Introduction: In this paper we report an unusual case of Cushing’s disease presenting with psychotic depression, paranoia, anorexia leading to severe weight loss culminating in 18% of her body weight. Case: A 22 year old female admitted with first episode psychosis to her local hospital displaying psychotic depressive symptoms, low mood, severe anorexia and mood congruent delusions regarding food contamination. Clinical manifestations of Cushing’s were recognised: cushingoid facies, facial plethora, hirsutism with striae and proximal myopathy. The degree of weight loss (70kg to 57kg) and paranoid ideation surrounding food necessitated caloric supplementation parenterally. Laboratory indices notable for hypokalaemia of 2.7nmol/l, male range testosterone level of 10.7nmol/l, DHEAS>27.1umol and suppressed gonadotrophins. Urine Free Cortisol was >25 times normal. Late night salivary cortisol was 13.4nmol/L(<2.6nmol/L). ACTH was raised at 74.0pg/ml in keeping ACTH dependent Cushing’s. MRI pituitary showed a bulky pituitary. CRF testing and Inferior Petrosal Sinus Sampling both indicated pituitary dependent Cushing’s disease. Following Metyrapone therapy and nutritional treatment the patient condition improved. She proceeded to transphenoidal pituitary exploration. Intraoperatively a very soft central lesion was excised and neuropathology confirmed a corticotroph adenoma. Post-operative morning cortisol at day 3 was 31nmol/l indicating early remission. 3 months post-operative there was remarkable improvement in mood, weight, cessation of anti-psychotics with normal diet and return of menses. She remained severely hypocortisolaemic 6 months post-op Conclusion: Cushing’s disease may present with severe psychiatric manifestation and significant weight loss. Clinicians need to be vigilant of psychosis as the primary presentation of Cushing’s disease.
We describe the case of a 24 year old man with metastatic non-seminomatous germ cell tumour who presented with hyperthyroidism and gynaecomastia associated with elevated human chorionic gonadotrophin(HCG). Following a 3 month history of gynaecomastia, flank pain, nausea and 7kg weight loss, the patient attended the emergency department with persistent vomiting. Initial laboratory investigations reported TSH <0.05mU/L (normal range 0.3-4.3) and free T4 29.5pmol/L (12-22), TPO antibodies negative, FSH <1 and LH 1 U/l, testosterone >52 nmol/L (9-29.0), bioactive prolactin 1048mU/L (63-245), SHBG 110.6 nmol/l (18.3-54.1), and oestradiol 3935pmol/L (<223). Clinical examination revealed bilateral tender gynaecomastia and supraclavicular lymphadenopathy. Testicular examination identified a left testis irregularity that was confirmed on ultrasound. Chest Radiograph revealed multiple bilateral opacities measuring up to 6 cm. Initial urine HCG was negative when tested on two occasions; however given suspicion for a HCG-secreting tumour, serum HCG was measured and reported as 503,944 IU/ml (<5) and AFP 17.6 IU/ml (0-5.0). The negative urine HCG is believed to be due to “hook effect”. CT revealed bulky retroperitoneal lymphadenopathy measuring 13 cm consistent with metastatic spread from the non-seminamatous germ cell tumour of testicular origin. Up front chemotherapy protocol with 4 cycles cisplatin based therapy was initiated given his disease burden and degree of symptoms. Radical orchidectomy was deferred until after chemotherapy - at which time germ cell tumour was only identified on immunohistochemistry staining. Over the 2 months following chemotherapy, all endocrinopathies resolved with corresponding reduction of HCG to 65.0 IU/ml. Symptoms of hyperthyroidism abated with treatment and his TFTs were biochemical normal. Oestrogen level also normalised with treatment. HCG-induced hyperthyroidism is a rare cause of hyperthyroidism. Endocrine manifestations occur in <5% germ cell tumour presentation but should be considered particularly when multiple endocrine abnormalities are present.
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