Application of Rhenium-186 Radiosynovectomy in Elbow Diffuse Pigmented Villonodular Synovitis. - A Case Report with Multiple Joint Involvement

After surgical therapy of diffuse pigmented villonodular synovitis (DPVNS), recurrence is seen in almost half of the patients. The effectiveness of radiosynovectomy (RSV) in preventing recurrence and complaints of DPVNS is well known. Elbow involvement in DPVNS is a very rare condition; therefore, RSV in elbow hasn’t been experienced widely. The aim of this case report is to show the effectiveness of RSV with rhenium-186 (Re-186) sulfide colloid. We applied Re-186 sulfide colloid to the elbow joint of DPVNS patients six weeks after arthroscopic synovectomy. As a result, the patient did not have any complaints, and our findings are compatible with residue or recurrence on magnetic resonance imaging (MRI) in sixth and twentieth month controls after administration. We concluded that Re-186 is an effective adjuvant therapy for the prevention of recurrence and complaints.     

Effects of impacted maxillary canines on root resorption of lateral incisors

Objectives

The aim of this study was to analyze the amount of root resorption of maxillary lateral incisors by relating the position, location, and angulation of the impacted canine using cone-beam computed tomography (CBCT).

Materials and methods

The study sample consisted of panoramic and CBCT radiographs of 46 patients with a unilateral impacted canine (16 males and 30 females; mean age: 19.53 ± 6.66 and 19.44 ± 5.77 years, respectively). Sector location and canine angulation were measured in panoramics. All tomographs were obtained using CBCT (NewTom 5G, QR, Verona, Italy) and three-dimensional (3D) reconstructions of the maxillary laterals assessed by Mimics 14.01 image analysis software.

Results

Upper lateral incisor volume was smaller on the impacted side (401.95 ± 83.69 mm³) than on the nonimpacted side (433.54 ± 92.6 mm³, P < 0.05). There were no significant differences of lateral root resorption volume when comparing the impacted canines being on the labial or palatal sides (P > 0.05), but impacted canine angulation was significantly steeper on the labial side (70.85°) than on the palatal side (46.09°, P < 0.05). The volume of root resorption of laterals when comparing the various positions of the canine in different sectors or canine angulation in 30^o intervals was not statistically significantly different (P > 0.05).

Conclusions

The impacted canines caused root resorption of lateral incisors. The angulation of the canine was steeper on the labial side than on the palatal side but root resorption of adjacent laterals was not different. There were no statistically significant differences in the amount of root resorption of the laterals when the canine was evaluated according to localization and angulation.

     

SUNCT and SUNA: an Update and Review

Purpose of Review

The purpose of this review is to provide an update on the clinical features, diagnosis, pathogenesis, epidemiology, and treatment of the rare primary headache disorders short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) and short-lasting unilateral neuralgiform headache attacks with autonomic symptoms (SUNA). Together these entities are known as short-lasting unilateral neuralgiform headache attacks (SUNHA).

Recent Findings

Recent case reports of secondary SUNCT and SUNA due to medullary infarcts support the theory that the trigeminohypothalamic pathway is involved in the pathophysiology of SUNHA. While medical therapy for SUNHA has not significantly changed, surgical therapy for refractory SUNCT and SUNA has made advancements with a recent case series demonstrating the efficacy of deep brain stimulation.

Summary

We will discuss the pathophysiology of both the pain and the autonomic symptoms experienced in SUNCT and SUNA attacks as well the medical, procedural, and surgical options for treatment with emphasis on recent advances. Specific secondary causes reported in the recent literature will be discussed in brief.

     

Evaluation of the thyroid disorders in children with familial Mediterranean fever

Clinical Rheumatology - Although it is well-known that autoimmune thyroid diseases are more common in most of the autoimmune connective tissue diseases, the relationship between autoinflammatory...     

Decreased Plasminogen Activator Inhibitor-1 Levels in Coronary Artery Aneurysmatic Patients

BACKGROUND: Matrix metalloproteinases (MMPs) have been implicated in the pathogenesis of arterial aneurysms through increased proteolysis of extracellular matrix proteins. Increased proteolysis due to elevated matrix degrading enzyme activity in the arterial wall may act as a susceptibility factor for the development of coronary aneurysms. Plasmin strongly stimulates pro-MMP enzyme conversion to the active form. Plasmin hyperactivity due to decreased plasminogen activator inhibitor-1 (PAI-1) may cause MMP over activity and coronary aneurysms. The aim of this study was to investigate the association between PAI-1 and presence of coronary aneurysms. METHODS: Twenty-three patients with aneurysmal coronary artery disease and stable angina were enrolled into study (Group 1). Twenty-two patients without coronary aneurysm were selected as a control group (Group 2). PAI-1 was measured in peripheral venous blood. RESULTS: The plasma PAI-1 level was lower in the coronary artery aneurysmatic patients compared to the control group (8.41 +/- 4.28 vs. 13.32 +/- 10.05 ng/ml, p = 0.037). Serum C-reactive protein (CRP) values were not significantly different between groups (3.83 +/- 1.08 vs. 4.01 +/- 1.35 mg/l, p >0.05). CONCLUSION: Increased matrix degrading enzyme activity can cause arterial wall destruction through increased proteolysis of extracellular matrix proteins. Unregulated plasmin hyperactivity due to decreased inhibition by PAI-1 may play an important role in coronary aneurysm formation.     

A common mutation of the insulin receptor substrate-1 gene is a risk factor for coronary artery disease

Insulin resistance is associated with increased risk of atherosclerosis. Insulin receptor substrate-1 (IRS-1) plays a key role in tissue insulin sensitivity. A common mutation (G972R) of the IRS-1 gene has been shown to impair IRS-1 function, and it has been associated with reduced insulin sensitivity and lipid abnormalities. This led us to investigate the role of the G972R mutation in predisposing individuals to coronary artery disease (CAD). The DNA of 318 subjects with angiographically documented coronary atherosclerosis (>50% stenosis) and 208 population control subjects was analyzed for the presence of the G972R mutation. This mutation was detected by nested polymerase chain reaction and BstNI restriction enzyme digestion. The frequency of the G972R mutation was significantly higher among patients with CAD than controls (18. 9% versus 6.8%, respectively; P<0.001). After controlling for other coronary risk factors, the relative risk of CAD associated with the G972R mutation was 2.93 (95% CI 1.30 to 6.60; P<0.02) in the entire cohort. This risk was found to be even higher in the subgroups of obese subjects (odds ratio [OR] 6.97, 95% CI 2.24 to 21.4; P<0.001) and subjects with clinical features of insulin resistance syndrome (OR 27.3, 95% CI 7.19 to 104.0; P<0.001). The IRS-1 gene variant was associated with a higher frequency of diabetes mellitus (14.9% among carriers versus 6.5% among noncarriers; P<0.01) and with a 60% increase of plasma total triglycerides (P<0.001). Also, plasma concentrations of total cholesterol and the ratio of total cholesterol to HDL cholesterol were significantly (P<0.001) higher among carriers than noncarriers, although to lesser a extent. These effects were independent of CAD status. The G972R mutation in the IRS-1 gene was found to be a significant independent predictor of CAD. Moreover, this mutation greatly increased the risk of CAD in obese subjects and in patients with the cluster of abnormalities of insulin resistance syndrome. Besides the increased frequency of diabetes, carriers showed a more atherogenic lipid profile, suggesting a potential role of the IRS-1 gene in the pathogenesis of lipid abnormalities associated with CAD.