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Article of the Month



Rosuvastatin-Induced Carotid Plaque Regression in Patients With Inflammatory Joint Diseases

In patient with rheumatoid arthritis (RA) there is an increased risk of cardiovascular (CV) disease. CV disease is a significant factor in the widening gap of mortality between patients with RA and the general population. The presence of carotid artery plaques is considered a strong CV risk factor. Patients with inflammatory joint disease have a high frequency of asymptomatic carotid plaques and these plagues have been shown to predict future acute coronary syndromes. Statins are often used for the reduction of these plaques and have being shown to induce regression of coronary atheroma volume and decrease the incidence of CV events in the general population. 86 patients with carotid plaques and inflammatory join disease were treated with rosuvastatin to obtain the LDL cholesterol goal and carotid plaque height was evaluated by ultrasonography. The median compliance with rosuvastatin treatment was 97.9%. At base line, the median number and height of the carotid plaques were 1.0 and 1.80mm (IQE 1.60-2.10). The mean change in carotid plaque height after r18 months of treatment with rosuvastatin was -0.19 +/- .35 mm with p < 0.0001. The mean baseline LDL cholesterol level was 4.0 +/- 0.9 mmoles/liter and the mean reduction in LDL cholesterol level was -2.3 mmoles/liter. After adjustment for age/sex/blood pressure, no linear relationship between a reduction in carotid plaque height and the level of LDL cholesterol exposure was observed during the study period. In addition, the amount of change of LDL cholesterol level during the study period did not influence the degree of carotid plaque height reduction. The study did show that intensive lipid-lowering treatment with rosuvastatin induced atherosclerotic regression and reduced the LDL cholesterol level significantly in patients with inflammatory joint disease. It also indicated that disease activity may influence the effect of anti-atherosclerosis treatment.


Arthritis & Rheumatology. Vol. 67, No. 7, July 2015 pp 1718-1728


Summary by: Alexander J. Feng, MD, PGY 3




Ultrastructural Changes of Brain Tissues Surrounding Hematomas After ICH

The aim of this study was to examine the cerebral ultrastructure surrounding the hematoma following an ICH using transmission electron microscopy (TEM) as correlated with clinical severity as determined by the Glasgow Coma Scale (GCS), the National Institutes of Health Stroke Scale (NIHSS), and bleeding volume. All patients, in this study, were diagnosed with a spontaneous ICH on CT scan that necessitated surgical evacuation, during which time brain tissue specimens were collected. The control group included individuals who underwent postmortem examination within one hour following death. Subjects with a history of systemic/chronic diseases were excluded. The patients were divided into subgroups with high GCS (GCS 9–11); intermediate GCS (GCS 6–8); and low GCS (GCS 3–5). More serious ultrastructural damage was seen in patients with greater NIHSS scores, lower GCS scores, and greater bleeding volumes. Additionally, bleeding volume was significantly related to both GCS and NIHSS scores, due to the decline in blood flow, which may increase intracranial pressures and decrease cerebral perfusion pressures, leading to brain tissue damage and neural dysfunctions. The high GCS group appeared to have more neuronal cellular damage, localized to the cell body, compared to patient with lower GCS scores began to show damage to extracelluar structures such as the myelin sheath and surrounding blood vessels, including loss of inter endothelial cell tight junctions. This study provided direct evidence that unfavorable structural change occurred in neurons after ICH, supporting neuroprotective strategies that aim to improve outcomes by reducing ICH-induced secondary pathologic processes.

European Neurology 2015; 74: 28-35

Summary by: Paul Hurd, MD, PGY3




Chronic Pain in Multiple Sclerosis Patients: Utility of Sensory Quantitative Testing in Patients with Fibromyalgia Comorbidity

Recent studies have shown that thermal and discomfort thresholds correlate with rates of chronic pain in multiple sclerosis patients. This study looks at multiple sclerosis patients with and without comorbid fibromyalgia and the correlation of chronic pain and thermal and discomfort thresholds.
One hundred and thirty three multiple sclerosis patients were assessed for chronic pain and fibromyalgia. The 1990 ACR diagnostic criteria of tender points was used by rheumatologists to assess for fibromyalgia. An algometer was used on the right forearm to assess the threshold and this was compared to 60 age matched control subjects. Researchers found 66% had chronic pain, 14% had neuropathic pain 17% had chronic pain and fibromyalgia. Thermal and discomfort thresholds were significantly lower in the patients with MS and fibromyalgia than the controls. The number of fibromyalgia tender points was also correlated with the thermal threshold values.  Further, female gender correlated significantly with the discomfort threshold.

Conclusion: Researchers believe that thermal threshold values with or without tender point exams can be a clinical tool for predicting the severity of chronic pain in multiple sclerosis patients. This also adds to our understanding of the pathophysiology of chronic pain in multiple sclerosis, however more research is needed.

European Journal of Neurology 2015. 73:257–263

Summary by: James Wilson, DO, PGY 3



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