The sonographic appearance of the normal adrenal gland in children varies with age. In newborns, the cortex is large and hypoechoic, whereas the medulla is relatively small and hyperechoic. With increasing age, the cortex becomes smaller and the medulla relatively larger. The cortex remains hypoechoic and the medulla hyperechoic until age 5-6 months, by which time the gland has become hyperechoic and smaller, with poor or absent sonographic differentiation between cortex and medulla. After 1 year of age, the appearance of the gland is similar to that of the adult gland, with straight or concave borders and a hypoechoic character.

A recent controlled American trial1 of treatment for Kawasaki disease compared the use of acetylsalicylic acid (aspirin) alone v aspirin at the same dose plus a single preparation of IV γ-globulin, which is not currently licensed in the United States. The dosage of IV γ-globulin was 400 mg/kg/d for four days, and the dosage of aspirin was 80 to 100 mg/kg/d for as many as 8 weeks. The results indicated that, if administered within ten days of onset of fever, the combined treatment significantly lowered the prevalence of coronary artery dilation and aneurysms detected at 2 and 7 weeks postenrollment. The IV γ-globulin-treated group showed significant and rapid reduction in fever, WBC count, and generalized inflammatory signs. Prior studies in Japan also showed benefit from IV γ-globulin.2 Because the etiology of Kawasaki disease is not known and the active component of the immune globulin has not been identified, it is not known whether all IV γ-globulin preparations currently licensed in the United States will be effective. Further studies are underway to compare different IV γ-globulin preparations and to determine the optimal dose and schedule of administration. Pediatricians should consider using IV γ-globulin and aspirin for the treatment of patients who meet the strict criteria for this syndrome.3 If IV γ-globulin is to be used, therapy should be initiated with any one of the products licensed in the United States and administered within ten days of the onset of illness at the dosage schedule described above. The efficacy of such therapy if initiated more than ten days after onset of illness or after aneurysms have been found has not yet been demonstrated.

Huntington's disease (HD) is a progressive neurodegenerative disorder, which is caused by expansion of a polyglutamine tract in the first exon of the huntingtin gene. Genetic testing allows the unambiguous diagnose of HD and the identification of individuals carrying the gene defect before onset of clinical symptoms. However, molecular markers that are suited to predict disease onset, monitor disease progression and asses the response to therapy are still not available. To identify HD-specific molecular markers we performed a comparative analysis of the autoimmune profile of symptomatic patients, presymptomatic gene carriers and a representative control cohort. Serum samples were tested for antigen/autoantibody interactions using a sequential arrangement of protein macroarrays and microarrays. The macroarrays contained E coli clones expressing approximately 10 000 human proteins and were used to characterise the autoimmune profile of 20 HD patients. Hereby, 273 human proteins were selected to generate a HD-specific protein microarray. Serum samples of 100 HD patients, 29 presymptomatic gene carriers and 100 healthy individuals were analysed using the HD-specific microarray. Thereby, several autoantigens were detected that represent putative molecular markers for HD. Further validation experiments are necessary to confirm the relevance of the identified molecular markers. The presence of HD-specific autoantibodies in serum samples supports the idea that progression of HD is associated with alterations of the immune system.

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