Cases reported "Hypopituitarism"

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1/108. A case of congenital hypopituitarism: difficulty in the diagnosis of ACTH deficiency due to high serum cortisol levels from a hypothyroid state.

    A three-month-old boy presented congenital hypopituitarism in which the hypothyroid state masked ACTH deficiency. Multiple anterior pituitary hormone deficiencies, including ACTH, were finally confirmed. High basal serum cortisol levels (up to 45.1 microg/dl) were observed during a stressful episode before L-thyroxine replacement therapy was started. Decreased morning serum cortisol levels (5.0 microg/dl or below) were observed on the sixth day of L-thyroxine replacement therapy despite mild hypoglycemia (lowest serum glucose level of 50 mg/dl). ACTH deficiency was then confirmed by insulin-induced hypoglycemia test (peak serum cortisol level of 4.9 microg/dl). The present findings showed that serum cortisol levels can be high during a stressful episode in an infant with ACTH deficiency and a coexisting hypothyroid state. Thus, the diagnostic evaluation of adrenal function soon after L-thyroxine replacement therapy is important in order to verify a possible subclinical ACTH deficiency, even in the presence of high serum cortisol levels before L-thyroxine replacement therapy.
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2/108. Severe non-infectious circulatory shock related to hypopituitarism.

    The authors report a case of refractory non-infectious circulatory shock with catecholamine and massive fluid loading-resistant features related to hypopituitarism. A 76-year-old man was admitted for shock after suffering from gastroenteritis for 3 days. He was pale and had sparse axillary and pubic hair and small testes. Right catheterization showed shock with low preload pressure and a low oxygen extraction ratio relevant for septic shock. Ultrasound tomography revealed a distended gallbladder due to a stone without peritoneal effusion. A non-inflammatory hydrops of the gallbladder was removed surgically. No microorganism was isolated. Cerebral computed tomography (CT) scan showed a pituitary mass. In the post-surgical period the shock became uncontrollable. Cortisol replacement therapy was instituted and clinical and hemodynamic improvement occurred after 2 h. Hormonal screening on admission before catecholamine administration showed a major decrease in all the hypothalamic-pituitary hormone concentrations. The patient died on day 15 with multiple organ failure. hypopituitarism, probably owing to pituitary adenoma, was the only disease identified in this case. hormone replacement therapy dramatically improved the clinical and hemodynamic status, although the role of an abdominal sepsis could not be eliminated. Arguments that pituitary hormone deficiency might increase the hemodynamic consequences of adrenal deficiency are discussed.
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3/108. hyponatremia-induced metabolic encephalopathy caused by Rathke's cleft cyst: a case report.

    Rathke's cleft cysts are sometimes associated with aseptic meningitis or metabolic encephalopathy due to hyponatremia. We treated such a case manifest by lethargy, fever and electroencephalographic abnormalities. A 68-year-old man was admitted to our ward after experiencing general malaise, nausea and vomiting and then high fever and lethargy. On admission, he was drowsy and had nuchal rigidity and Kernig's sign. Physically, he was pale with dry, thickened skin. He had lost 5.0 kg of body weight in the last month. His serum sodium was 115 mEq/l. He had a low serum osmotic pressure (235 mOsmol/l) and a high urine osmotic pressure (520 mOsmol/l). His urine volume was 1200-1900 ml/24 h with a specific gravity of 1008-1015. The urine sodium was 210 mEq/l. He did not have an elevated level of antidiuretic hormone. Electroencephalograms showed periodic delta waves over a background of theta waves. With sodium replacement, the patient become alert and symptom free, and his electroencephalographic findings normalized. However, the serum sodium level did not stabilize, sometimes falling with a recurrence of symptoms. magnetic resonance imaging clearly delineated a dumbbell-shaped intrasellar and suprasellar cyst. The suprasellar component subsequently shrunk spontaneously and finally disappeared. An endocrinologic evaluation showed panhypopituitarism. The patient was given glucocorticoid and thyroxine replacement therapy, which stabilized his serum sodium level and permanently relieved his symptoms. A transsphenoidal approach was performed. A greenish cyst was punctured, and a yellow fluid was aspirated. The cyst proved to be simple or cubic stratified epithelium, and a diagnosis of Rathke's cleft cyst was made. The patient was discharged in good condition with a continuation of hormonal therapy. Rathke's cleft cyst can cause aseptic meningitis if the cyst ruptures and its contents spill into the subarachnoid space. Metabolic encephalopathy induced by hyponatremia due to salt wasting also can occur if the lesion injures the hypothalamus and pituitary gland.
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4/108. Idiopathic giant-cell granulomatous hypophysitis mimicking acute meningitis.

    A 32-year-old woman presented with severe headache, photophobia, fever, nausea, vomiting, and worsening vision. She had also noted several months of amenorrhea. She was febrile to 38.9 degrees C. Laboratory evaluation revealed a markedly elevated erythrocyte sedimentation rate. Lumbar puncture revealed a cerebrospinal fluid lymphocytic pleocytosis and an elevated protein level. Endocrine studies revealed evidence of panhypopituitarism without diabetes insipidus. A magnetic resonance imaging study showed a 2-cm pituitary mass with optic chiasmal compression. The patient had a trans-sphenoidal resection of the mass. pathology revealed multinucleated giant cells in necrotic debris, but no evidence of pituitary tumor. Studies looking for evidence of systemic granulomatous disease were negative. The patient was considered to have idiopathic giant-cell granulomatous hypophysitis. After surgery, the patient's vision improved and hormone replacement therapy was initiated. This case illustrates that idiopathic giant-cell granulomatous hypophysitis should be considered in the differential diagnosis of a patient presenting with a pituitary mass, hypopituitarism, and meningitis-like symptoms.
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5/108. Successful pregnancy by intracytoplasmic sperm injection after radiotherapy-induced azoospermia.

    A 27-year-old male, who underwent excision and radiotherapy for a pineal gland germinoma four years previously, subsequently developed panhypopituitarism and, thus, complete azoospermia. Gonadotrophin replacement therapy resulted in the production of a small number of motile spermatozoa which were used for Intracytoplasmic Sperm Injection (ICSI) into oocytes obtained from his wife. After successful fertilization and embryo transfer, a singleton intrauterine pregnancy was achieved which resulted in the normal delivery of a morphologically normal male live infant at term.
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6/108. Cystic lymphocytic hypophysitis, visual field defects and hypopituitarism.

    A 45-year-old man presented with anterior pituitary failure, requiring thyroxine, hydrocortisone and androgen replacement. An MRI scan revealed a large cystic pituitary mass and thickening of the pituitary stalk. Over three years, diabetes insipidus and bitemporal hemianopia developed and the cystic mass had enlarged on MR scanning. Transphenoidal resection was performed with normalisation of the visual fields. histology revealed lymphocytic hypophysitis, which is rare in men. The presentation with cystic enlargement is unique.
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7/108. Effect of long-term treatment with recombinant human growth hormone on erythropoietin secretion in an anemic patient with panhypopituitarism.

    We studied the effect of treatment with recombinant human GH in an anemic patient with panhypopituitarism in which hemoglobin (Hb) concentration remained as low as 11.0 g/dl in spite of appropriate replacement with thyroid and adrenocortical hormones. Recombinant human GH was subcutaneously and constantly infused for 12 months using a portable syringe pump at a rate of 0.25 U/kg/week. After the treatment with human GH plasma erythropoietin (EPO) levels increased from 12.2 to 25.1 mIU/ml, with a concomitant increase of Hb concentration to 13.6 g/dl. When the administration of human GH was interrupted, both plasma EPO levels and Hb concentrations decreased. There was a close correlation between plasma GH and EPO levels before and during the human GH administration (y=2.444x 1 3.423, r=0.641, p<0.05). plasma GH levels were well correlated with Hb concentrations before and during human GH administration (y=0.529x 11.313, r=0.690, p<0.01). plasma IGF4 levels were also correlated with Hb concentrations (y=0.007x 10.874, r=0.832, p<0.001), but not with plasma EPO levels. These findings suggest that GH treatment may be useful in anemic patients with panhypopituitarism.
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8/108. coronary artery bypass grafting in patients with hypopituitarism.

    Three patients with angina pectoris and hypopituitarism underwent coronary artery bypass grafting. The patients received perioperative replacement steroid and thyroid hormone therapy, and there were no complications. Careful perioperative hormonal management is necessary for patients with hypopituitarism.
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9/108. Combined pituitary hormone deficiency caused by a novel mutation of a highly conserved residue (F88S) in the homeodomain of PROP-1.

    Mutations in the pituitary-specific paired-like homeodomain transcription factor, PROP-1, result in combined pituitary hormone deficiency. We studied a Brazilian girl, offspring of first cousins, who presented with short stature and deficiencies of GH, TSH, PRL, LH, and FSH. Her cortisol response to hypoglycemia was determined at age 4.9, 10.7, and 14.1 yr and remained normal. magnetic resonance imaging at the age of 9 yr revealed an anterior pituitary lobe of diminished height (3 mm; normal, 4.5 /- 0.6), but radiography revealed a sella turcica volume above the normal mean. Direct sequencing of the PROP-1 gene revealed homozygosity for a novel 263T>C transition that results in the replacement of a highly conserved phenylalanine by serine at codon 88 (F88S). F88 constitutes the hydrophobic core of the first helix of the homeodomain of PROP-1, and the substitution by the polar residue serine is expected to alter the secondary structure and impair binding of the mutated PROP-1 to dna target sequences. The F88S mutation (which corresponds to murine F85S) was introduced into the murine Prop-1 complementary dna and its consequences on dna binding and trans-activation were assessed in vitro. In contrast to wild-type Prop-1, the F88S mutant showed no significant dna binding to a PRDQ9 Prop-1 response element in gel shift assays. transcriptional activation of a luciferase reporter gene containing a PRDQ9 site upstream of a simian virus 40 promoter was reduced to approximately 34% compared with that of wild-type Prop-1 in transiently transfected TSA-201 human embryonic kidney cells. The F88S mutation further expands the repertoire of mutations in PROP-1.
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10/108. A case of lymphocytic infundibuloneurohypophysitis showing diabetes insipidus followed by anterior hypopituitarism associated with thrombasthenia.

    We report a case of a 42-year old male patient with diabetes insipidus followed by anterior hypopituitarism associated with thrombasthenia. The patient had been diagnosed with thrombasthenia since the age of 19. He was admitted and diagnosed as diabetes insipidus in 1995. Although T1-weighted image of magnetic resonance imaging (MRI) showed empty sella and partial pituitary stalk hypertrophy, the anterior pituitary functions were normal at that time. Three years later, he was re-admitted after an episode of general malaise and impotence in 1998. Endocrinological studies revealed adrenal insufficiency, hypothyroidism and hypogonadism. T1-weighted image of MRI demonstrated the thickening of pituitary stalk and neurohypophysis. Analysis of anti-pituitary antibodies by immunoblotting identified a major band at 61.5 kDa. The diabetes insipidus was controlled by desmopressin acetate and the shrinkage of pituitary stalk was seen after hormonal replacement therapy including glucocorticoid and thyroid hormone. We suggested that this case represented lymphocytic infundibuloneurohypophysitis, in which a chronic inflammatory process occurred in infundibulum and/or neurohypophysis and that hypopituitarism developed possibly due to damage to the pituitary portal vessels caused by a thickened pituitary stalk, although a pituitary biopsy was not done because of the risk of bleeding in thrombasthenia. The pituitary autoantibodies in sera from patients with hypopituitarism may be helpful to characterize the patient with lymphocytic hypophysitis.
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