleagues compared the electrocardiogram scans of 92 patients with psoriatic arthritis to those of 92 age- and sex-matched nonpsoriatic, nonarthritic control subjects.

“The major finding of our study,” they report, “is a statistically significantly longer PR interval in the patients with psoriatic arthritis compared to individuals without psoriasis or arthritis” (159.6 vs 151.3 milliseconds, respectively; p = 0.021). Compared with controls, the mean PR interval was 8.3 milliseconds, 5.5% longer, in patients with psoriatic arthritis.

“Although the clinical relevance of this finding is questionable since the absolute difference was small, the importance of the observation is the implication of atrioventricular node involvement in the psoriatic arthritis systemic disease,” Dr. Zisman and colleagues note.

The abnormal prolongation of the PR interval was asymptomatic, requiring no additional intervention. No statistical difference was apparent with respect to the QRS interval or other ventricular conduction disturbances studied.

There was no apparent effect of methotrexate or nonsteroidal anti-inflammatory drug therapy on the cardiac conduction properties examined; the effects of the newer biological treatments were not assessed in this study.

Dr. Zisman and colleagues conclude, based on their observations that “a prospective study with prolonged followup is warranted to elucidate the clinical significance of our observed conduction abnormalities.”

Reference:
J Rheumatol 2008;35:2379-2382.

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CT needed to assess bone loss and lung involvement in COPD

2008-12-22T18:05:12-05:00

NEW YORK (Reuters Health) - Computed tomography (CT) of the chest can serve a dual purpose in patients with chronic obstructive pulmonary disease (COPD), measuring both the severity of emphysema and vertebral bone density, physicians in Japan report.

The multiple extrapulmonary features associated with COPD indicate that it is a systemic disease, Dr. Toyohiro Hirai and colleagues at Kyoto University note in the December issue of the journal Chest; one such feature is osteoporosis. However, the association between the degree of pulmonary involvement and loss of bone density is unclear.

Their cross-sectional survey included 65 clinically stable men with COPD and no history of bone disease or use of corticosteroids or other medicines that influence bone metabolism. The average patient age was 68.8 years old.

The average CT scan density of the thoracic vertebrae (T4, T7 and T10) was used to determine bone mineral density, and the percentage of low-attenuation area in the lungs was used as a quantitative measure of pulmonary emphysema.

“Percentage of low-attenuation area in the lungs correlated with bone density more closely than other risk factors for osteoporosis, such as age, BMI, FEV1, smoking, and PaO2,” Dr. Hirai’s group reports.

Moreover, their forward stepwise multiple regression analysis showed that only percentage of low-attenuation area in the lungs and BMI could predict bone density in these patients, indicating that COPD itself is a risk factor for osteoporosis.

CT scanning, they conclude, “is a useful tool for the management of COPD not only as a pulmonary disease, but also as a systemic disease,” with the potential for establishing strategies for decreasing osteoporotic fractures.

Reference:
Chest 2008;134:1244-1249.

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Rapid heart and respiration rates predict posttraumatic stress disorder

2008-12-22T18:02:14-05:00

NEW YORK (Reuters Health) – As indicators of arousal, elevations in the heart and respiration rates immediately after a traumatic event are predictive of future posttraumatic stress disorder (PTSD), Australian researchers report.

“Fear-conditioning models posit that increased arousal at the time of trauma predicts subsequent PTSD. This multisite study evaluated the extent to which acute heart rate and respiration rate predict subsequent chronic PTSD,” Dr. Richard A. Bryant, from the University of New South Wales, Sydney, and colleagues state.

The study featured 955 patients who were seen immediately after a traumatic injury at four centers in Australia from April 2004 to February 2006; the patients were then evaluated 3 months later for PTSD using the Clinician-Administered PTSD Scale-IV. The patients were also screened major depressive disorder using the Mini-International Neuropsychiatric Interview.

PTSD was identified in 90 patients (10%) and major depressive disorder in 159 (17%). The average heart rate at the time of the event in PTSD patients was higher than that in non-PTSD patients, 90.16 vs. 84.84 beats/min (p < 0.01), as was the respiration rate, 20.24 vs. 18.58 breaths/min (p < 0.001).

By contrast, heart rate and breathing rate did not differ significantly by depression status, according to the report in the November issue of the Journal of Clinical Psychiatry.

A heart rate of at least 96 beats/min increased the odds of PTSD by 2.12-fold and a respiration rate of 22 breaths/min increased the odds by 2.42-fold.

“This study provides the first large-scale multisite evidence that elevated heart rate and respiration rate in the immediate aftermath of traumatic injury are associated with subsequent PTSD,” the authors emphasize.

Nonetheless, there is insufficient evidence to start using heart and breathing rates as screening tools for PTSD. The findings do, however, suggest possible starting points for examining the mechanisms that underlie this disorder.

Reference:
J Clin Psychiatry 2008;69:1694-1701.

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