Hirsutism casued by ovarian and adrenal cancer
Information on hirsutism and hair removal treatments
Tumor Induced Hirsutism (Ovarian / Adrenal)
Hirsutism is a hair development disorder in women. Its primary manifestation is excess hair growth in a male-like pattern in various body parts. Hirsutism is caused by various underlying ailments most of which are endocrine disorder related.
The endocrine triggered causes are marked by an excess and hyperactivity of the steroidal hormone androgen, which is the key regulator of human hair production and development. Non-androgenic causes of hirsutism are quite rare. On the other hand, there is also an idiopathic factor, which is the second most common cause of hirsutism. Other androgenic causes are hyperandrogenism, hypothyroidism, the hyperandrogenic insulin-resistant acanthosis nigricans syndrome (HAIR-AN), 21-hydroxylase non-classic I adrenal hyperplasia (late-onset CAH), 21 -hydroxylase-deficient congenital adrenal hyperplasia, hyperprolactinemia, Cushing’s syndrome and androgenic tumors. Androgenic tumor induced hirsutism is relatively rare with an incidence between one per 300 and one per 1000 hirsute cases.
Androgen-secreting tumors can be of the following kinds:
Apparent symptoms of tumor related hirsutism
This kind of hirsutism shows a speedy hair growth pattern, virilization (clitoral enlargement), masculinization and other androgenic symptoms over a span of 3–6 months. Whereas, PCOS triggered hirsutism develops over several years. But one must note that many younger patients with signs of virilization may have another ailment called the hyperandrogenic insulin-resistant acanthosis nigricans syndrome, which also causes hirsutism. Androgenic tumors are also marked by Cushingoid features.
Clinical evaluation of tumor induced hirsutism
Androgen-secreting tumors are more commonly ovarian in origin and rarely sourced to the adrenal cortex. Experts warn that suppression and stimulation tests are not totally effective for diagnosis of these androgenic tumors and should be discouraged. Androgen-producing tumors are most correctly diagnosed with detailed clinical investigations and should not be based on mere biochemical indicators. The various effective clinical procedures, both for adrenal and ovarian tumors, are as follows:
Tests for serum testosterone levels
A single serum total testosterone level investigation is vital to detecting an ovarian tumor. A circulating testosterone count of 2.5 or more times the upper limits of the normal level for that particular examination or 200 or more ng/dL could indicate ovarian androgen-secreting tumors. However, only 20 percent to 30 percent of cases recording these test scores actually have tumors. In most cases, they come up with stromal hyperplasia (hyperthecosis) or hilar cell hyperplasia. Moreover, in one set of tests, 50 percent of tumors were detected in women whose testosterone counts were less than 200 ng/dL. On the other hand, a lesser degree of testosterone elevation indicates increased ovarian androgen secretion without tumor and is more suggestive of PCOS.
A test result that reports that DHEAS is greater than twice normal or more than 700 µ-g/dL in a pre-menopausal woman or more than 400 µ-g/dL a postmenopausal women, could indicative an adrenal tumor.
Ultrasound and CT scan
The hirsute patient should also be checked for pelvic masses. For ovarian masses the medical examination should include pelvic ultrasound or abdomen/pelvic computed tomography (CT) scan. A magnetic resonance or computed tomography is necessary for the adrenal gland related tumors.
The patient should undergo a prolactin test. If the test results show a porlactin level of more than 50 ng/dL, then it could suggest a prolactinoma.
A research-based evaluation of tumor-triggered hirsutism
A particular research based on clinical assessment was conducted in an endocrinology clinic in the Netherlands to exclude enzyme deficiencies and virilizing tumors. This demonstrative survey included 84 consecutive women who were tested for ‘hormone level sensitivity and specificity to identify virilizing adrenal tumors’. Hormone counts of 14 women with either an adrenal carcinoma (n=12) or an adrenal adenoma (n=2) were compared with the hormone scores of the women with hirsutism (n=73) as well as to the controls (n=31). Serum values of total testosterone, androstenedione, DHEAS, DHEA, and cortisol was also checked. A 24-hour urinary 17-ketosteroid excretion measure was also conducted. The process included a 5-day dexamethasone suppression investigation. On the 6th day a urinary sample was obtained between 8 and 9 am.
The survey results were as follows: An increased basal total testosterone or DHEAS value diagnosed all 14 patients with adrenal carcinomas or adenomas and 36 of 73 women with hirsutism of non-neoplastic source. It also concluded that ‘the combined test sensitivity was 100 percent’ and ‘specificity was 50 percent’ for the confirmation of adrenal tumors.