PubMed · 612561
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T K Thusoo, S M Gulati, K K Pandey, Satyanand. 1977. Non-functioning adrenal cortical carcinoma.. https://pubmed.ncbi.nlm.nih.gov/612561/
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Cushing's syndrome during pregnancy is most often caused by an adrenal cortical tumour; it is a rare event which bears poor foetal and maternal prognoses. We report 3 cases of adrenal cortex carcinoma diagnosed during pregnancy (after 24, 27 and 28 weeks respectively of amenorrhea) and revealed by local tumoral signs in 2 cases and by pulmonary embolism in the third. Because hair growth was moderate and weight gain as well as high blood pressure had mistakenly been attributed to the pregnant state, these clinical features of hypercortisolism has only lately been related to tumoral secretion. The hypercortisolic state was firmly established by comparing the patients' urinary cortisol levels (677, 941 and 2,167 micrograms/day) and 20-hour salivary cortisol levels (9.9, 15 and 25.3 micrograms/ml) with values obtained in women at the same stage (88 +/- 11.4 micrograms/day and 2.31 +/- 0.25 micrograms/ml). The aetiological diagnosis was made by the finding of a highly increased salivary testosterone levels (50, 34 and 95 pg/ml; normal = 8.6 +/- 4 pg/ml), and by magnetic resonance imaging which showed unilateral adrenal masses of 3, 8 and 20 cm in diameter respectively. These 3 cases illustrate the difficulty of the clinical diagnosis of hypercortisolism during pregnancy. Assessment of the unbound steroids and magnetic resonance imaging are the most useful methods for an early diagnosis, thus preventing the severe complications which may otherwise reveal this rare pathological condition.
The usefulness of non-specific chemotherapy for advanced adrenocortical carcinoma (ACC) is controversial. We report on 2 young female patients (25 and 19 yr) who presented with a clinical picture of Cushing's syndrome due to histologically confirmed ACC. The first patient underwent radical surgery, but after a disease-free interval of 6 months a local recurrence was apparent. She was reoperated and treated with 6 courses of cisplatin and etoposide chemotherapy. Mitotane (8 g daily) was begun, but 2 months later debulking surgery was again performed. A second-line chemotherapy with the etoposide, adriamycin, cisplatin (EAP) scheme attained a partial remission lasting 7 months, then metastatic spread to the brain led to death of the patient. The survival time was 30 months. The second patient underwent radical surgery and adjuvant mitotane (4 g daily), but multiple lung and mediastinal metastases were diagnosed after an interval of 29 months. Chemotherapy with the EAP regimen (6 courses) without interrupting mitotane attained a partial remission lasting 21+ months. We suggest that the EAP scheme is active in advanced ACC and that its association with mitotane is feasible.
61 Lysodren -treated dogs with hyperadrenocorticism are compared with 36 untreated dogs with the same disease. 75.14% of the treated dogs had pituitary-dependent-hyperadrenocorticism (PDH) whereas this diagnosis was found in 63.89% of the untreated dogs. A functioning adrenocortical tumor (FAT) was found in 13.11% of the treated dogs but was evident in 22.22% of the untreated dogs. Simultaneous pituitary and adrenal Cushing's syndrome (PDH/FAT) were found in 11.48% of the treated and 8.33% of the untreated cases. Sex distribution was equal in both groups. Overall slightly more females than males were affected by the disease. Poodles (38.14%) and dachshunds (23.71%) were the mainly affected races. Race-distribution of diseased animals is compared to the overall race-distribution in a ten years statistic (1981-1990) of all necropsied animals (Walter und Schwegler, 1992). The mean age of Lysodren -treated dogs with a PDH diagnosis (10.0 years) is lower as the mean age of untreated dogs with the same diagnosis (10.3 years). Reasons for this unexpected finding are discussed.