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By: S. Jorn, M.A., M.D., M.P.H.
Clinical Director, Kaiser Permanente School of Medicine
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Children with inguinal hernias and/or inguinal masses should be suspected of testicular feminization. In contrast to dysgenetic gonads with a Y 73, 74, 75 and76 chromosome, the occurrence of gonadal tumors is relatively late, rarely before age 25, and the overall incidence is less, about 5–10%. Therefore, gonadectomy should be performed at approximately age 16–18, to allow endogenous hormonal changes and a smooth transition through puberty. Because of the importance of prophylactic gonadectomy, detection of this syndrome demands careful investigation for other affected family members. About a third of the patients have negative family histories and presumably represent new mutations. In the past, conventional wisdom warned against unthinking and “needless” disclosure of the gonadal and chromosomal sex to a patient with complete androgen insensitivity. This attitude has changed as, more and more, patients desire and appreciate a full understanding of themselves. Although infertile, these patients are certainly completely female in their gender identity, and this should be reinforced rather than challenged. We now strongly advocate combining a truthful education L A with appropriate psychological counseling of patient and parents. Incomplete Androgen Insensitivity A spectrum of disorders, all due to an X-linked recessive trait, are known as incomplete forms of testicular feminization. Incomplete androgen insensitivity is one-tenth 76 as common as the complete syndrome. The clinical presentation ranges from almost complete failure of virilization to essentially complete phenotypic masculinization. Between these poles exist examples of mild clitoromegaly and slight labial fusion to significant genital ambiguity. Males have been described whose only indication of androgen insensitivity was azoospermic or severe oligospermic infertility. Indeed, the incidence may approach 40% or more of men with infertility due to azoospermia 77 or severe oligospermia. However, the defect in androgen receptor function may be so subtle that some affected men are fertile. The undervirilized fertile male syndrome is another manifestation of this androgen receptor disorder. The diversity of presentation represents variable manifestations of the same mutant gene. The biochemical abnormality depends upon the degree of function of the androgen receptor or postreceptor events. Molecular analysis of the androgen receptor gene in individuals with androgen insensitivity has demonstrated a spectrum of disorders in which both the complete and 71 partial forms result from androgen receptor gene mutations.
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Genetic Service, St Mary’s Hospital, Manchester) 76 Prenatal diagnosis Chorionic villus sampling Chorionic villus sampling is a technique in which fetally derived chorionic villus material is obtained transcervically with a flexible catheter between 10 and 12 weeks’ gestation or by transabdominal puncture and aspiration at any time up to term. Both methods are performed under ultrasound guidance, and fetal viability is checked before and after the procedure. The risk of miscarriage related to sampling in the first trimester in experienced hands is probably about 1–2% higher than the rate of spontaneous abortions at this time. Dissection of fetal chorionic villus material from maternal decidua permits analysis of the fetal genotype. The main indications for chorionic villus sampling include the diagnosis of chromosomal disorders from familial translocations and an Figure 14. The advantage of this method of testing is the earlier timing of the procedure, which allows the result to be available by about 12 weeks’ gestation in many cases, with earlier termination of pregnancy, if required. These advantages have led to an increased demand for the procedure in preference to amniocentesis, particularly when the risk of the disorder occurring is high. If prenatal diagnosis is to be achieved in the first trimester it is essential to identify high risk situations and counsel couples before pregnancy so that appropriate arrangements can be made and, when necessary, supplementary family studies organised. Fetal blood and tissue sampling Fetal blood samples can be obtained directly from the umbilical Figure 14. Blood sampling enables rapid fetal karyotyping in cases presenting late in the second trimester. Fetal skin biopsy has proved effective in the prenatal diagnosis of certain skin disorders and fetal liver biopsy has been performed for diagnosis of ornithine transcarbamylase (otc) deficiency. In this method in vitro fertilisation and embryo culture is followed by biopsy of one or two outer embryonal cells at the 6–10 cell stage of development. The reported rate of pregnancy is about 20% per Hunter syndrome cycle and confirmatory genetic testing by chorionic villus Menke syndrome Lowe oculocerebrorenal syndrome biopsy or amniocentesis is recommended for established. This method may be more acceptable to some Autosomal trisomies (21, 18 and 13) couples than other forms of prenatal diagnosis, but has a very Familial chromosomal rearrangements limited availability. The rapid P expansion of molecular techniques in the past few decades has A T led to a better understanding of human genetic disease. The orientation of the phosphate groups defines the 5 5 3 and 3 ends of the molecules. The D ra non-template strand is therefore referred to as the sense strand and the template strand as the anti-sense strand. The genetic code Protein product the basis of the genetic code lies in the order of bases along Figure 15. A group of three nucleotides constitute the coding unit and is referred to as the codon. Each codon specifies a particular amino acid enabling correct polypeptide assembly during protein production. As there are only 20 amino acids, most are specified by more than one codon and the genetic code is therefore said to be degenerate.
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Surprisingly, the androgen receptor concentration is constant throughout the cycle. The biochemical dialogue between the fetoplacental unit and the mother must pass back and forth through the decidua. The classic view of the decidua conformed to its designation as a thin line in anatomical diagrams, a minor, inactive structural component. A specific role for the a-subunit has not been apparent; however, gonadotropin receptors are present in the endometrium 65 and in vitro, a-subunit acts synergistically with progesterone to induce decidualization of endometrial cells. Decidual cells are derived from the stroma cells of the endometrium, under the stimulation of progesterone. Thus, they appear during the luteal phase and continue to proliferate during early pregnancy, eventually lining the entire uterus, including the implantation site. There is no evidence that these proteins are secreted into the circulation, therefore they serve as autocrine and paracrine 67, 68 agents. The amino acid sequence and the chemical and biological properties of decidual prolactin are identical to those of pituitary prolactin. Decidual prolactin synthesis and release are controlled by the placenta, fetal membranes, and decidual factors. A protein named decidual prolactin-releasing factor has been purified from the placenta, and an inhibiting protein, which blocks the 68 stimulatory activity of the releasing factor, has been purified from decidua. Lipocortin-1 is a calcium and phospholipid binding protein, present in the placenta and decidua, that inhibits phospholipase A 2 and responds to glucocorticoids. Lipocortin-1 inhibits decidual prolactin release but in a mechanism independent of phospholipase action and independent of glucocorticoids. The prostaglandin 70 system is not involved in decidual prolactin production, and corticoid steroids do not affect decidual prolactin release. There is good reason to believe that the amniotic fluid prolactin is derived from the decidua. In vitro experiments indicate that the passage of prolactin across the fetal membranes is in the direction of the amniotic cavity. The amniotic fluid concentration correlates with the decidual content, not maternal circulating levels. Amniotic fluid prolactin reaches peak levels in the first half of gestation (about 4000 ng/mL) when maternal plasma levels are approximately 50 ng/mL and fetal levels about 10 ng/mL. Finally, amniotic fluid prolactin is unaffected by bromocriptine treatment (which reduces both fetal and maternal circulating levels to baseline levels).
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Examination of peripheral blood smears to detect morulae in peripheral blood monocytes or granulocytes is insensitive. Ehrlichiosis and anaplasmosis can be severe or fatal in untreated patients or patients with predisposing conditions, and initiation of therapy early in the course of disease helps minimize complications of illness. Failure to respond to doxycycline within the frst 3 days suggests infection with an agent other than Ehrlichia or Anaplasma species. Treatment should continue for at least 3 days after defervescence; the standard course of treatment is 7 to 14 days. Unequivocal evidence of clinical improvement generally is evident by 1 week, although some symptoms (eg, head ache, weakness, malaise) can persist for weeks after adequate therapy. As with other rickettsial diseases, when a presumptive diagnosis of ehrlichiosis is made, doxycycline should be started immediately and should not be delayed pending laboratory confrmation of infection. Human-to-human transmission of ehrlichiosis or anaplasmosis, except in rare cases associated with transfusion of blood products, has not been documented. A risk of blood transfusion infection should be considered in areas with endemic infection. Prophylactic administration of doxycycline after a tick bite is not indicated because of the low risk of infection. In addition, a collaborative report providing recom mendations for “Diagnosis and Management of Tickborne Rickettsial Diseases” is available at The most common manifestation is nonspecifc febrile illness, which in young infants may lead to evaluation for bacterial sepsis. Other manifestations can include the follow ing: (1) respiratory: coryza, pharyngitis, herpangina, stomatitis, bronchiolitis, pneumonia, and pleurodynia; (2) skin: hand-foot-and-mouth disease, onychomadesis (periodic shed ding of nails), and nonspecifc exanthems; (3) neurologic: aseptic meningitis, encephalitis, and motor paralysis; (4) gastrointestinal/genitourinary: vomiting, diarrhea, abdominal pain, hepatitis, pancreatitis, and orchitis; (5) eye: acute hemorrhagic conjunctivitis and uveitis; (6) heart: myopericarditis; and (7) muscle: myositis. Neonates, especially those who acquire infection in the absence of serotype-specifc maternal antibody, are at risk of severe disease, including sepsis, meningoencephalitis, myocarditis, hepatitis, coagu lopathy, and pneumonitis. Infection with enterovirus 71 is associated with hand-foot-and mouth disease, herpangina, and in a small proportion of cases, severe neurologic disease, including brainstem encephalomyelitis and paralytic disease, and secondary pulmonary edema/hemorrhage and cardiopulmonary collapse. Patients with humoral and combined immune defciencies can have persistent central nervous system infections, a dermatomyositis-like syndrome, and/or disseminated infec tion. Severe, multisystem disease is reported in hematopoietic stem cell transplant patients and children with malignancies. As a group, human parechoviruses (formerly echoviruses 22 and 23, and others) appear to cause similar clinical diseases as enteroviruses, including febrile illnesses, exanthems, sepsis-like syndromes, and respiratory tract, gastrointestinal tract, and cen tral nervous system infections. Neonates and young infants have presented with more severe clinical disease and long-term sequelae than have older children. The nonpolio enteroviruses include more than 100 distinct serotypes formerly subclassifed as group A coxsackieviruses, group B coxsackieviruses, echoviruses, and newer numbered enteroviruses. They are spread by fecal-oral and respiratory routes and from mother to infant prena tally, in the peripartum period, and possibly via breastfeeding. Enteroviruses may survive on environmental surfaces for periods long enough to allow transmission from fomites.
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