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      Duplication of the pituitary gland - plus syndrome

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          Abstract

          Duplication of the pituitary gland (DPG) is a very rare developmental anomaly that is often associated with other anomalies – the DPG-plus syndrome and occurs due to splitting of the rostral notochord and prechordal plate during blastogenesis. DPG with the constellation of associated anomalies as in our patient has not been reported previously. This article illustrates the importance of imaging the brain in all patients with obvious midline facial anomalies and the complementary role of MRI and CT in such cases.

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          Most cited references16

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          Defects of blastogenesis.

          Ginevra Zanni, Catherine J Reynolds, John Opitz … (2002)
          Ever more frequent and closer involvement by clinical geneticists and counselors in the prenatal assessment of development mandates a better understanding of all stages of human ontogeny, but especially those of earliest development during which most of the lethal and all of the gross, multiple and complex defects of morphogenesis arise. Because of the phenomenon of universality, i.e., identical molecular inductive mechanisms involved in the process of embryonic pattern formation in all vertebrates, experimental animals indeed are a most valuable approach to an understanding of the causal and formal aspects of development and are beginning to forge essential, strong bonds between molecular biologists and clinicians in a mutually supportive discipline of developmental biology. However, to grieving parents of a stillborn fetus with, say, Pentalogy of Cantrell, sirenomelia or otocephaly, mouse data offer little comfort or reassurance about recurrence; thus, it is imperative to make ever more effective a science of human teratology (sensu lato) with participating reproductive geneticists, obstetricians, neonatologists, ultrasonographers, pediatric/fetal pathologists, cytogeneticists and pediatric geneticists to generate the diagnostic, pathogenetic and causal data necessary to counsel and to comfort the parents. Few molecular data exist on causes of blastogenetic defects in humans; however, the phenomenon of parsimony, whereby the same "morphogenetic" molecule, say, sonic hedgehog (SHH), is "deployed" simultaneously or sequentially during the morphogenesis (and even the histogenesis) of several/many embryonic primordia, makes it likely that a genetic/epigenetic disturbance of such an inductive system will have multiple effects on blastogenetic, organogenetic and perhaps also histogenetic events in the embryo. If causally defined, such a pattern of anomalies constitutes pleiotropy, and the embryo/fetus can be said to have a syndrome. If cause is unknown, the presumption of pleiotropy is less certain, and the fetus/infant may be said to have an "association" with low empiric recurrence risk. Copyright 2002 Wiley-Liss, Inc.
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            Hypothalamic and pituitary development: novel insights into the aetiology.

            Daniel Kelberman, M. Dattani (2007)
            The anterior pituitary gland is a central regulator of growth, reproduction and homeostasis, and is the end-product of a carefully orchestrated pattern of expression of signalling molecules and transcription factors leading to the development of this complex organ secreting six hormones from five different cell types. Naturally occurring and transgenic murine models have demonstrated a role for many of these molecules in the aetiology of combined pituitary hormone deficiency (CPHD). These include the transcription factors HESX1, PROP1, POU1F1, LHX3, LHX4, TBX19, SOX2 and SOX3. The expression pattern of these transcription factors dictates the phenotype that results when the gene encoding the relevant transcription factor is mutated. The highly variable phenotype may consist of isolated hypopituitarism, or more complex disorders such as septo-optic dysplasia and holoprosencephaly. Since mutations in any one transcription factor are uncommon, and since the overall incidence of mutations in known transcription factors is low in patients with CPHD, it is clear that many genes remain to be identified, and the characterization of these will further elucidate the pathogenesis of these complex conditions and also shed light on normal pituitary development.
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              MR, CT, and plain film imaging of the developing skull base in fetal specimens.

              Angela H Brodie, Carrie Chong, Franz Seibert … (2000)
              The developing fetal skull base has previously been studied via dissection and low-resolution CT. Most of the central skull base develops from endochondral ossification through an intermediary chondrocranium. We traced the development of the normal fetal skull base by using plain radiography, MR imaging, and CT. Twenty-nine formalin-fixed fetal specimens ranging from 9 to 24 weeks' gestational age were examined with mammographic plain radiography, CT, and MR imaging. Skull base development and ossification were assessed. The postsphenoid cartilages enclose the pituitary and fuse to form the basisphenoid, from which the sella turcica and the posterior body of the sphenoid bone originate. The presphenoid cartilages will form the anterior body of the sphenoid bone. Portions of the presphenoid cartilage give rise to the mesethmoid cartilage, which forms the central portion of the anterior skull base. Ossification begins in the occipital bone (12 weeks) and progresses anteriorly. The postsphenoid (14 weeks) and then the presphenoid portion (17 weeks) of the sphenoid bone ossify. Ossification is seen laterally (16 weeks) in the orbitosphenoid, which contributes to the lesser wing of the sphenoid, and the alisphenoid (15 weeks), which forms the greater wing. MR imaging can show early progressive ossification of the cartilaginous skull base and its relation to intracranial structures. The study of fetal developmental anatomy may lead to a better understanding of abnormalities of the skull base.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Indian J Radiol Imaging
                Journal ID (iso-abbrev): Indian J Radiol Imaging
                Journal ID (publisher-id): IJRI
                Title: The Indian Journal of Radiology & Imaging
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 0971-3026
                ISSN (Electronic): 1998-3808
                Publication date (Print): Jan-Mar 2016
                Volume: 26
                Issue: 1
                Pages: 126-130
                Affiliations
                [1]Department of Radiodiagnosis, Military Hospital, Amritsar, India
                [1 ]Department of Radiodiagnosis, Nijjer Scan and Diagnostic Centre, Amritsar, India
                Author notes
                Correspondence: Dr. Debraj Sen, Department of Radiodiagnosis, Military Hospital, Amritsar - 143 001, India. E-mail: sendebraj@ 123456gmail.com
                Article
                Publisher ID: IJRI-26-126
                DOI: 10.4103/0971-3026.178361
                PMC ID: 4813062
                PubMed ID: 27081236
                SO-VID: 281b08ac-26a6-4878-824e-895a07b51327
                Copyright © Copyright: © 2016 Indian Journal of Radiology and Imaging
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

                History
                Categories
                Subject: Neuro

                ScienceOpen disciplines: Radiology & Imaging
                Keywords: basilar artery duplication,blastogenesis,craniopharyngeal canal,duplication of pituitary gland,epignathus teratoma
                Data availability:
                ScienceOpen disciplines: Radiology & Imaging
                Keywords: basilar artery duplication, blastogenesis, craniopharyngeal canal, duplication of pituitary gland, epignathus teratoma

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