Cases reported "Hypopituitarism"

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1/15. sodium and water disturbances in patients with Sheehan's syndrome.

    Sheehan's syndrome has been attributed to ischemic damage of the pituitary gland or hypothalamic-pituitary stalk during the peripartum period. Well-described clinical features of Sheehan's syndrome include hypothyroidism, adrenal insufficiency, hypogonadism, growth hormone deficiency, hypoprolactinemia, and different sodium and water disturbances. The occurrence of sodium and water disturbances associated with Sheehan's syndrome depends on the degree of pituitary damage, time of onset since the initial pituitary insult, and concurrent medical conditions that also may play a role in sodium and water balance. We present a patient with Sheehan's syndrome with severe chronic hyponatremia; discuss a potential problem in the patient's management; and review the literature for various sodium and water disturbances, including acute and chronic hyponatremia as well as overt and subclinical central diabetes insipidus. Although Sheehan's syndrome is more prevalent in developing countries, the increasingly large immigrant population within the united states warrants better awareness of this syndrome and its potential complicating sodium and water disturbances. Prompt diagnosis and an understanding of the pathogenic mechanisms of sodium and water disturbances associated with Sheehan's syndrome may avoid potential treatment-related complications.
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2/15. Infundibulohypophysitis in a man presenting with diabetes insipidus and cavernous sinus involvement.

    Infundibulohypophysitis is an unusual inflammatory condition that affects the infundibulum, the pituitary stalk, and the neurohypophysis and may be part of a range that includes lymphocytic hypophysitis. Lymphocytic hypophysitis occurs mainly in women and most often presents in the later stages of pregnancy. Infundibulohypophysitis usually presents with diabetes insipidus and the cause remains unclear. The case of a 46 year old man with a 12 week history of polyuria and polydipsia is reported. Cranial diabetes insipidus was diagnosed on the basis of a water deprivation test. Initial cranial and pituitary imaging studies were normal. He subsequently developed symptoms of panhypopituitism over a period of 6-9 months and then, more acutely, developed diplopia secondary to a fourth nerve palsy. Further brain imaging studies disclosed an enhancing pituitary stalk and a left cavernous sinus lesion. An initial trial of immunosuppressive treatment did not help symptoms significantly. The diagnosis of infundibulohypophysitis was made on histological evidence. The patient was treated with prednisolone and methotrexate. At 9 months he is well, without symptoms, and the radiological abnormalities have resolved.
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3/15. An autopsy case of adrenal insufficiency 20 years after hypophysectomy: relation between stress and cause of death.

    A 63-years-old man was found dead with the body soaking in water lying face up on a riverbank. autopsy and diatom examination demonstrated that the cause of death was drowning. He had undergone hypophysectomy 20 years earlier. autopsy, pathological and endocrinological findings demonstrated secondary and chronic hypothyroidism, hypogonadism, and adrenal insufficiency. The cadaver had fallen into the river, and received numerous wounds such as abrasions and subcutaneous hemorrhage. Moreover, it was suspected that he had developed hypothermia before death. Cortisol in the blood and 17- OHCS in urine were within the reference range. We suspect that the adrenocortical hormone was secreted into the blood as a result of various stresses due to wounds and hypothermia. However, it was suspected that sufficient hormone might not be secreted due to chronic adrenal insufficiency. This insufficient cortisol causes the decrease in the stress resistance, and might influence his cause of death. Moreover, as hypothyroidism decreases thermogenesis, he might have fallen into hypothermia easily. In addition, because both adrenocortical insufficiency and hypothyroidism caused the hypoglycemia, he might have fallen into the loss of consciousness. Therefore, it was considered that he had died by drowning, in relation to the adrenocortical insufficiency and panhypopituitarism.
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4/15. hypoglycemia secondary to endocrine deficiencies.

    hypoglycemia secondary to endocrine deficiencies is uncommon, but it occurs. The endocrine deficiency may be of hypothalamic-pituitary origin or may be due to primary failure of the adrenal gland or the thyroid gland. If hypoglycemia is suspected, the diagnosis should be established immediately by measurement of the blood sugar level. Blood should also be obtained for subsequent use in confirming the diagnosis of the endocrine disease responsible for causing the hypoglycemia. A 50% dextrose in water solution should immediately be injected, and fluid therapy consisting of 5% dextrose in normal saline should be initiated. Intravenous cortisone should be given if primary or secondary adrenal cortical insufficiency is suspected until the results of the biochemical tests become available. If hypothyroidism is suspected, intravenous L-thyroxine should be given carefully in addition to the cortisone treatment. Failure in recognizing hormone deficiencies as the cause of hypoglycemia in some patients and failure in promptly correcting the condition may lead to fatal consequences.
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5/15. A case of postpartum hypopituitarism (Sheehan's syndrome) associated with severe hyponatremia and congestive heart failure.

    A case of a 69-year-old woman with postpartum hypopituitarism (Sheehan's syndrome) associated with congestive heart failure and severe hyponatremia is reported. She developed congestive heart failure after cholecystectomy, and marked improvement was noted by treatment with oxygen, digoxin, furosemide, and dopamine. Two weeks after surgery, she became confused, and hyponatremia, 106 mEq/l, was detected. She was referred to us. Past history revealed postpartum hemorrhage at the age of 34, followed by a failure to lactate, menoschesis, and loss of pubic hair and axillary hair. Hypertonic saline (1.5%) infusion and water restriction increased her serum sodium concentration into the low normal range. Despite hyponatremia, serum vasopressin was not suppressed. Basal levels of pituitary hormones were low, and they did not respond to provocation tests. Marked impairment of water excretion was noted, and plasma vasopressin was not suppressed during a water-loading test. These results suggest that inappropriately increased vasopressin played an important role in impaired water excretion, and this defect could have been responsible for the development of hyponatremia and congestive heart failure in this patient.
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6/15. diabetes insipidus: a postpartum complication.

    Sheehan's syndrome and diabetes insipidus were diagnosed in a 31-year-old woman seven months after postpartum bleeding with a short duration of hypotension. The diagnosis of diabetes insipidus was established by the inability to concentrate urine during water deprivation and the marked increase in urinary osmolality after administration of 1-Desamino-8-D-arginine-vasopressin (DDAVP). Obstetricians should be aware of diabetes insipidus as a postpartum complication.
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7/15. hyponatremia of hypothyroidism. Appropriate suppression of antidiuretic hormone levels.

    A hypothyroid, 72-year-old woman with idiopathic hypopituitarism manifested severe hyponatremia, plasma hypoosmolality, and inappropriately elevated urine osmolality suggestive of a syndrome of inappropriate antidiuretic hormone secretions. The hyponatremia did not respond to demeclocycline hydrochloride, and antidiuretic hormone (ADH) levels measured by a specific radioimmunoassay were appropriately suppressed. Subsequent replacement therapy with levothyroxine sodium resulted in correction of the hyponatremia. Thus, both direct assay as well as hormone blockade failed to show an action of ADH in mediating the water retention.
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8/15. Nocturnal diuresis in panhypopituitarism.

    Although impaired water diuresis in adrenocortical insufficiency is well-known, little attention has been paid to the diuretic pattern at night. In two cases of panhypopituitarism, the nocturnal diuretic pattern was found to be quite different from that in the morning, and marked diuresis did occur after water loading at night, without any significant change of serum cortisol which remained at a low level throughout the day. At the antidiuretic stage in the morning, urine osmolality continued to rise gradually, in spite of the water loading, to the level of 666 mOsm/liter. At the water restriction test, the urine was concentrated only to the same level of 600-700mOsm/liter. At the ascending stage of urine osmolality, exogenously injected pitressin showed little antidiuretic effect, although the kidney was able concentrate urine to the higher level later. In the morning, 3 liters of 5% glucose infusion failed to produce a marked diuresis in spite of extreme plasma dilution and expansion. furosemide immediately induced diuresis even in the morning and the kidney recovered its ability to respond to pitressin. Glucocorticoid also improved the diuretic pattern in the morning, but a latent period of about 2 hr was always observed before the appearance of the effect. What happened during this latent period was unclear, but it was interesting to note that a mechanism similar to that which induces diuretic response seemed to occur without glucocorticoid at night.
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9/15. Chronic hypernatremia, hypovolemia and partial hypopituitarism in sarcoidosis: a case report.

    A syndrome of chronic hypernatremia (range 148 to 161 mmoles/l) and partial hypopituitarism (growth hormone and gonadotropin deficiencies) is reported in a 27 year-old man with sarcoid hypothalamic involvement. The patient did not complain of thirst and spontaneous fluid intake was not sufficient to restore the serum sodium to normal. However, when larger amounts of water were given (50 ml/kg for 180 min), the plasma osmolality returned to normal values in 3 hours. blood volume values were found subnormal on two occasions on free diet (63 and 74% of the theorical normal values) and plasma renin activity was elevated (22 ng/ml/hour). plasma vasopressin (AVP) concentrations (range < 1 to 1.9 pg/ml) were inappropriately low for the degree of plasma osmolality and remained markedly subnormal when hypertonic saline was infused (NaCl 5%, 10 ml/min for 60 min). However, the secretory stores and hemodynamic control of AVP release were intact since a rise in plasma AVP to 10.8 pg/ml was observed after induction of arterial hypotension with sodium nitroprusside infusion. These results provide further direct evidence fo the dysfunction of the thirst mechanism and the osmotic contol of AVP release. They support the concept that osmoreceptor areas are anatomically distinct from the neurohypophyseal AVP secretory system and that neural inputs from baroreceptor and osmoreceptor cells are completely separated.
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10/15. Primary empty sella syndrome with panhypopituitarism, diabetes insipidus, and visual field defects.

    A 58 year old woman with a history of hypothyroidism was evaluated for marked visual impairment and found to have the primary empty sella syndrome with multiple endocrine abnormalities. Visual field determination revealed preservation of vision only in the left inferior quadrants bilaterally. Failure of growth hormone (hGH), cortisol and prolactin to respond to insulin induced hypoglycaemia (0.1 U/kg), of luteinizing hormone (LH) and follicle stimulating hormone (FSH) to respond to gonadotrophin releasing hormone (GnRH, 100 microgram) and of thyrotrophin (TSH) and prolactin to increase after thyrotrophin releasing hormone (TRH, 500 microgram), confirmed the diagnosis of panhypopituitarism. Following water deprivation with a 9% loss in body weight, her urine osmolality remained at 204 mOsm./kg H2O), indicating that she had posterior pituitary deficiency as well. During surgical exploration, which was performed in an effort to improve her markedly impaired vision, a compromised vascular supply to the left optic nerve and chronic arachnoiditis was demonstrated. This case represents one extreme of functional impairment in a syndrome which is generally considered benign and which rarely requires therapeutic intervention. Our patient is compared to 29 reported cases of the primary empty sella syndrome with visual field defects. The operative findings in eight of these cases are reviewed. The need for a multidisciplinary approach and close follow-up of patients with an empty sella and functional deficits is emphasized. Surgical intervention including lysis of adhesions and chiasmapexy has been effective in selected cases in reversing or stabilizing visual field abnormalities.
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