BACKGROUND: Cranial autonomic dysregulation is a common symptom of patients suffering from cluster headache or migraine. The peripheral vascular dysfunction may increase the risk for ischemic or hemorrhagic strokes, myocardial infarction, retinal vasculopathy, cardiovascular mortality, and peripheral artery diseases. Furthermore, it may also manifest with ocular symptoms, e.g., increased lacrimation, conjunctival injection, and facial swelling.
METHODS: We here report a case of a patient with migraine and ocular signs of a vascular dysregulation that have led to persisting changes of conjunctival vessels and to a corneal arcus.
CONCLUSIONS: Autonomic vascular dysregulation may not only cause headaches but also persisting changes of ocular tissues, e.g., conjunctival vessel alterations and a corneal arcus.

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A 25-year-old male patient presented with complaints of blurred vision in both eyes since 2 years. The patient was a known case of nephrotic syndrome with dyslipidaemia for which he was on diuretics and lipid-lowering agents for 3 years. On examination, his visual acuity was 6/9 in both eyes with cloudy cornea and arcus juvenilis. Fundus examination was within normal limits. On systemic work-up, his lipid profile was deranged with increased serum total cholesterol, very low density lipoprotein, low density lipoprotein and triglyceride. The serum high density lipoprotein was decreased. Renal function test revealed elevated serum creatinine with significant proteinuria. Renal biopsy was suggestive of dense deposit disease on immunofluorescence and transmission electron microscopy. Ocular manifestation of dense deposit disease is characterised by retinal drusen, pigmentary atrophy, choroidal neovascular membrane and atypical serous retinopathy. To the best of our knowledge, anterior segment changes in dense deposit disease has not been reported. This is the first case reporting cloudy cornea with arcus juvenilis in a case of dense deposit disease.

BACKGROUND: Arcus lipoides corneae is a common bilateral degenerative disorder with ageing but only rarely occurs unilaterally. Clinically visible cream-coloured ring-shaped corneal opacities are caused by excessive lipoid deposits in the corneal stroma. Our aim is to discuss theoretical aspects of the possible impact and pathomechanism of unilateral ptosis in unilateral arcus lipoides.
METHODS: The authors report the case of a 70-year-old female patient who was treated for chronic pancreatitis and hyperlipoproteinemia. She had congenital ptosis on the left side, and an arcus lipoides corneae in her left eye. The patient underwent extracapsular cataract extraction, and irregular high-grade astigmatism developed. An irregularity of the wound healing was apparent from the keratometric values, which decreased after removal of the corneal sutures.
CONCLUSIONS: The known etiological factors of unilateral arcus lipoides, like contralateral stenosis of the internal carotid artery, traumatic or iatrogenic hypotony, chronic iridocyclitis of the eye were absent in our patient.

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Premature corneal arcus may identify individuals with hyperlipidaemia and increased cardiovascular risk. We have attempted to quantitate relationships through determination of graded prevalence of corneal arcus with age for 81 males and 73 females suffering from heterozygous familial hypercholesterolaemia (HFH) at presentation, and for 280 male and 353 female unselected patients (age range 16-76 years) attending a country general practice. Some degree of arcus affected 50% of HFH patients by age 31-35 years, and 50% of practice patients by age 41-45 years. Complete full ring arcus affected 50% of the familial hypercholesterolaemia (FH) group by age 50 years, with only 5% similarly affected in the non-FH group. Arcus grade with age was advanced by some 5 years in males versus females. Premature arcus potentially alerting to HFH can be broadly defined for males and females combined, as heavy full ring by age 50 years, or any degree of arcus by age 30-35 years. Arcus grade was not related to the presence of coronary disease. Accelerated development of corneal arcus with age is an indicator of HFH, but premature arcus is not an additional marker of premature coronary disease for individual cases of HFH.

A Fish-Eye Disease family has been recently discovered in Bordeaux, being made up 3 homozygous and 3 heterozygous patients for a recessive hereditary anomaly of LCAT. The influence of the enzyme on the plasma lipoprotein composition and its role in cholesterol efflux explain, at least for a part, the pathophysiology of the lipidic corneal clouding which is the single symptom in the homozygous patients. The comparison of the molecular biology data resulting from the analysis of the patient\'s LCAT gene with those which have been obtained in other FED patients as in patients with classic LCAT deficiency allows to differenciate biochemically both pathologies. It allows too the differentiation between primary and secondary (Tangier disease, apo A-I deficiency, A-I and C-III deficiency) LCAT deficiencies, which may be all associated with a Corneal arcus. The profile of the lipidic parameters most often measured in plasma (Total cholesterol, HDL-cholesterol, cholesterol esterification rate, lipidogramme, apo A-I, apo A-II, LCAT mass and activity) is practically pathognomonic of this affection and consequently authorizes its differential diagnosis. In spite of the striking deficiency of HDL as of their atherogenesis preventing markers these patients do not show any sign of early cardio vascular disease.