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  • Author: Ana Valea x
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Severe hepatocytolisis syndrome - a challenge in medical therapy of Cushing’s disease


Introduction Cushing’s disease is a rare endocrine disorder characterized by persistent hypercortisolism due to excessive, autonomous ACTH secretion by a pituitary adenoma. Transsphenoidal adenomectomy is the main therapeutic option in Cushing’s disease. When imaging studies are unable to demonstrate an obvious pituitary mass complete tumor resection is difficult and often encumbered by risk of relapse. Medical therapy is a second-line option or the first-line treatment for patients with high surgical risk, incomplete surgical resection or relapse. Rarely classic clinical manifestations limit the selection of medical therapy for Cushing’s disease. Case presentation We present the case of a male patient with Cushing’s disease complicated with diabetes mellitus and severe hepatocytolisis syndrome with no visible pituitary adenoma on MRI studies. In the absence of technical equipment petrosal sinus sampling could not be performed in order to improve surgery outcome

Conclusion The presence of unbalanced diabetes and severe hepatocytolisis syndrome made it impossible to use steroidogenesis inhibitors (mitotane, ketoconazole, metyrapone, etomidate) or inhibitors of ACTH secretion as pasireotide that represent a new option in achieving control of hypercortisolism

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Subclinical Cushing’s syndrome with bilateral adrenal tumours in a patient with gallbladder multiple stone: therapeutical options


Introduction The field of Cushing syndrome is a various area; there are still subjects incompletely clarified as the subclinical pattern as well as cortisol producing bilateral adrenal tumours.

Case presentation The paper presents a 67-year old male case previously known with metabolic complications. He had an abdominal ultrasound done for unspecific complains and multiple gallbladder stones together with a right adrenal tumour were found. Later the computer tomography revealed bilateral adrenal tumours of almost 1.5 centimetres diameters (right larger than left) and a morning plasma cortisol level of 2.58 micrograms/ decilitre after low dose of dexametasone suppression test confirming the subclinical Cushing syndrome. After 6 months the endocrine and imagery profile was similar but the gallbladder patter aggravated so surgery was performed (together with right adrenalectomy) by a laparoscopic procedure. The blood pressure profile improved after surgery.

Conclusion Subclinical Cushing syndrome diagnosis is challenging especially if metabolic complications or bilateral adrenal tumours are presented. Based on our observations in this case unilateral adrenalectomy improved the metabolic pattern

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From headache to Rathke’s cleft cyst followed by diabetes insipidus with panhypopituitarism


Introduction The Rathke cyst represents an unusual benign tumour derived from Rathke’s cleft remnants. The diagnosis is potential seen at any age. The most frequent signs are mostly mass effects as headache, visual field defects and hypopituitarism.

Case presentation 30-year old female is admitted for persistent headache that was later associated with secondary amenorrhea and visual field defects for the last two years. The clinical data are consistent with high levels of serum prolactin, gonadotropes deficiency, as well as central hypothyroidism. The magnetic resonance imagery found a pituitary tumour of 2.7 centimetres with extrapituitary extension up to the optic chiasm. Surgery was performed in order to remove the tumour. The pathologic report confirmed a Rathke’s cleft cyst. Diabetes insipidus associated with panhypopituitarism was diagnosed and treated after the procedure. Close follow-up is necessary.

Conclusion This case highlights the fact that headache sometimes embraces a severe neoplasia diagnosis and that the iatrogenic complications after surgery are lifelong care demanding

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Infertility as the onset of Cushing’s disease: is pasireotide a treatment option?


Introduction Cushing’s disease is a complex endocrine disorder characterized by excessive glucocorticoid secretion caused by an ACTH-secreting pituitary adenoma. Hyperandrogenism and menstrual disorders such as amenorrhea and oligomenorrhea complete the clinical picture of Cushing’s syndrome. Infertility is relatively common, involving complex pathogenetic mechanisms, which differ depending on the cause of hypercortisolism.

Case presentation We present the case of a female patient diagnosed with Cushing’s disease during the investigations carried out to assess infertility. After transsphenoidal adenomectomy, the patient underwent treatment with pasireotide and dopamine agonists, achieving normalization of gonadotropin and estradiol levels.

Conclusion Current guidelines recommended transsphenoidal adenomectomy as first-line therapy in an attempt to correct hypercortisolism and restore fertility in patients with Cushing’s disease. In case of relapse pasireotide and dopamine agonists can be effective in normalizing the hormonal profile

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Menopause and prolactin secreting tumours


Introduction Prolactinomas without galactorhhea may be considered menopause or not diagnosed. This is a cases series.

Case1. 76-year female with menopause at age of 52 was discovered at 66 yrs with high prolactin and a pituitary micro-nodule. Bromocriptin was continued for 6 years then switched to cabergoline with constant imagery. The patient did not display at all galactorrhea. Osteoporosis was diagnosed at age of 66 with previous 2 fragility fractures.

Case2. 45-year female is known with secondary amenorrhea (without galactorrhea) for the last 7 years being considered menopause. She experienced headaches thus a MRI was performed and found a pituitary tumour of 1.5cm. Low FSH with increased prolactin was revealed. Cabergoline was started. Within 2 months the menses resumed and headache mildly improved. After 3 months prolactin normalised under weekly 2 mg of cabergoline. Periodical prolactin control is necessary as well as a pituitary scan at 6 months.

Case3. 39-year female had a 3 yrs history of secondary amenorrhea. A prolactin of 117ng/mL and a microprolactinoma of 0.77cm were found. Cabergoline was started and progressively increased up to 1.5mg per week. The prolactin quickly normalised up to 8ng/mL within 4 months. She was followed for 2 years and the imagery found a tumour reduction to 0.44cm.

Conclusion Prolactinomas associate a great variety of clinical presentations. They interfere with menopause by mimicking it in cases without galactorrhea. Also a newly diagnosed prolactinoma during menopause needs long term therapy and followed-up for especially for bone safety.

Open access