Lipedema is a chronic vascular disease almost exclusively of female sex, characterized by the deposit of fat on the legs, with an "Egyptian column" shape, orthostatic edema, hypothermia of the skin, alteration of the plantar support, and negativity of Stemmer's sign. The etiology and pathogenesis of this disease are still the object of study, and therapy is very difficult. Various authors have described morphologic and functional alterations of prelymphatic structures and of lymphatic vessels. The big veins remain untouched in the phlebograms and an alteration of the skin elasticity is demonstrated. The present authors have studied by dynamic lymphoscintigraphy 12 women patients suffering from lipedema, and compared the results with those of 5 normal subjects and 5 patients suffering from idiopathic lymphedema who were sex and age matched with the patients suffering from lipedema. The patients suffering from lipedema showed an abnormal lymphoscintigraphic pattern with a slowing of the lymphatic flow that presented some analogies to the alterations found in the patients suffering from lymphedema. A frequent asymmetry was also noticed in the lymphoscintigraphic findings that is in contrast to the symmetry of the clinical profile.
Here we describe the case of a 41-year-old woman with a history of Cushing disease who had previously undergone unsuccessful neurosurgery, followed by stereotactic radiosurgery. More than 4 years after this treatment, she presented severe visual impairment, which started in the left eye and was documented by neuro-ophthalmic evaluation. Radiological assessment by contrast-enhanced magnetic resonance (MR) imaging initially suggested the diagnosis of glioma of the optic nerve and the patient started corticosteroid treatment (first with prednisone, 80 mg/day, followed by dexamethasone, 8 mg/day). Despite the therapy, vision in the left eye rapidly worsened until light was no longer perceptible; similar symptoms and signs also developed in the right eye, evolving to complete temporal hemianopsia. The clinical evidence was confirmed by the rapid progression of the MR picture, which showed homogeneous enhancement of the chiasm and optic nerves. On the basis of these findings, the original diagnosis of glioma was excluded, and radiation-induced optic neuropathy was diagnosed. As corticosteroids had proved inefficacious, hyperbaric oxygen (HBO) therapy was promptly instituted and vision steadily started to improve. This improvement was documented and confirmed by the progressive recovery of the visual field in the right eye and the changes in the sequential follow-up MR scanning. Optic neuropathy is an infrequent but dramatic complication of radiation therapy. Symptoms develop, on average, 12 months after treatment, and the onset may be acute and characterized by the progressive loss of vision in one or both eyes. HBO has already been used to treat this complication, but its efficacy is still controversial. Here, in addition to describing this particular case, which presented a significantly delayed radiation injury of the optic pathways, we provide a brief literature review and discuss some important points. 154 813-818 European Journal of Endocrinology
Objectives Superficial vein thrombosis in non-varicose veins of the lower limbs is rather frequent and may be underestimated. This study aims to evaluate the prevalence of inherited or acquired thrombophilia in a sample of outpatients with the disease. Method An observational study was conducted on 73 consecutive superficial vein thrombosis patients tested for inherited or acquired thrombophilia. Results Sixty of 73 patients with superficial vein thrombosis completed the testing protocol, while 13 dropped out; 46 of 60 patients were found to have a thrombophilia (76.6%). The types detected were: factor V Leiden (31/60, i.e. 51.6%), prothrombin mutation (2/60, i.e. 3.3%), MTHFR mutation (23/60, i.e. 38.3%), antiphospholipid antibodies (5/60, i.e. 8.3%), protein C deficit (1/60, i.e. 1.6%), protein S deficit (1/60, i.e. 1.6%), and antithrombin deficit (0/60, i.e. 0%). Conclusions Among patients with superficial vein thrombosis in non-varicose veins, testing demonstrated a high prevalence of thrombophilia. The most common form proved to be factor V Leiden. As thrombophilia was found to be a major cause of superficial vein thrombosis in non-varicose veins, the authors recommend that patients with superficial vein thrombosis in non-varicose veins be investigated for thrombophilia.
Stasis microangiopathy includes all the pathological changes in the microcirculation and interstitium due to venous hypertension. Venous valve incompetence occurring in the superficial or deep venous system or in both is the most common cause of venous hypertension, a pathological condition that plays a key role in most or all clinical signs of chronic venous disease, including edema and venous ulcers. The aim of the first and main part of this review is to focus on the various pathogenetic mechanisms of stasis microangiopathy triggered by venous hypertension, including hemodynamic and hemorheological alterations, inflammation, and functional alterations. The rationale underlying the current available treatment options of stasis microangiopathy is mentioned briefly in the second part of the review.
Objective: To evaluate the recurrence of telangiectases in patients who had previously been treated by sclerotherapy. Design: Retrospective single patient group study with 5-year follow-up. Setting: Centra Studi Malattie Vascolari ‘J. F. Merlen’, Frosinone, Italy. Patients and methods: The records of 52 patients who had been treated by sclerotherapy for leg telangiectases 5 years earlier were reviewed. Patients had been reviewed at yearly intervals. The reappearance of telangiectases at the initial treatment site and at new sites had been recorded at each review. Results: In 77% of patients studied (40/52) new telangiectases appeared. Of these, 67% (35/72) were in a different area and 56% (29/52) were in the same area (χ2 = N.S.). In 46% of cases (24/52) telangiectases occurred both in the area treated originally and in additional areas. In 48% of cases affected by a recurrence (19/40), the additional telangiectases were of minimal extent requiring little if any treatment. Conclusions: Sclerotherapy of telangiectases treats the consequences of the disease and does not address the cause. Consequently, patients often suffer recurrence of their telangiectases. This may be regarded as an evolution of the disease, affecting new veins, rather than true recurrence. Maintenance treatment will often be required to sustain the results following the initial course of sclerotherapy.
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