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Androsteroma

 
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Last reviewed: 12.07.2025
 
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Androsteromas - virilizing tumors - are a rare pathology (1-3% of all tumors); a virilizing, hormonally active tumor of the adrenal cortex, originating mainly from its reticular zone, excessively secreting corticosteroids, but mainly androgens, and characterized by a clinical picture similar to congenital dysfunction of the adrenal cortex. Androsteromas can reach large sizes - up to 1000-1200 g.

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Epidemiology

Androsteroma disease can occur at any age, in both females and males. Women are predominantly affected, mostly under 35 years of age. The researchers' indication of the rarity of androsteroma in men may be due to the difficulty of diagnosis - in adult men, virilization is less noticeable and, apparently, some of their androsteromas occur under the guise of hormonally inactive adrenal tumors.

Pathogenesis

The pathogenesis of androsteroma is caused by increased production of hormones, mainly androgens, by the tumor tissue. Pathological examination reveals a tumor of the adrenal cortex. It is usually soft and encapsulated. Histologically, the tumor mainly contains dark cells characterized by pronounced polymorphism. In some cases, the histological picture of the tumor resembles the structure of the reticular zone of the adrenal cortex. In malignant androsteroma, pronounced polymorphism, cellular atypia, infiltrative growth of tumor cells, and multiple foci of necrosis are noted. In malignant androsteroma, metastasis to the retroperitoneal space, liver, and lungs may occur.

Androsteroma is usually widely encapsulated, the cut surface is red-brown, often with foci of necrosis, hemorrhage and cystic-changed areas. Tumors usually have one or more enzyme defects that cause the tumor tissue to produce excess amounts of androgens. The cells are compact, normal in size, with vesicular nuclei; they form cords and acinar structures. In malignant tumors, pronounced nuclear and cellular polymorphism and atypism are noted. Such cells form syncytial and alveolar structures; a discomplexed type of structure is encountered. Mitoses are rare. In children, virilizing tumors are usually malignant.

Symptoms androsteromas

The clinical picture in patients with androsteroma is caused by excessive production of male sex hormones - androgens - by the tumor. The degree of virilization depends on the hormonal activity of the tumor and the duration of the disease. In females, androsteroma is manifested by virilization of varying degrees. The subcutaneous fat layer decreases, the muscles stand out, their mass increases, the voice becomes rougher, lower; hair growth is noted on the body and limbs; on the face - in the form of a beard and moustache, while on the head they fall out, a bald spot is formed. The mammary glands undergo more or less pronounced atrophy. Menstruation begins to be confused and soon stops. A change in the external genitalia is characteristic - a significant increase and virilization of the clitoris. The well-being of patients in the early stages of the disease remains good. Physical strength and performance may even increase (the effect of androgens).

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Diagnostics androsteromas

CT is used to visualize the adrenal glands, which most often reveals a unilateral adrenal tumor. CT data are of decisive importance in diagnosing androsteroma. Differential diagnostics should be carried out with bilateral virilizing adrenal hyperplasia. For this purpose, tests are performed with the introduction of ACTH and dexamethasone. Due to a certain autonomy of the tumor, i.e. independence of its function from the regulatory influence of the pituitary gland, the introduction of ACTH and dexamethasone is not accompanied by a change in the excretion of 17-KS. X-ray examination (suprarenography) is combined with retrograde or infusion pyelography. Of other diseases accompanied by virilization, one should remember about ovarian tumors producing androgens, adrenoblastomas. In these cases, the excretion of 17-KS is unchanged or moderately increased inadequately to the degree of virilization. The diagnostic method is a gynecological examination and X-ray diagnostics (oxypelviography).

An enlarged ovary on one side gives grounds to suspect a tumor. There are isolated cases of virilization syndrome development due to lipoid cell tumor of the ovary with ectopic tumor of the adrenal cortex in the ovary. The same diagnostic tests are used, including gynecography. Hormonal studies in women with ovarian tumors reveal increased secretion of androsterone, etiocholanolone, pregnanetriol and testosterone glucuronide. When metapyrone or chorionic gonadotropin is administered, a noticeable increase in these steroids is noted. In boys, androsteroma should be distinguished from premature puberty associated with damage to the central nervous system, pineal tumor, and testicular tumor. With all this pathology, the excretion of 17-ketosteroids does not reach such a high level as with androsteroma. Neurological symptoms are present with intracerebral processes.

Despite the seemingly bright clinical picture of the disease, androsteroma is often diagnosed late, and patients are treated for several years for ovarian dysfunction, baldness, constitutional hirsutism, etc. In the case of children, in addition to the described signs, premature physical and sexual development occurs in girls according to the heterosexual type, and in boys according to the isosexual type. Bone age is ahead of the passport age. As a result of early closure of growth zones, patients remain short even after recovery. Body weight usually does not increase, sometimes weight loss is noted. In the late stages, exhaustion, weakness occur, pain may occur due to the large size of the tumor.

Patients with androsteroma do not show the same major metabolic disturbances as patients with glucosteroma. The amount of androgens determined in urine and blood sometimes increases tens of times.

Clinical case of androsteroma

Patient G.N., born in 1987, consulted an endocrinologist at the RCH in the summer of 2011 with complaints of hair growth all over her body over the past 2-3 years, absence of menstruation over the past three months, weight loss of 10 kg over the past 2 years, increased sensitivity, unexplained aggression, mood lability, and constant weakness.

Considers herself ill for about 2-3 years, when she began to notice weight loss against the background of a good appetite, the appearance of increased hair growth on the body, an irregular menstrual cycle. In the last few months, these symptoms have worsened, menstruation has completely stopped. She went to the doctor for the first time.

Heredity for endocrinological diseases is not burdened. Gynecological anamnesis: menstruation since 14 years, regular, light, painless. Currently - amenorrhea. There were no pregnancies.

On examination, the patient's condition is satisfactory. Height is 168 cm, weight is 52 kg, BMI is 18 kg/m2. Normostenic body type. Hair growth is male-type. The skin is dry. The visible mucous membranes are clean, pale, no hyperpigmentation. The thyroid gland is not palpable. In the lungs, vesicular breathing is heard, no wheezing. The boundaries of relative cardiac dullness are within the age norm. The heart rate is increased (96 beats/min), the heart sounds are muffled. BP is 100/60 mm Hg (in a sitting position). Orthostatic test is negative. The pulse is of satisfactory filling, there is no pulse deficit. The abdomen is soft, painless. The liver is not enlarged, the dimensions according to Kurlov are 9x8x7 cm. The spleen is not enlarged. There is no peripheral edema or pastosity.

Research results

DHEA-S = 1460.7 (N-80.2 - 511.7 mcg/dl), Testosterone = 13.4 (N 0.17 - 4.13 nmol/l), Cortisol = 8.2 (N 3.7 - 24.0 mcg/dl), ACTH = 14.2 (N-0-46 pg/ml). The content of LH, FSH, STH, 17-hydroxyprogesterone, estradiol, somatomedin-c are within normal limits.

Computer tomography - multiple nodular formations of both adrenal glands. Adenomas. Histological examination of the biopsy - dark cell adenoma of the adrenal cortex with massive hemorrhages. Ultrasound of the uterus and appendages - the condition corresponds to hypoestrogenism.

Based on the anamnesis and clinical and laboratory data, a clinical diagnosis was made: Androsteroma of both adrenal glands.

The patient underwent left adrenalectomy and resection of the right adrenal gland. During the month after surgery, the patient noted restoration of the menstrual cycle, stabilization of weight, stabilization of mood, and a qualitative improvement in her well-being. Postoperative examination results: DHEA-S = 161.3 mcg/dl, Testosterone = 1.27 nmol/l.

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Differential diagnosis

Differential diagnosis should be made with congenital dysfunction of the adrenal cortex, Stein-Leventhal syndrome, virilizing ovarian tumor in women, in men and boys with testicular tumor, as well as with other types of premature puberty. Given that half, according to our data, and according to some observations even more, of androsterone are malignant, the issues of early diagnostics are of great importance. In case of successful tumor removal, the symptoms of the disease undergo a fairly rapid regression.

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Treatment androsteromas

The only treatment for androsteroma is surgery - removal of the adrenal gland affected by the tumor.

Forecast

With early diagnosis and timely surgical treatment, benign androsteroma has a favorable prognosis. With malignant androsteroma and the presence of metastases, the prognosis is unfavorable.

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