The lower extremities are oriented at right angles to the axes of the thorax and the adjacent limbs near the union of the ischium belong to the opposite twin. Embryology
During embryonic development, twins can form from the splitting of a single embryo (monozygotic) which forms identical twins or the twins can arise from separate oocytes in the same menstrual cycle (dizygotic) which forms fraternal twins. Although the latter is more frequent, monozygotic is the reason conjoined twins can develop. In monozygotic twinning for conjoined twins such as ischiopagi, the twins form by the splitting of a bi-laminar embryonic disc after the formation of the inner cell masses. Thus, making the twins occupy the same amnion which can lead to a conjoining of the twins as a result of the twins not separating properly during the twinning process. Separation occurring between the seventh and thirteenth days should result in a monochorionic, monoamniotic identical twins sharing a yolk sac. If separation of the twins occur in the later stages of development prior to the appearance of the primitive streak and axial orientation, then it can be predicted that conjoined twins will develop. The origin of exactly what goes wrong to produce ischiopagus or any conjoined twin is a result by either incomplete fission or double overlapping inducing centers on the same germ disc.
Medications that extend or prolong the QT interval (macrolides, antihistamines, beta-2 agonists) should be avoided in these patients to prevent cardiac death. Epidemiology
Gitelman syndrome is estimated to have a prevalence of 1 in 40,000 homozygous people . The ratio of men to women affected is 1:1. This disease is encountered typically past the 1st decade of life, during adolescence or adulthood but can occur in the neonatal period. Heterozygous carriers of the SLC12A3 gene mutations are 1% of the population. Parents with Gitelman syndrome have a low probability of passing the disorder to their offspring roughly 1 in 400 unless they are both carriers of the disease. History
The condition is named for Hillel Jonathan Gitelman (1932– January 12, 2015), an American nephrologist working at University of North Carolina School of Medicine. He first described the condition in 1966, after observing a pair of sisters with the disorder. Gitelman and his colleagues later identified and isolated the gene responsible (SLC12A3) by molecular cloning. References
External links

"Gitelman syndrome". MedlinePlus. U.S. National Library of Medicine.