Several disease-modiying therapies can be used for relapsing MS or for exacerbations. Examples include in terferons 31 a (Rebi), 31 b (Betaseron), and glatiramer acetate (Copaxone), which lower relapse rates by a third (Rudick, 201l). Data concerning safety in pregnancy are limited but overall reassuring (Amato, 2010; Salminen, 2010). In clinical trials, natalizumab (Tysabri), an :4-integrin antagonist, especially when combined with interferon 31a, significantly reduced MS clinical relapse rates (Polman, 2006; Rudick, 2006). In a review of 35 pregnancies, irst-trimester drug exposure did not worsen outcomes (Hellwig, 2011). If these drugs are used in pregnancy, the neonate should be monitored for thrombocytopenia and anemia (Alroughani, 2016).
Fetal exposure in 89 pregnancies to ingolimod (Gilenya), another immune-modulating drug, was associated with six fetal malformations and nine spontaneous losses. Because of this and associated animal teratogenicity, its use in pregnancy is not recommended. Due to its prolonged persistence, contraception is recommended for 2 months ater drug cessation (Alroughani, 2016; Karlsson, 2014).
Prevention of relapses postpartum is aforded by treatment with intravenous immunoglobulin (I I G) , given in a dose of 0.4 g/kg daily for 5 days during weeks 1, 6, and 12 (Argyriou, 2008).
his adult-onset neurodegenerative disease stems from an autosomal dominant expanded CAG trinucleotide repeat within the Huntington gene on chromosome 4. It is characterized by choreoathetotic movements, progressive dementia, and psychiatric manifestations. Because the mean age of onset is 40 years, Huntington disease rarely complicates pregnancy. Prenatal diagnosis is discussed in Chapter 14 (p. 288). Prenatal screening is controversial, and because this usually is a late-onset adult disease, extensive counseling is important (Schulman, 2015).
approximately 1 in 7500 persons. It is more common in women, and its incidence peaks in their 20s and 30s. he eti ology is unknown, but genetic factors likely playra role. Most patients demonstrate antibodies to the acetylcholine receptor, although 10 to 20 percent are seronegative (Drachman, 2015).
he latter often have antibodies to muscle-specific tyrosine kinase (MuSK), which regulates assembly of the acetylcholine receptor subunits at the neuromuscular junction (Pal, 201l).
Cardinal features of myasthenia are weakness and easy fatigability of facial, oropharyngeal, extraocular, and limb muscles. Deep tendon reflexes are preserved. Cranial muscles are involved early and disparately, and diplopia and ptosis are common. Facial muscle weakness causes diiculty in smiling, chewing, and speaking. In 85 percent of patients, the weakness becomes generalized. Other autoimmune diseases may coexist, and hypothyroidism should be excluded. The clinical course is marked by exacerbations and remissions, especially when it first becomes clinically apparent. Remissions are not always complete and are seldom permanent. Systemic diseases, concurrent infections, and even emotional upset may precipitate exacerbations, of which there are three types: 1.
Myasthenic crises-characterized by severe muscle weakness, inability to swallow, and respiratory muscle paralysis.
2.
Rtactory crises-characterized by the same symptoms but unresponsive to the usual therapy.
3.