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      Unilaterales Sicca-Syndrom Translated title: Unilateral dry eye syndrome

      brief-report

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          Abstract

          Es wird über den Fall eines streng einseitigen Sicca-Syndroms bei einem männlichen Patienten berichtet. Im Rahmen einer Stufendiagnostik konnte das Spektrum möglicher Ursachen immer weiter eingegrenzt werden, wobei v. a. die MRT-morphologische Darstellung der Tränendrüsenloge auf der betroffenen Seite wichtige diagnostische Informationen lieferte. Schlussendlich konnte in Zusammenschau der Befunde und in Verbindung mit der Anamnese des Patienten eine traumatisch bedingte Atrophie der Tränendrüse als auslösender Faktor eruiert werden.

          Translated abstract

          This article presents the case of a strictly unilateral dry eye syndrome in a male patient. Based on a stepwise diagnostic procedure the spectrum of possible causes could be gradually limited, whereby the magnetic resonance imaging of the lacrimal gland in particular provided important diagnostic information. Ultimately, in the synopsis of the findings and combined with the medical history of the patient, a traumatic atrophy of the lacrimal gland could be determined as the triggering factor.

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          Most cited references5

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          Anatomy and histopathology of the human lacrimal gland.

          To review the anatomy and histopathologic changes of the human main lacrimal gland.
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            Estrogen prevention of lacrimal gland cell death and lymphocytic infiltration.

            Previous studies have shown that ovariectomy causes necrosis of lacrimal acinar cells, apoptosis of plasma cells and gland lymphocytic infiltration. Both, lacrimal gland cell death and lymphocytic infiltration were prevented by androgen treatment. Since estrogens are removed by ovariectomy, and the synthetic estrogen diethylstilbestrol has been shown to affect some biochemical correlates of lacrimal secretion, the purpose of this study was to determine the effect of 17-beta-estradiol treatment on ovariectomy-induced cell death and lymphocytic infiltration. Sexually mature female New Zealand white rabbits (4-4.5 kg) were ovariectomized and divided into two groups. One group was treated with 0.5 mg kg(-1) per day 17-beta-estradiol, and the other group with vehicle alone. A third group of sham operated rabbits was used as controls and they also were treated with vehicle alone. Six days after surgery, the animals were euthanized, the lacrimal glands removed and processed for analysis of apoptosis as assessed by DNA fragmentation, and for morphological examination. DNA fragmentation was determined using the TUNEL assay and agarose gel electrophoresis. Sections were also stained for rabbit thymic lymphocyte antigen (RTLA), and rabbit CD18. Labelled nuclei and stained areas were quantified by automated densitometry. Ovariectomized rabbits showed a significant increase in the values for degraded DNA as a percent of total nuclear area (2.90+/-0.40%) compared to sham operated rabbits (0.73+/-0.22%). 17-beta-estradiol treatment in ovariectomized rabbits prevented the increase in DNA degradation. Examination of TUNEL assay at higher magnification (40x) confirmed previous studies showing that ovariectomy caused apoptosis of interstitial cells. Significant numbers of bulging cells of very pale appearance under light microscopy, also confirm previously identified necrotic cells in acinar regions. Treatment with 17-beta-estradiol prevented this necrosis. Increased numbers of RTLA(+) and CD18(+) interstitial cells were also evident after ovariectomy. 17-beta-estradiol treatment prevented the increase in the number of lymphoid cells. We confirmed previous observations that suggest that glandular atrophy observed after ovariectomy is likely to proceed by necrosis of acinar cells rather than apoptosis, and that ovariectomy triggers an inflammatory response in the gland. These results suggest that in addition to androgens, estrogens also seem to play a role to maintain lacrimal gland structure and function. A decrease in available estrogen levels could trigger both lacrimal gland apoptosis and necrosis, as well as lymphocytic infiltration. Although, the effect of estrogens in these experiments seems to be direct and not through androgens, the possibility of the role of an autocrine and/or paracrine factors, promoted by estrogen on lacrimal gland cells still needs to be investigated.
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              The relationship between apoptosis and atrophy in the irradiated lacrimal gland.

              Atrophy is generally considered to be a true late effect of radiation. However, in serous glands, atrophy was thought to be a consequential late effect because serous cells die within hours of irradiation and the apparent effects of atrophy are observed contemporaneously with radiation treatment. Therefore, to determine the pathogenesis of atrophy in serous glands, it is necessary to differentiate between parenchymal loss as a result of direct radiation death of serous cells and parenchymal loss as a result of serous cell death that is secondary to fibrosis, vascular damage, or precursor cell death. The lacrimal glands of 62 rhesus monkeys have been irradiated to single doses of 2.5 to 20 Gy and examined at intervals of 4 hr to 112 days postirradiation. Serous cells (nuclei) and acini were counted in at least 30 high power fields per (dose, time) point. At each dose and time of sacrifice, the average number of nuclei per acinus and the average number of acini per high power field were calculated. Also at each dose and time, the distribution of the number of nuclei per acinus was examined to determine how the frequency of acinar sizes changed as a function of irradiation. The number of cells per acinus appears to rise initially, but this is likely a result of the degranulated cells being physically smaller, yielding an artificially higher count. Within 4 days after 12.5 Gy, the average number of nuclei per acinus approaches control values and remains within the range of controls for at least 112 days. The number of acini per high power field decreases steadily for 30 days after 12.5 Gy. From 30 to 112 days, there is some recovery of this number, but it remains well below control values. At 24 hr, the number of nuclei per acinus shows a distinct dose response up to 20 Gy. However, at 30 days there is no evidence of a dose response for this parameter. These results indicate that even though serous cells die in significant numbers within hours of irradiation, the atrophy of the lacrimal gland (and by extension, the parotid gland) is a result of the death of the serous stem cell or precursor. Consequently, protection of serous cells from radiation apoptosis will not diminish serous gland atrophy.
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                Author and article information

                Contributors
                Juliane.Jakob@med.uni-jena.de
                Journal
                Ophthalmologe
                Ophthalmologe
                Der Ophthalmologe
                Springer Medizin (Heidelberg )
                0941-293X
                1433-0423
                9 July 2020
                9 July 2020
                2021
                : 118
                : 6
                : 587-589
                Affiliations
                GRID grid.275559.9, ISNI 0000 0000 8517 6224, Universitätsklinikum Jena, ; Am Klinikum 1, 07747 Jena, Deutschland
                Author information
                http://orcid.org/0000-0003-4611-9210
                Article
                1168
                10.1007/s00347-020-01168-5
                8187192
                32647926
                b698d083-3ade-4cf8-8c06-fea0a7ef975d
                © The Author(s) 2020

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                History
                Funding
                Funded by: Universitätsklinikum Jena (8979)
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                © Springer Medizin Verlag GmbH, ein Teil von Springer Nature 2021

                keratitis superficialis punctata,contusio bulbi,stufendiagnostik,mrt,tränendrüsenatrophie,superficial punctate keratitis,contusion of the bulb,stepwise diagnostic procedure,magnetic resonance imaging,lacrimal gland atrophy

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