Circulating microaggregates as biomarkers for the Post-COVID syndrome.

CoVID-19 can develop into Post-COVID syndrome of potentially high morbidity, with procoagulation and reactivation of dormant viral infections being hypothesized pathophysiological mechanisms. We report on a patient suffering from fatigue, post exertional malaise, pain and neurological symptoms as a consequence of the second CoVID infection. Using live confocal microscopy on native whole blood samples we detected microaggregates of thrombocytes, leukocytes and plasma proteins in peripheral blood. In addition, there was specific cellular immunological reactivity to EBV. Upon anticoagulatory and virustatic pharmacological therapy we observed dissolution of microaggregates and significant stable clinical remission. We suggest to consider circulating microaggregates as a morphological indicator of chronic post-COVID syndrome.

Lisch corneal dystrophy is genetically distinct from Meesmann corneal dystrophy and maps to xp22.3.

PURPOSE: There is an ongoing discussion whether Lisch corneal dystrophy (band-shaped and whorled microcystic dystrophy of the corneal epithelium) represents a disorder that is different from Meesmann corneal dystrophy. The purpose of this study was to evaluate at the molecular level if Lisch and Meesmann corneal dystrophies are genetically distinct. METHODS: We examined at the slit lamp a total of 48 members of a family with an aggregation of Lisch corneal dystrophy. Genomic DNA was extracted from leukocytes of the peripheral blood of seven affected and six unaffected members of this family. Mutational hotspots in the cornea-specific keratin genes K3 and K12 were scanned for mutations by single-strand conformation analysis. To test for linkage to the keratin K3 or K12 loci or for X-chromosomal inheritance, six (K3) and four (K12) microsatellite markers each flanking the keratin loci as well as 22 microsatellite markers covering the X-chromosome were typed. Linkage was analyzed using the MLINK and FASTMAP procedures. RESULTS: A total of 19 trait carriers were identified in six generations of the family. No hereditary transmission from father to son was observed. Linkage was excluded for the keratin K3 and K12 genes. Furthermore, single-strand conformation analysis detected no mutations in these genes. Multipoint linkage analysis revealed linkage with a maximum likelihood of the odds (LOD) score of 2.93 at Xp22.3. Linkage was excluded for Xp22.2 to Xqter. CONCLUSIONS: Lisch corneal dystrophy is genetically different from Meesmann corneal dystrophy. Evidence was found for linkage of the gene for Lisch corneal dystrophy to Xp22.3.

A new, band-shaped and whorled microcystic dystrophy of the corneal epithelium.

Five family members and three unrelated patients (four women, four men, 23 to 71 years old) had a dystrophy of the corneal epithelium. Direct slit-lamp examination showed bilateral or unilateral, gray, band-shaped, and feathery opacities that sometimes appeared in whorled patterns. Retroillumination showed intraepithelial, densely crowded, clear microcysts. Light and electron microscopy disclosed diffuse vacuolization of the cytoplasm of epithelial cells in the affected area. Visual acuity was so reduced in three patients that abrasion of the corneal epithelium was performed. The corneal abnormalities recurred within months, with the same reduction in visual acuity as before. The corneal opacities were progressive in two patients but diminished noticeably in another after he began using a hard contact lens. We found no other ophthalmic irregularities or associated systemic abnormalities and no indication of drug-induced keratopathy.

Schnyder's dystrophy. Progression and metabolism.

In the first long-term cohort study of Schnyder's corneal dystrophy the authors examined affected and unaffected members of two unrelated families in 1975 and 1976 respectively, and again in 1984. They identified carriers, catalogued changes in the diffuse and crystalline corneal opacities which characterize this dystrophy and analysed the patient's lipid metabolism. Corneal opacities never regressed. Progression was more frequent in diffuse than in crystalline opacities. Both crystalline and diffuse opacities reappeared and progressed following penetrating keratoplasty. Mean cholesterol levels in the carrier group were above normal and six had a moderate type IIa dyslipoproteinemia; conversely, two carriers had low apo B. The degree of corneal opacification showed no relationship to dyslipoproteinemia. Schnyder's corneal dystrophy appears to involve the corneal lipid metabolism only and not to be a systemic disease.

[Epithelial corneal basement membrane dystrophy]. / Die Epitheliale Hornhaut-Basalmembrandystrophie.

Dystrophy of the basement membrane of the corneal epithelium is an autosomal-dominant disease. Three distinct forms of opacity occur, either in isolation or in combination with one another. These are (1) dotlike opacities, (2) maplike opacities and (3) fingerprint lines. The present paper describes a family in which 6 members show only the characteristic signs of superficial maplike corneal opacities. There have been no recurrent corneal erosions. In addition, 7 "isolated cases" are described in which both the pure and combined forms of opacity have been observed. The dotlike opacities are demonstrable only when maplike alterations are also present. The patholomechanism leading to these dotlike changes cannot be explained by aberrance of the basement membrane alone. Cases of the three forms of opacity which may occur as secondary phenomena have to be distinguished from the dystrophic form.

[Differential diagnosis of hereditary vitreoretinal degenerations ]. / Differentialdignose hereditärer vitreoretinaler Degenerationen.

Vitreoretinal degenerations constitute the main cause of manifestation of an amotio retinae during youth. Seven different hereditary forms can be distinguished. For the individual types, characteristic or obligatory symptoms can be postulated. In this connection, five main symptoms of hereditary vitreo-retinal degenerations are presented: (1) foveal retionoschisis, (2) "white plains", (3) peripheral retinoschisis, (4) vitreal strands with insertion on the retina, (5) peripheral band-shaped vitreoretinal degeneration.