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  • Title: [Clinical, histopathologic and immunohistochemical studies of chronic sialectatic parotitis in childhood and adolescence].
    Author: Ussmüller J, Donath K.
    Journal: Klin Padiatr; 1999; 211(3):165-71. PubMed ID: 10412127.
    Abstract:
    UNLABELLED: Chronic sialectatic parotitis (CSP) causes problems in differential diagnosis and therapy. CSP shows the typical clinical features of chronic recurrent parotitis and will be investigated histopathologically only after ultimative parotidectomy. The etiology and pathogenesis of these unspecific inflammations is still unknown. Therefore no causal therapy is available and a lot of different trials (sialogoga, gland massage, infrared light, antibiotics, antiphlogistics, Trasylol, duct occlusion, duct ligation, gland denervation, radiotherapy) are not successful in the long run. MATERIAL AND METHOD: The salivary gland registry of the University of Hamburg (1965-1996) contains 22 infants and juvenile patients showing very severe courses of CSP. These cases have been investigated clinical (ultrasound, sialography), histopathological (paraffin embedded sections, histomorphometry of the ectatic duct lumina) and immunohistochemical (CK-MNF, AKTIN, KiM4) in a retrospective study to research the pathogenesis of CSP. RESULTS: Recurrent and always very dolent parotid swelling occurs between the age of 3 and 14 years for the first time. The courses vary from 3 months until 25 years. Local findings as well as ultrasound and sialographic features allow no certain differentiation of chronic recurrent parotitis. Conservative therapy fails in each case and leads to the necessity of surgical treatment. Histopathological three different stages of development can be observed: Initial stages show regular lobular architectonic structure of the parotid gland parenchyme with duct ectasies surrounded by slight inflammation of lymphocytes and plasmacells. Advanced stages are characterized by an increase of periductal inflammation and the appearance of lymphfollicels. Nearly complete lymphatic transformation of the parenchyme with destruction of the lobular formation dominates the terminal "immunologic" stage. Some cases show multiple myoepithelial islands within this lymphatic stroma typically observed in benign lymphoepithelial lesions. Whether bacteria nor primary obstructive changes can be observed. The histomorphometric analyses of the average and maximal luminal duct diameters show marked increase of 39% respectively 46% from and- vanced to terminal stages of CSP. Therefore the pathognomonic duct ectasies seem to depend on the progredient inflammation and are not due to a hereditary malformation of the duct system. Immunohistochemical terminal stages show follicular lymphatic hyperplasia (KiM4) expressing overshooting humoral immune reaction of MALT. CONCLUSION: Concerning the pathogenesis CSP corresponds to a immunopathological disorder of MALT and seems to be a prestage of benign lymphoepithelial lesion. Consequently important changes in the diagnosis and therapy of CSP lead to early histopathological investigation to differentiate the stage of inflammation. In stage III conservative parotidectomy should be carried out because spontaneous healing can not be expected. In contrast initial cases should be treated at first by glucocorticoids and immunosuppressives.
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