Prognosis
In the short term, the exposure to increased levels of ACTH or glucocorticoids, the former due to ectopic ACTH production and the latter an indirect effect of the increase in ACTH, an adrenal adenoma, or exogenous long-term steroid therapy, the results are in line with the discussion above regarding prolonged exposure to stress. In the relatively short term, patients with increased exposure to glucocorticoids experience proximal muscle wasting and weakness. Proximal muscle is defined as the proximal muscles of the upper and lower extremities. Assessment finding of proximal muscle weakness include determination that the patient has difficulty standing from a sitting position without the use of arms or arm-swinging momentum. The patient, after a course of specific questioning, may be determined to have difficulty in performing or completing tasks which require use of the biceps, triceps, and deltoid groups. This might be reflected in a decrease in participation in certain sporting events depending on use of upper extremities such as racquet sports, baseball, bowling or basketball. The affected patient may not be able to performs tasks around the house such as changing a light bulb, painting, or difficulty in putting up dishes or getting dishes out of high cabinets.
These patients also encounter difficulty maintaining constant weight, with common adipose deposition to supraclavicular or abdominal trunk locations, as a result of the process of stress-induced gluconeogenesis, impairment of glut4 protein, and glucose intolerance. Sudden weight gain, especially in the face, shoulders and trunk may lend a psycho-social facet to the patient condition. When coupled with the depression caused by hypercortisolism, the combined set of symptoms may lead to a drastic change in the patient�s interaction with strangers, friends, family, and even medical professionals. Patients may simply give up on goals and objectives, fall behind in meeting financial obligations, and experience an overall decrease in the quality of life which medicine seeks to maintain.
The Cushing�s patient, regardless of exact etiology may struggle with decreases in overall mental abilities, the inability to retain new information, forgetfulness, and pseudo-Alzheimer�s phenomena (Best). Common psychological events include depression and lack of motivation, because of the abundance of glucocorticoid-to-glucocorticoid receptor activity at the neuronal level, which leads ultimately to decreased use of the neuron, atrophy and possibly death of the affected cell and surrounding neuronal tissue. Such neuronal effects are at least long-term, and quite possibly permanent to some extent
The effects of prolonged glucocorticoid exposure on the cardiovascular system are at least detrimental, as proven by history and morbidity/mortality data from as far back as the 1950�s. (DeGroot 1763) While the role of cortisol cannot be underestimated, most of this effect is presumed to be indirect, the combination of injurious factors including the permissive action of glucocorticoids on vasopressors and failure to regulate blood sugar levels. The body systems remain unchecked in regulation of, or failure to effectively regulate, blood pressure. The presence of glucose in plasma increases plasma osmotic pressure, while insulin is relatively inhibited from action by glucocorticoids.
In addition to the primary effects of exposure to glucocorticoids, the Cushing�s patient is likely to suffer from secondary or tertiary effects of prolonged levels of cortisol. One example may be prerenal and or renal-renal failure, secondary to a combination of decreased renal perfusion, taxation by increased glucose levels, and hypertension. Renal compromise can result in derangement of serum electrolytes, and thereby effect coronary functioning. Resultant arrythmias can result in underperfusion of cerebral tissue, leading to further compromise of body systems. While all of this sounds quite morbid and fatalistic, changes in medicine and research over the past 50 years has lead to a better prognosis now than in times past.
In 1952, mortality of patients with ACTH-secreting pituitary adenomas was 50% within 5 years. Of these, 46% of the deaths were secondary to bacterial infection and 40% secondary to cardiovascular and renal complications related to prolonged exposure to glucocorticoids and mineralocorticoids. In 1961, a similar mortality total was reported with different causes, with infection responsible for only 15% and cardiovascular effects due to hypertension represented about 20%, with about 60% accredited to post-operative adrenal crisis or metastasis of adrenal cancer to other organs. In 1971, only 30% of Cushing�s patients died within 5 years of diagnosis, most from cardiovascular disease or infection in spite of decreased post operative mortality. (DeGroot 1763)
In cases of tumors which secrete ACTH exogenously, the prognosis is less positive. The chance of metastasis is higher, and therefore so is the chance of reappearance of an ACTH-secreting malignancy within 3-10 years of original operative cure. (DeGroot 1763) DeGroot also states that recurrence of an ACTH-secreting tumor after initial surgical cure is a grave sign, as it indicates metastasis. (1764)
Cushing�s was once considered a fatal condition. Longevity has improved drastically with the advent of research, cause determination, and advances in surgery and pharmacology. The effects of chronic exposure to increased cortisol, whatever the cause, lead to a wide range of detrimental changes to the organism and its psyche. These changes have their roots at the cellular level and are neither imagined nor benign. We owe it to our patient, profession, and own well-being to recognize that stress and Cushing�s are similar enough to warrant our respect and care. Where possible, as medical providers, we should advocate for treatment of causes of increased stress and make every effort to ensure that we ourselves remain aware of the potential for damages it can inflict on living organisms.