Complex regional pain syndrome type I: a comprehensive review.

BACKGROUND: Complex regional pain syndrome type I (CRPS I), formerly known as reflex sympathetic dystrophy (RSD), is a chronic painful disorder that usually develops after a minor injury to a limb. This topical review gives a synopsis of CRPS I and discusses the current concepts of our understanding of CRPS I in adults, the diagnosis, and treatment options based on the limited evidence found in medical literature. CRPS I is a multifactorial disorder. Possible pathophysiological mechanisms of CRPS I are classic and neurogenic inflammation, and maladaptive neuroplasticity. At the level of the central nervous system, it has been suggested that an increased input from peripheral nociceptors alters the central processing mechanisms. METHODS: A literature search was conducted using, as electronic bibliographic database, Medline from 1980 until 2014. RESULTS: An early diagnosis and multidisciplinary treatment are necessary to prevent permanent disability. CONCLUSIONS: The pharmacological treatment of CRPS I is empirical and insufficiently effective. Further research is needed regarding the therapeutic modalities discussed in the guidelines. Physical therapy is widely recommended as a first-line treatment. The efficacy of local anesthetic sympathetic blockade as treatment for CRPS I is questionable.

Modification of the lipidic and coagulative pattern in postmenopause women: effect of hormone replacement therapy.

AIM: We evaluated the changes of lipidic and coagulative pattern during menopause and the influence of hormone replacement therapy (HRT) on these parameters. METHODS: We considered 158 patients divided into 2 groups: Group I consisted of 127 women in physiological/surgical menopause and Group II of 31 women with childbearing potential. Subsequently, we considered a group III formed of 34 patients from menopausal women (group I) who underwent three months of HRT. We evaluated total-cholesterol (TC), HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C), triglycerides (TG), lipoprotein (a) (Lpa), fibrinogen, antithrombin III (ATIII), factor VII (FVII) and tissue factor pathway inhibitor (TFPI). RESULTS: We found a worse lipid profile in the post-menopausal group compared to controls (TC 243.8+/-29.7 vs 217.9+/-32.7 mg%, P=0.002; TG 121.5+/-68.4 vs 88.6+/-53.0 mg%, P=0.039; LDL-C 163.0+/-27.9 vs 136.2+/-29.6 mg%, P=0.004; HDL-C 60.9+/-14.9 vs 64.1+/-14.6 mg%, P=ns). With regard to the coagulative pattern, fibrinogen was significantly higher in the post-menopausal group (fibrinogen: 273.3+/-67.4 vs 243.8+/-39.5 mg%, P=0.013; ATIII 112.2+/-11.7 vs 117.5+/-12.7% %, P=0.059; FVII 121.6+/-11.3 vs 117.6+/-10.8 mg%, P=ns; TFPI activity 2.5+/-2.3 vs 2.1+/-1.1 U/mL, P=ns; TFPI antigen 120+/-38 vs 127+/-39 U/mL, P=ns). Comparing the same parameters, before and after three months of HRT, in patients of Group III we observed a significant improvement of TC and TG levels (TC from 232.3+/-42.7 to 215.2+/-37.6 mg%, P=0.0001; TG from 103.7+/-56.8 to 95.0+/-44.3 mg%, P=0.059; HDL-C from 62.3+/-12.9 to 63.6+/-12.6 mg%, P=ns; LDL-C from 149.3+/-38.7 to 132.6+/-34.5 mg%, P=0.0001). The following changes were observed with regard to coagulative parameters: fibrinogen from 270.9+/-69.4 to 253.2+/-56.2 mg%, P=0.07; ATIII from 113.5+/-11.4 to 110.8+/-13.2 mg%, P=0.198; FVII from 108.6+/-18.0 to 104.4+/-17.5 mg%, 0.014. TFPI activity from 2.6+/-2.3 to 2.3+/-1.4 U/ml, P=ns; TFPI antigen from 68+/-13 to 87+/-22 U/mL, P=0.001. CONCLUSION: Our data confirm the presence of an alteration in lipidic and coagulative pattern in post menopausal women and positive changes after HRT.

Inefficiency of renin-angiotensin inhibitors in preventing atrial fibrillation in patients with a normal heart.

AIM: Recent scientific evidence has emphasized the possible role of inhibitors of the renin-angiotensin system in preventing arrhythmic relapses in patients with paroxysmal or persistent atrial fibrillation and co-existing left ventricular hypertrophy or left ventricular dysfunction. METHODS: In order to verify the effects of these drugs on patients with a normal heart, we collected a series of 187 patients admitted to our division of cardiology for paroxysmal or persistent atrial fibrillation. All patients underwent cardioversion (with antiarrhythmic drugs and/or by electrical cardioversion) and were discharged in sinus rhythm. Episodes of recurrent arrhythmia were recorded during a mean follow-up period was 2 years. Patients were subdivided into 2 groups according to therapy: group 1 comprised patients receiving renin-angiotensin system inhibitors, group 2 comprised those not receiving therapy with these agents. All 91 patients in group 1 and 76 of those in group 2 had hypertension. Among the 91 patients in the group 1, 55 were treated with angiotensin-converting enzyme (ACE) inhibitors and 36 with angiotensin receptor blockers. There were no statistically significant differences in cardiovascular risk factors or antiarrhythmic drug use between the 2 groups. RESULTS: In group 1, 83% of patients experienced <2 recurrences of atrial fibrillation during the follow-up period, while 17% had >2 episodes. In group 2, 86% of patients experienced <2 relapses during the follow-up period, while the remaining 14% had >2 relapses. There was no statistically significant difference between the 2 groups (P=0.85). A subgroup analysis showed that treatment with angiotensin receptor blockers, beta-blockers, diuretics, and calcium-channel blockers brought no advantage in sinus rhythm maintenance. CONCLUSION: In our sample of hypertensive patients with a healthy heart, treatment with ACE inhibitors showed no statistically significant advantage in the prevention of atrial fibrillation relapses.