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Although genetic etiologies of many lymphatic dysplasia syndromes associated with\n                    <jats:styled-content style=\"fixed-case\">PIL<\/jats:styled-content>\n                    have been identified, the pathogenesis of isolated\n                    <jats:styled-content style=\"fixed-case\">PIL<\/jats:styled-content>\n                    (with no associated syndromic features) remains unknown. Familial cases and occurrence at birth suggest genetic etiologies in certain cases. Recently,\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    55 deficiency with hyperactivation of complement, angiopathic thrombosis, and PLE (the\n                    <jats:styled-content style=\"fixed-case\">CHAPLE<\/jats:styled-content>\n                    syndrome) has been identified as a monogenic form of\n                    <jats:styled-content style=\"fixed-case\">PIL<\/jats:styled-content>\n                    . Surprisingly, loss of\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    55, a key regulator of complement system leads to a predominantly gut condition. Similarly to other complement disorders, namely paroxysmal nocturnal and hemoglobinuria (\n                    <jats:styled-content style=\"fixed-case\">PNH<\/jats:styled-content>\n                    ) and atypical hemolytic uremic syndrome (\n                    <jats:styled-content style=\"fixed-case\">aHUS<\/jats:styled-content>\n                    ),\n                    <jats:styled-content style=\"fixed-case\">CHAPLE<\/jats:styled-content>\n                    disease involves pathogenic cross\u2010activation of the coagulation system, predisposing individuals to severe thrombosis. The observation that complement system is overly active in\n                    <jats:styled-content style=\"fixed-case\">CHAPLE<\/jats:styled-content>\n                    disease introduced a novel concept into the management of\n                    <jats:styled-content style=\"fixed-case\">PLE<\/jats:styled-content>\n                    ; anti\u2010complement therapy. While\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    55 deficiency constitutes a treatable subgroup in the larger pool of patients with isolated\n                    <jats:styled-content style=\"fixed-case\">PIL<\/jats:styled-content>\n                    , the etiology remains to be identified in the remaining patients with intact\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    55.\n                  <\/jats:p>","DOI":"10.1111\/imr.12715","type":"journal-article","created":{"date-parts":[[2018,12,18]],"date-time":"2018-12-18T20:12:24Z","timestamp":1545163944000},"page":"20-32","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":35,"title":["CHAPLE syndrome uncovers the primary role of complement in a familial form of Waldmann's 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