14% of twins and 41% of triplets are even born very preterm, compared to 1.7% in singletons.Drugs known as betamimetics can be used to relax the muscles of the uterus and delay birth in singleton pregnancies. There is some evidence that these drugs can also reduce the risk of preterm birth for twin pregnancies, but existing studies are small. More data is required before solid conclusions can be drawn. Likewise, existing studies are too small to determine if a cervical suture is effective for reducing prematurity in cases of multiple birth.As a result of preterm birth, multiples tend to have lower birth weight than singletons. Exceptions are possible, however, as with the Kupresak triplets, born in 2008 in Mississauga, Ontario, Canada. Their combined weight was 17 lbs, 2.7 oz, which set a world record. Two of the triplets were similar in size and, as expected, moderately low birth weight. The two combined weighed 9 lbs, 2.7 oz. The third triplet, however, was much larger and weighed 8 lbs. individually. Cerebral palsy
Cerebral palsy is more common among multiple births than single births, being 2.3 per 1,000 survivors in singletons, 13 in twins, and 45 in triplets in North West England. This is likely a side effect of premature birth and low birth weight. Incomplete separation
Multiples may be monochorionic, sharing the same chorion, with resultant risk of twin-to-twin transfusion syndrome. Monochorionic multiples may even be monoamniotic, sharing the same amniotic sac, resulting in risk of umbilical cord compression and nuchal cord.
This is likely due to the fact that the absence of myeloperoxidase leads to increased neutrophil phagocytosis and degranulation as well as increased development of the adaptive immune system. That is, other aspects of the immune system typically compensate for the lack of myeloperoxidase, leading to relatively mild symptoms. Nonetheless, myeloperoxidase-deficient individuals have been found to experience more chronic inflammatory conditions (such as rheumatoid arthritis, pulmonary/skin inflammation, kidney/heart disease, etc.) than individuals with sufficient myeloperoxidase. Researchers hypothesize this may be a result of heightened adaptive immune system activity in individuals with myeloperoxidase deficiency. There is also some evidence that congenital myeloperoxidase deficiency is correlated with higher rates of malignant tumors. Types
MPO deficiency is broken down into two categories: primary/congenital and secondary/acquired. Primary MPO deficiency is an autosomal recessive genetic disorder, which is caused by mutations in the myeloperoxidase gene on chromosome 17q23. There are several different known mutations of this gene which all lead to myeloperoxidase deficiency.Secondary MPO deficiency, on the other hand, occurs in various clinical situations as a result of hematological neoplasm, disseminated cancers, some drugs, iron deficiency, lead intoxication, thrombotic disease, renal transplantation, severe infectious disease, diabetes mellitus, neuronal lipofuscinosis, or pregnancy. Secondary MPO deficiency is typically partial, meaning only a portion of the affected individual’s neutrophils lack functional myeloperoxidase. Diagnosis
Myeloperoxidase deficiency can be diagnosed via flow cytometry and cytochemical stains. Various devices can divide up leukocyte (white blood cell) populations based on their size and peroxidase activity.