2. Discussion
Despite the significant advance in human research, the delineated
pathogenesis of conjoined twins remains a mystery. Two
major theories have been proposed. According to the fusion
theory, occurrence of the anomaly is determined by the end of the
second week of gestation when two heterozygotic embryos fuse
together to form a common embryonical structure containing two
embryonic discs but a single yolk sac. DNA analysis of both the
autosite and the parasite respectively has demonstrated the latter
to be virtually always homozygotic [5]. The latter theory has been
rejected, but a report is published to present a dizygotic origin of
twins [6]. The fission theory implies incomplete division of the
embryo followed by subsequent fusion at 14e15 days after fertilization
resulting in conjoined twinning. The meaning of ischemic
atrophy in the pathogenesis of double monstrosity has been
debated. Early malnourishment in one of twins induces selective
degeneration in the upper half of the body and makes it totally
dependent for growth on the autosite [5]. The factors that cause
this selective atrophy are not discernible, but the oversensitivity of
the brain, heart and lungs to ischemia are noted [7]. Joined twins
at the site of either abdomen or thorax result from union at the
extreme rostral aspect of the early embryonic disc, primarily
involving only the septum transversum in omphalopagus, but both
the septum and the cardiac primordium in thoracopagus. The
latter comprises a small portion of all reported heteropagus twins
because a defective heart of the autosite is unable to support the
viability of both fetuses [2]. Albeit by the definition, thoracopagus
parasiticus must involve abnormal heart (duplication of cardiac
primordium in symmetrical twins) some authors have reported
heteropagus parasiticus without heart involvement in the autosite
2. DiscussionDespite the significant advance in human research, the delineatedpathogenesis of conjoined twins remains a mystery. Twomajor theories have been proposed. According to the fusiontheory, occurrence of the anomaly is determined by the end of thesecond week of gestation when two heterozygotic embryos fusetogether to form a common embryonical structure containing twoembryonic discs but a single yolk sac. DNA analysis of both theautosite and the parasite respectively has demonstrated the latterto be virtually always homozygotic [5]. The latter theory has beenrejected, but a report is published to present a dizygotic origin oftwins [6]. The fission theory implies incomplete division of theembryo followed by subsequent fusion at 14e15 days after fertilizationresulting in conjoined twinning. The meaning of ischemicatrophy in the pathogenesis of double monstrosity has beendebated. Early malnourishment in one of twins induces selectivedegeneration in the upper half of the body and makes it totallydependent for growth on the autosite [5]. The factors that causethis selective atrophy are not discernible, but the oversensitivity ofthe brain, heart and lungs to ischemia are noted [7]. Joined twinsat the site of either abdomen or thorax result from union at theextreme rostral aspect of the early embryonic disc, primarilyinvolving only the septum transversum in omphalopagus, but bothการ septum และ primordium หัวใจใน thoracopagus ที่หลังประกอบด้วยส่วนเล็ก ๆ ของแฝด heteropagus รายงานทั้งหมดเพราะหัวใจบกพร่องของ autosite ไม่สนับสนุนการชีวิตของทั้งสอง fetuses [2] แม้ว่าตามนิยาม thoracopagusparasiticus ต้องเกี่ยวข้องกับหัวใจผิดปกติ (ซ้ำหัวใจprimordium ในคู่สมมาตร) ผู้เขียนบางมีรายงานheteropagus parasiticus โดยหัวใจมีส่วนร่วมในการ autosite
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