Atherosclerosis, some serum inflammatory markers in psoriasis.

AIM: Psoriasis is an autoimmune inflammatory disease which is associated with increased inflammatory markers and atherosclerosis. We wanted to investigate whether there is a relationship between some inflammatory markers and subclinical atherosclerosis markers. METHODS: We studied 60 psoriasis patients and 50 healthy controls. Demographic, biochemical parameters, C3, C4, d-dimer, CRP, fibrinogen and YKL-40 (human cartilage glycoprotein-39) levels were measured. After measuring carotid intima-media thickness (cIMT) and aortic elasticity parameters such as aortic strain, (beta) stiffness index and compliance, statistical comparisons were done. RESULTS: Patients with psoriasis had significantly higher diastolic blood pressure, CRP, fibrinogen, C3, uric acid levels, ß-stiffness index, and cIMT values than the control group. cIMT was correlated with CRP, YKL-40 and psoriasis area and severity index (PASI) score (r=0.219, P=0.038; r=0.225, P=0.033 and r=0.275, P=0.034). Aortic strain (%), aortic compliance and aortic stiffness index were correlated with C3 (r=-0.349, r=-0.526 and r=0.235) and fibrinogen (r=-0.354, r=-0.275 and r=0.289), all P values <0.05, but not with PASI score. The presence of psoriasis was related to aortic strain (ß±SE: -2.055±0.861, P=0.019) and ß-stiffness index (ß±SE: 2.934±1.143, P=0.012). CONCLUSION: Serum C3, CRP, fibrinogen and YKL-40 levels are elevated as well as increased cIMT and impaired aortic elasticity in psoriasis. CRP, YKL-40 and PASI score are correlated with cIMT. Increased serum C3 and fibrinogen levels correlate negatively with aortic strain and aortic compliance, and correlate positively with the ß-stiffness index.

Lichen simplex chronicus as a symptom of neuropathy.

BACKGROUND: The main cause of lichen simplex chronicus (LSC) is not known but there is evidence to suggest that neurological abnormalities may be implicated in its aetiology. AIM: To investigate neuropathy in patients with LSC on the limbs. METHODS: In total, 23 consecutive patients [15 women (65.2%) and 8 men (34.8%); mean +/- SD age 48.2 +/- 14.03 years, range 20-71] with LSC on the limbs were included in the study. Mean +/- SD duration of disease was 22.86 +/- 21.38 months (range 1-60). Radiography, magnetic resonance imaging (MRI) and electrophysiological studies were performed for all patients. RESULTS: In total, 8 patients (34.8%) had LSC on the arms and 15 patients (65.2%) had LSC on the legs; 3 (37.5%) of the 8 patients with LSC on the arms and 6 (40%) of the 15 patients with LSC on the legs had radiculopathy in the electrophysiological studies. The prevalence of radiculopathy in patients with LSC on the limbs was higher than in asymptomatic subjects in the electrophysiological studies. CONCLUSIONS: Damage to the peripheral nervous system, such as radiculopathy and neuropathy, can play a critical role in the aetiology of LSC on the limbs. Both nerve-root compression in MRI scans and radiculopathy in nerve-conduction studies are common findings in asymptomatic subjects, but they seem to be more common in patients with LSC on the limbs. Therefore, these patients should be evaluated for the possibility of underlying neuropathy.

Acquired port-wine stain related to acoustic neuroma.

Port-wine stains are frequently seen congenital vascular malformations consisting of ectatic dermal capillaries. Acquired port-wine stain that develops later in life is an uncommon vascular lesion that is morphologically identical to a congenital port-wine stain. In the majority of acquired port-wine stains, the aetiology is unknown, but trauma is an important causative factor. Other proposed aetiologies include chronic sun exposure, hormonal changes, frostbite injury, obstruction of the peritoneovenous shunt, herpes zoster infection, and cerebral arteriovenous malformation. Here we report the first case of a patient who had an acquired port-wine stain related to a solid brain tumour.