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Pituitary metastasis occurs rarely in cancer patients and often remains undiagnosed. However, early detection and appropriate treatment can improve the patient's quality of life and possibly prolong survival. Herein, we describe the case of a 52-year-old woman with panhypopituitarism caused by metastases to the hypothalamus and pituitary from primary breast cancer. She had a 5-year history of breast cancer with metastases to the bones 1.5 years after initial diagnosis and mastectomy. She presented with severe headaches, generalized fatigue, dizziness, hypotension, difficulties with balance and coordination, polyuria, and polydipsia. Laboratory work-up revealed panhypopituitarism (central diabetes insipidus; hypothyroidism; and low prolactin, gonadotrophin, and adrenocorticotropic hormone levels), and magnetic resonance imaging confirmed the pituitary and hypothalamic involvement. She received hormone replacement therapy, radiation therapy of the sella turcica and suprasellar lesion, and chemotherapy, with significant improvement of her clinical status, but she died 15 months later.
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PMID:Panhypopituitarism due to metastases to the hypothalamus and the pituitary resulting from primary breast cancer: a case report and review of the literature. 1993 72

Recurrent autoimmune hypophysitis is a rare autoimmune endocrine disease involving lymphocytic infiltration and chronic pituitary inflammation. It is even more rare than primary hypophysitis. The objective of the study was to evaluate the efficacy of glucocorticoid treatment combined with azathioprine for treating three cases of recurrent autoimmune lymphocytic hypophysitis encountered within a two-year period. The clinical features and follow-up data of these cases were analyzed, including results of treatment with glucocorticoids combined with azathioprine. All three patients were female and presented with the following clinical characteristics: case 1 was a 22-year-old with headache and diplopia; case 2 was a 70-year-old with dry mouth, polydipsia, and polyuria; case 3, a 32-year-old, with polydipsia, polyuria and menstrual disorders with headache and dizziness. Regarding recurrence, case 1 recurred 4 months after surgery and again 14 months after discontinuing prednisone; case 2 relapsed 16 months after receiving high-dose methylprednisolone pulse therapy; and case 3 recurred during the period of prednisone dose reduction. The patients were treated with glucocorticoids plus azathioprine, and positive responses were seen in all three cases. Symptoms were relieved, and MRI revealed significant reduction of lesions during follow-up. Pituitary function resumed in cases 1 and 3; permanent hypopituitarism was present in case 2. At last follow-up, MRI showed no further recurrence of disease in any patient. Treatment and responses of these patients with autoimmune hypophysitis suggest that glucocorticoid therapy combined with azothioprine is effective treatment for recurrent autoimmune hypophysitis. Endocrine and radiologic studies are an essential part of follow-up.
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PMID:Recurrent autoimmune hypophysitis successfully treated with glucocorticoids plus azathioprine: a report of three cases. 2166 39

Nephrogenic diabetes insipidus (NDI) is caused by the inability of renal collecting duct cells to respond to arginine vasopressin (AVP)/antidiuretic hormone (ADH). We present the case of a 7-year-old boy with a history of excretion of large amounts of dilute urine and polydipsia since infancy. The boy had several vomiting episodes with mild dehydration during the first 3 years of life. There was no evidence of headaches, dizziness or visual problems. He drinks between 2 and 3 L/day and has 24-hour diuresis of 2 liters, now. He has prepubertal appearance with appropriate weight [+0.85 standard deviation score (SDS)] and height (+0.15 SDS) for his age. His intelligence was also normal. The water deprivation test showed low urine osmolality after 8 hours of dehydration. After desmopressin administration, urine osmolality remained low. Serum osmolality was in the normal range for sex and age before and after desmopressin administration. This indicated a nephrogenic form of diabetes insipidus. Molecular analyses revealed a P286L [p.Pro(CCC)286Leu(CTC)] mutation in the AVPR2 gene, that was inherited from his mother. This patient is the first case with genetically confirmed X-linked inherited form of NDI in the Republic of Macedonia. Molecular analysis confirmed the clinical diagnosis and enabled genetic advice for this family.
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PMID:X-Linked Recessive form of Nephrogenic Diabetes Insipidus in a 7-Year-Old Boy. 2593 2

A 49-year-old female with history of daily inhaled corticosteroid use for asthma presented to a concussion clinic 7 wk after sport-related head injury with headache, visual blurring, dizziness, nausea, fatigue, polydipsia, and polyuria. Examination revealed difficulty with vestibuloocculomotor testing due to nausea and visual straining. Cranial computed tomography/magnetic resonance imaging was unremarkable. Laboratory testing revealed critically low serum cortisol, hypernatremia, and urine studies suggesting diabetes insipidus. The patient was referred to the emergency department. Intravenous fluid resuscitation, corticosteroids, and desmopressin led to significant symptomatic relief. She was maintained on oral hydrocortisone after cosyntropin test revealed adrenal insufficiency. Her clinical picture suggested chronic subclinical adrenal suppression from inhaled corticosteroids which was exacerbated by hypopituitarism from concussion combined with diabetes insipidus. Adrenal insufficiency should be considered in athletes with history of corticosteroid use and endocrine-related symptoms after concussion, because this can create significant morbidity and can mimic traditional symptoms of concussion.
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PMID:Sport-Related Concussion Preceding Adrenal Insufficiency and Hypopituitarism. 3191 17

Hyponatremia can be asymptomatic or have a wide range of clinical presentations such as headaches, muscle cramps, nausea, seizures, coma, cerebral edema and may even result in death. Despite it has been suggested that duloxetine has a relatively less risk of hyponatraemia, the number of case reports are increasing. A 45- year old female patient with complaints of fear, anxiety, sleeplessness and headache was started on duloxetine (30 mg/day). In the first week of the treatment, she was admitted to the emergency service with dizziness, dry mouth, polyuria and polydipsia. She had to be transferred to the intensive care unit because of agitation, loss of consciousness and a generalized tonic-clonic seizure. Blood levels of Sodium (Na+), Potassium (K+) and Chlorine (Cl-) were, respectfully, 121 mmol/L, 2.7 mmol/L and 87 mmol/L. Brain imaging displayed cerebral edema. Electrolyte levels were regulated with saline infusions. Amitriptyline was initiated for the ongoing headache and anxiety. In outpatient visits, hyponatremia did not recur in the following 3 months. Low dose duloxetine was associated with severe hyponatremia signs and symptoms in an individual who was not previously considered as high risk for hyponatraemia. The patient's history did not reveal any complaints related to hyponatremia when she was treated with sertraline two years ago. Based on these, we discussed the risk factors for hyponatremia and risky antidepressant classes.
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PMID:Duloxetine Induced Hyponatremia. 3259 91


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