Adrenal crisis occurs when you cannot produce enough aldosterone and/or cortisol to meet your body’s needs, resulting in electrolyte abnormalities, hypoglycemia, OR poor circulation (as evidenced by low blood pressure). 

CAH is only one cause of adrenal crisis, but it is not the only one.  So will these people show signs of CAH?  To the degree that sudden withdrawal of medication can leave them unable to produce adequate amounts of aldosterone and cortisol---yes.  But, CAH is also usually characterized by the overproduction of androgens.  Someone with asthma who is being treated with steroids will certainly not overproduce androgens, so the answer is also no. 

Below are excerpts of an emedicine article on adrenal crisis.  If the link gives you trouble, you may have to go to the emedicine home page and register as a user.  It’s free.  If you go down to the section on causes, you will see that rapid withdrawal of steroids is one of the causes of adrenal crisis. 

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http://www.emedicine.com/med/topic65.htm

Pathophysiology: The adrenal cortex produces 3 steroid hormones: glucocorticoids (cortisol), mineralocorticoids (aldosterone, 11-deoxycorticosterone), and androgens (dehydroepiandrosterone). The androgens are relatively unimportant in adults, and 11-deoxycorticosterone is a fairly weak mineralocorticoid in comparison to aldosterone. The hormones of importance in acute adrenal crisis are cortisol and aldosterone.

Cortisol enhances gluconeogenesis and provides substrate through proteolysis, protein synthesis inhibition, fatty acid mobilization, and enhanced hepatic amino acid uptake. Cortisol indirectly induces insulin secretion to counterbalance hyperglycemia but also decreases insulin sensitivity. Cortisol also has a significant anti-inflammatory effect through stabilizing lysosomes, reducing leukocytic responses, and blocking cytokine production. Phagocytic activity is preserved, but cell-mediated immunity is diminished in situations of cortisol deficiency. Finally, cortisol facilitates free water clearance, enhances appetite, and suppresses adrenocorticotropic hormone (ACTH) synthesis.

Aldosterone is released in response to angiotensin II stimulation, hyperkalemia, hyponatremia, and dopamine antagonists. Its effect on its primary target organ, the kidney, is to promote reabsorption of sodium and secretion of potassium and hydrogen. The mechanism of action is unclear; an increase in the sodium- and potassium-activated adenosine triphosphatase (Na⁺/K⁺ ATPase) enzyme responsible for sodium transport, as well as increased carbonic anhydrase activity, has been suggested. The net effect is to increase intravascular volume.

Adrenocortical hormone deficiency results in the reverse of these hormonal effects, producing the clinical findings of adrenal crisis.

Primary adrenocortical insufficiency occurs when the adrenal glands fail to release adequate amounts of these hormones to meet physiologic needs, despite release of ACTH from the pituitary. Infiltrative or autoimmune disorders are the most common cause, but adrenal exhaustion from severe chronic illness also may occur.

Secondary adrenocortical insufficiency occurs when exogenous steroids have suppressed the hypothalamic-pituitary-adrenal (HPA) axis. Too rapid withdrawal of exogenous steroid may precipitate adrenal crisis, or sudden stress may induce cortisol requirements in excess of the adrenal glands’ ability to respond immediately.

Serum chemistry: Abnormalities are present in as many as 56% of patients. Hyponatremia is common (although not diagnostic); hyperkalemia, metabolic acidosis, and hypoglycemia also may be present.