Cases reported "Diseases in Twins"

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1/13. lung development in diamniotic twins discordant for complete urinary tract obstruction.

    OBJECTIVES: To investigate the effect of anhydramnios on the lung development of 1 twin in the presence of a normal amniotic fluid volume in its diamniotic co-twin. methods: Three sets of diamniotic twins, discordant for complete urinary tract obstruction and anhydramnios, were followed prospectively with regular ultrasound scans and after delivery. RESULTS: All 3 twins with complete urinary tract obstruction and anhydramnios died within 2 days after birth, with confirmed severe pulmonary hypoplasia. In every case the twin with a normal amount of surrounding amniotic fluid had a normal postnatal outcome. CONCLUSIONS: The observation that a normal amniotic fluid volume in one sac does not protect the anhydramniotic twin from pulmonary hypoplasia has important implications for the aetiology of the condition and for the possibility of therapeutic septostomy. These results are discussed in relation to previous human and animal studies.
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2/13. central nervous system in twin reversed arterial perfusion sequence with special reference to examination of the brain in acardius anceps.

    The twin-reversed arterial perfusion (TRAP) sequence, or acardia, is the most severe complication in monozygotic twinning. Although more than 400 cases with TRAP sequence were reported since 1533, thorough investigations of the brain in those cases with a rudimentary head remained infrequent. We report a TRAP sequence with microcephaly and a severely rudimentary brain anlage. Neuropathologic examination clearly demonstrated two types of change: (1) developmental arrest of brain at the prosencephalic stage (holoprosencephaly), and (2) hypoxic damage to the holospheric brain mantle with cystic change (hydranencephaly). With reference to previous studies in experimental animals showing that lack of oxygen during early embryogenesis can induce severe disruptions of head-brain and heart formation, it is concluded that oxygen deficiency due to TRAP may be responsible not only for the encephaloclastic changes in the acardius anceps, but for the developmental arrest of the brain cases as well. This would make it unnecessary to postulate additional primary causes such as asymmetric zygote cleavage (Schwalbe, '07) for the maldevelopment.
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3/13. In utero development of hypertensive necrotizing pulmonary arterial lesions: report of a case associated with premature closure of the ductus arteriosus and pulmonary hypoplasia.

    Premature closure of the ductus arteriosus (PCDA) is an uncommon defect in which pulmonary hypertension (PH) has been documented by echocardiography in patients and by direct measurement after experimental PCDA in animals. The pulmonary vascular histology in human cases has received little attention but in the few recorded observations the vessels were either normal or showed increased muscularity. We report the case of a 31 week hydropic female stillborn monozygotic twin in whom postmortem examination disclosed PCDA and hypoplasia of the lungs. Atypical plexiform lesions with necrotizing pulmonary arteritis were present. These lesions represent vascular consequences of severe pulmonary hypertension produced by greatly enhanced blood flow through a restricted vascular bed resulting from the combined effects of these two abnormalities. The findings in this case of PCDA with presumed severe PH indicate that severe pulmonary vascular changes can develop in utero and that the interval of time needed for development of such chances in secondary PH is relatively short.
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4/13. Colonic pneumatosis intestinalis in preterm infants: different to necrotising enterocolitis with a more benign course?

    Necrotising enterocolitis (NEC) is the predominant immaturity-associated disease of the bowel in the preterm neonate and leads to substantial mortality and long-term morbidity. Diagnostic features of NEC include, apart from the clinical presentation, laboratory and radiological parameters. Pneumatosis intestinalis (PI) on abdominal radiographs is regarded as a criterion of definitive proof for this disease entity. The objective of this presentation is to link the topographic pattern of PI to the clinical course in cases of suspected NEC. We report two cases of radiological appearance of colonic PI indicative of NEC without associated laboratory and/or macroscopic evidence of the disease, and with minor clinical symptoms only. Data from animal studies indicate that decreased blood supply to the small bowel is associated with more extensive bowel damage as compared to impaired colonic perfusion. Therefore the topographical distribution of PI might be a more specific sign as the general presence or absence of PI. CONCLUSION: The topographical pattern of pneumatosis intestinalis may be predictive of the clinical course of inflammatory bowel disease in preterm infants.
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5/13. Multiple cystic and focal encephalomalacia in infancy and childhood with brain stem damage.

    Two cases are described in which damage to the brain stem was associated with extensive necrosis of the cerebral hemisphere. In the first case--a monochorionic twin--there was clear evidence that injury of an ischaemic or hypoxic type had occurred during fetal life and some evidence that an inadequate share of the placental circulation was an important aetiological factor. In the second case death occurred 4 yr after an asphyxial episode at birth. The lesions in the hemispheres and brain stem were extensive, although less than in the first example. The lesions are discussed in the context of our knowledge of the anatomy and physiology of the developing nervous system. Although they cannot as yet be fitted into the concepts of "critical periods" and "vulnerable periods" of development, this is perhaps because observations on human cases are scanty in comparison with the extensive animal studies which have been reported. The lesions are contrasted and compared with those seen in animals.
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6/13. Monozygous twin brothers discordant for photosensitive epilepsy: first report of possible visual priming in humans.

    PURPOSE: The interaction of genetic predisposition and the environment in the development of epilepsy is often discussed, but, aside from some animal reflex epilepsies, little evidence supports such interaction in the development of reflex epilepsy in humans. methods: We describe the history of a 16-year-old boy in whom photosensitive epilepsy developed after a period of weekly exposures to high-intensity light flashes. RESULTS: Both he and his clinically unaffected monozygotic twin were found to be photosensitive. CONCLUSIONS: This case report suggests that some genetic forms of human reflex epilepsy may be elicited by repeated environmental exposure to the appropriate stimulus, similar to some of the stimulus-induced epilepsies seen in animals.
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7/13. Foetal kidney maldevelopment in maternal use of angiotensin ii type I receptor antagonists.

    We report renal lesions observed in a foetus exposed throughout pregnancy to angiotensin ii type I (AT 1) receptor antagonists. The mother suffered from essential hypertension and was treated with Cozaar (losartan 50 mg). autopsy examination of the foetus revealed severe renal lesions, including tubular dysgenesis, hypertrophy of the endothelial and medial cells lining the arterial and arteriolar walls, hyperplasia of the juxtaglomerular apparatus and poorly developed vasa recta. Similar lesions have already been observed in foetuses of women treated with angiotensin-converting enzyme antagonists and also in foetuses and neonates of animals undergoing experimental blockade of the renin-angiotensin system. The purpose of this report is to describe structural lesions observed in the kidneys, and, particularly, vascular lesions. Our results suggest that the use of AT 1 receptor antagonists during pregnancy may have a severe deleterious effect on kidney development in the foetus.
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8/13. Asplenia syndrome in a pair of monozygotic twins.

    Asplenia syndrome is one of the heterotaxy syndromes, which many familial and animal studies suggest are caused by the loss of adequate genetic control of normal left-right asymmetry development. Moreover, there has not been any environmental factor documented to cause these syndromes. Asplenia syndrome occurring in a pair of monozygotic twins is reported. In view of the negative family history, a new germline mutant gene might be the aetiology of our patients. Both twins are associated with some degree of discordant complex heart defects within the context of a high degree of "mirror-image" of the unpaired thoracoabdominal organs. CONCLUSION: This report implies that sporadic asplenia syndrome might associate with new mutations and further genetic study may be indicated. These monozygotic twins' discordant phenotypes imply that some unidentified factors play an important role in their ultimate development of the same genetically determined abnormalities.
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9/13. anomia for animals in a child.

    The occurrence of anomia which particularly affected the category of animals is described in a 12-year-old boy. This difficulty cannot be accounted for by frequency or familiarity and is unaffected by whether the stimulus is a line drawing, photograph or model. The deficit does not represent development lag, as normal children of the same naming age differ qualitatively. The results, which include a one year follow-up, are discussed in relation to unitary versus multiple semantic systems. The disorder includes a disturbance of memory arising during the developmental period. It is suggested that items which are involved in daily actions can be more easily remembered than those which are identified by sensory features alone, and that the preserved learning of motor skills in acquired amnesia may be of relevance.
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10/13. amyotrophic lateral sclerosis in dizygotic twins.

    A pair of dizygotic twins developed typical amyotrophic lateral sclerosis during adulthood. The concordance for this disease in these two patients of nonconsanguineous parentage with no family history of the disorder suggests the possibility of sublethal intrauterine injury to anterior horn cells. Infectious or toxic exposure during the twins' intimately shared milieu in the prenatal period could have resulted in a neuronal "abiotrophy" that would not have become clinically apparent until decades later. If such a prenatal neuronal injury plays a role in the pathogenesis of amyotrophic lateral sclerosis, it becomes clear that attempts at experimental animal transmission of the disease from affected adults would fail even if the offending agent were viral.
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