Non-classical CAH is a milder form of what my children have. My children have salt-wasting CAH. Salt-wasting CAH infant will die without treatment. The non=classical CAH can die if very ill or surgery and not given extra cortisol (cortef). It is a stress (physical) stress hormone for illness. It is a hormone that they do not produce enough. And they produce too much male hormone. Also without treatment they grow too fast but end up as a short adult if not treated. Early treatment is desired and that is why it is important that all infants in every state have CAH screening newborn blood test... it is progessive condition.

My email is preston@kreative.net 

I think genetic testing is also a good idea. I had it done and my insurance paid for it. It was done locally and sent to Dr. Maria New's office in New York City. There is a link for her homepage on this web page below the banner.

 

http://www.medhelp.org/nadf/nadf5.htm

here is a fact sheet about CAH from NADF (National Adrenal Diseases
Foundation). 505 Northern Blvd, Great Neck, NY 11021, 516-487-4992, email:
NAFD@aol.com

The author of the CAH article is:Phyllis W Speiser, MD

http://www.lij.edu/education_and_research/research/faculty-interests/speiser.html

North Shore - Long Island Jewish Health System
Phyllis W Speiser, MD
E-mail  speiser@nshs.edu

She co-wrote this article. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=Display&DB=PubMed

21-Hydroxylase-deficient nonclassic adrenal hyperplasia is a progressive disorder: a multicenter study.

Moran C, Azziz R, Carmina E, Dewailly D, Fruzzetti F, Ibanez L, Knochenhauer ES, Marcondes JA, Mendonca BB, Pignatelli D, Pugeat M, Rohmer V, Speiser PW, Witchel SF.

Departments of Obstetrics and Gynecology, The University of Alabama at Birmingham, 35249-7333, USA.

OBJECTIVE: Our aim was to determine whether the clinical features of 21-hydroxylase-deficient nonclassic adrenal hyperplasia are correlated with either age at symptom onset or age at presentation, or both, and with the degree of adrenocortical abnormality.

STUDY DESIGN: In a multicenter cohort design 220 women with nonclassic adrenal hyperplasia, with a basal or adrenocorticotropic hormone-stimulated 17-hydroxyprogesterone level >30.3 nmol/L, were studied, either prospectively (n = 39) or retrospectively (n = 181). Patients were stratified by age of presentation into 5 groups: (1) <10 years (n = 25), (2) 10 to 19 years (n = 64), (3) 20 to 29 years (n = 83), (4) 30 to 39 years (n = 30), and (5) 40 to 49 years (n = 16). Two patients >50 years old were excluded from the analysis because of age.

RESULTS: Ninety-two percent of patients <10 years old had premature pubarche at presentation, whereas clitoromegaly and acne were each present in only 20% of these younger subjects. With only patients > or =10 years old considered, presenting clinical features included hirsutism (59%), oligomenorrhea (54%), acne (33%), infertility (13%), clitoromegaly (10%), alopecia (8%), primary amenorrhea (4%), and premature pubarche (4%). Among the patients >/=10 years old, the prevalence but not the degree of hirsutism increased significantly with age.

Basal levels of 17-hydroxyprogesterone in adolescents were significantly higher than the levels found either in children (<10 years old) or women 40 to 49 years old (P <.01 and P <.03, respectively), although no difference was noted in the stimulated 17-hydroxyprogesterone levels between age groups. The adrenocorticotropic hormone-stimulated levels but not the basal levels of 17-hydroxyprogesterone were significantly higher in patients with clitoromegaly than in women without clitoromegaly. Alternatively, there were no differences in either basal or stimulated 17-hydroxyprogesterone levels between patients with and those without hirsutism, acne, or alopecia.

CONCLUSION: In children <10 years old the most common presenting complaint was premature pubarche, whereas hirsutism and oligomenorrhea were more common in older patients. The prevalence of hirsutism increased with age, suggesting the progressive nature of nonclassic adrenal hyperplasia. Furthermore, the adrenocorticotropic hormone-stimulated levels of 17-hydroxyprogesterone were higher in patients with clitoromegaly, which suggests that the degree of adrenocortical dysfunction in nonclassic adrenal hyperplasia determines, at least in part, the clinical presentation.