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Primary adrenal malignancy
Published in Anju Sahdev, Sarah J. Vinnicombe, Husband & Reznek's Imaging in Oncology, 2020
Ayshea Hameeduddin, Anju Sahdev, Rodney H Reznek
Adrenocortical carcinoma has a bimodal age distribution, occurring before the age of 5 years and in the fourth to fifth decades. About 50% of adrenal carcinomas are functional in adulthood and most commonly cause Cushing's syndrome. The definitive treatment for adrenal carcinoma is surgery; the prognosis is nevertheless poor. CT remains the most widely used imaging technique to identify and stage adrenal carcinomas; 70% are >6 cm, 30% are calcified and heterogeneous in appearance after IV injection of contrast medium.
Test Paper 1
Published in Teck Yew Chin, Susan Cheng Shelmerdine, Akash Ganguly, Chinedum Anosike, Get Through, 2017
Teck Yew Chin, Susan Cheng Shelmerdine, Akash Ganguly, Chinedum Anosike
Features suggestive of adrenal carcinoma on imaging include large size (>5 cm); invasion of other organs like liver, kidney, IVC, or diaphragm; calcification; central heterogeneous area of low density (tumour necrosis); peripheral nodular enhancement on contrast-enhanced images; and delayed washout. A HU of <37 on contrast-enhanced CT at 5–15 minutes after contrast injection is diagnostic of a benign adrenal lesion.
Case 72: A Rapidly Deteriorating Patient
Published in Layne Kerry, Janice Rymer, 100 Diagnostic Dilemmas in Clinical Medicine, 2017
Adrenal carcinoma is a rare cancer that tends to affect both young children and adults in their fourth or fifth decades of life. Typical symptoms include virilisation in children, and Cushing's syndrome (glucocorticoid excess) and/or Conn's syndrome (mineralocorticoid excess). Non-functional tumours may present with abdominal pain and ‘red-flag’ warning signs, including weight loss. The cancer is highly aggressive, with a 5-year survival rate of 20%–35%. Metastases are often present at the time of diagnosis.
Patients with suspected benign tumors and glial fibrillary acidic protein autoantibody: an analysis of five cases
Published in International Journal of Neuroscience, 2019
Qingmei Huang, Huacai Yang, Tianni Liu, Huiming Xu, Baikeng Chen, Si Liu, Wenfeng Li, Youming Long, Cong Gao
At present, the pathogenesis of GFAP astrocytopathy is still unclear. Similar to autoimmune encephalitis, it may be associated with the presence of tumors. The expression of GFAP has also been reported in some paraneoplastic cases. To date, there have been three large-scale human studies of GFAP astrocytopathy and tumors from the Mayo Clinic, USA [1], a research team from Italy [4], and our study of GFAP astrocytopathy in Chinese patients [2]. The study by Lennon et al. [1] reported that 34% of patients had tumors. Of these, 66% of tumors appeared within 2 years after the onset of related neurological symptoms. In 22 patients, the tumors were observed after the neurological symptoms, including 15 cases of ovarian teratoma, three cases of adrenal carcinoma, two cases of glioma, one case of head and neck squamous cell carcinoma, and one case of multiple myeloma. The study by Iorio et al. [4] reported three patients (14%) with a history of tumor (one case each of breast carcinoma, ovarian carcinoma, and thymoma). No tumor was found in our previous studies [2,10], but as the number of cases has increased, five patients (12.5%) were found to have tumors, similar to the study by Iorio et al. Two cases were reported to have meningioma, of which one case was pathologically confirmed as meningioma after surgery, and the other three cases had suspicious tumors.
Postmenopausal androgen-secreting ovarian tumors: challenging differential diagnosis in two cases
Published in Climacteric, 2019
E. Arteaga, A. Martinez, J. Jaramilo, P. Villaseca, M. Cuello, P. Valenzuela, R. Gejman, J. E. Blumel
Herein, we present two cases of hyperandrogenism in postmenopausal age (testosterone >100 ng/dl) due to ASOT that show heterogeneity in the presentation of these disorders. Both cases manifested as the slow development of hirsutism, one with virilization, and the exacerbation of libido, symptoms that must be attributed to the increase in testosterone levels. If we analyze the possible causes of hyperandrogenism in postmenopause (Table 3)1, we can state that the slow progression of the disease and the lack of cushingoid appearance made the existence of a malignant disease, such as adrenal carcinoma, very unlikely. Also, symptoms starting at a mature age allowed us to rule out a diagnosis of congenital adrenal hyperplasia or polycystic ovary syndrome, which give symptoms earlier on in life. Also, they did not mention the use of androgens and had no clinical elements of acromegaly. The diagnosis was circumscribed to an ovarian origin for the androgen excess with a very low possibility of a testosterone-only-secreting adrenal adenoma.
Primary pigmented nodular adrenocortical disease (PPNAD) as an underlying cause of symptoms in a patient presenting with hirsutism and secondary amenorrhea: case report and literature review
Published in Gynecological Endocrinology, 2018
Ewa Cyranska-Chyrek, Dorota Filipowicz, Ewelina Szczepanek-Parulska, Marta Nowaczyk, Urszula Ambroziak, Sadegh Toutounchi, Łukasz Koperski, Tomasz Bednarczuk, Blazej Meczekalski, Marek Ruchała
Meanwhile, CT scan demonstrated normal adrenal glands without nodules what made adrenal carcinoma, adenoma, or macronodular hyperplasia less probable. Additionally, we pursued single-photon emission computed tomography (SPECT-CT) with the use of iodomethyl-norcholesterol (I-131), which showed symmetrically increased uptake in both glands. MRI of the pituitary and chest X-ray were normal. Echocardiogram did not show any atrial mass suggestive of myxoma. Densitometry of femoral neck and spine revealed mild osteopenia; T-score respectively (−) 1.5 and (−) 1.3. Vaginal ultrasound examination revealed dysfunctional ovaries with absence of the dominant follicle and the volume 8.7 ml (right) and 7.3 ml (left). The endometrium was 6 mm. Uterus length was 3.6 cm, while a-p diameter 2.4 cm.