Cases reported "Hypoglycemia"

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1/24. Hypoglycaemia induced by adrenal gland neoplasia (Anderson's syndrome) : report of a case.

    A patient with hypoglycaemia associated with an adrenal neoplasia (Anderson's syndrome) is reported. Endocrinological investigation showed increased secretion of cortisol and catecholamines as well as an increased urinary steroid excretion along with profound inhibition of both basal and stimulated insulin secretion. During IVGTT, Conard's coefficient was reduced. The hyperglycemic response to glucagon injection was blunted, suggesting that liver glycogen stores were decreased or unavailable.
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2/24. anorexia nervosa with severe liver dysfunction and subsequent critical complications.

    A twenty-year-old woman with anorexia nervosa (body mass index=11) suffered from severe liver dysfunction (aspartate aminotransferase 5,000 IU/l, alanine aminotransferase 3,980 IU/l, prothrombin time 32%), hypoglycemia (serum glucose 27 mg/dl), and pancreatic dysfunction (amylase 820 IU/l, lipase 558 IU/l). She fell into a depressive state with irritability, which was not improved by intravenous glucose. Despite treatment with plasmapheresis for the liver dysfunction, she subsequently developed pulmonary edema, acute renal failure, gastrointestinal bleeding, and disseminated intravascular coagulation. Hemodialysis, mechanical ventilation and drug therapy including prednisolone, prostaglandin E1, and branched-chain amino acid, improved her critical condition. In this case, malnutrition may have been the cause for the liver dysfunction and subsequent complications.
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3/24. Adrenal crisis presenting as hypoglycemic coma.

    An 18-month-old male infant presented with hypoglycemic coma and clinical signs of bronchopneumonia. He was suspected of suffering from septic shock. The patient progressed to irreversible multiple organ failure before the diagnosis of adrenal crisis was established. Plasma levels of ACTH and cortisol remained undetectable. renin and aldosterone were normal. An autopsy failed to demonstrate any adrenal gland cortical tissue. Immunohistochemical staining demonstrated the presence of all pituitary hormones except ACTH, establishing the diagnosis of isolated ACTH deficiency. intensive care clinicians should consider adrenal crisis in non-diabetic children with hypoglycemia and rapid circulatory deterioration.
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4/24. Lymphocytic hypophysitis: its expanding features.

    Lymphocytic hypophysitis is classically defined as an inflammatory disorder confined to adenohypophysis. However, it has recently been indicated that infundibuloneurohypophysitis underlies some subsets of central diabetes insipidus (DI). Therefore, lymphocytic hypophysitis can be considered a syndrome including disorders of both the anterior pituitary (lymphocytic adenohypophysitis) and the posterior pituitary (lymphocytic infundibuloneurohypophysitis). We describe a 77-yr-old woman with lymphocytic hypophysitis presenting with headache, diplopia, general malaise and appetite loss. Head magnetic resonance imaging (MRI) demonstrated pituitary swelling and dura mater thickening on the dorsum sella. Endocrinological investigations revealed both anterior and posterior pituitary dysfunction associated with primary hypothyroidism due to Hashimoto's thyroiditis. headache and diplopia spontaneously disappeared, and anterior pituitary dysfunction, general malaise and appetite loss improved after taking 10 mg hydrocortisone daily, although ACTH hyposecretion persisted. Pituitary swelling was thereafter reduced but the dura mater thickening persisted. We suggest that this case may represent a variant of lymphocytic hypophysitis in which chronic inflammatory process involves both the anterior and the posterior pituitary gland, infundibulum, dura mater on the dorsum sella and cavernous sinus. Regarding expanding features of lymphocytic hypophysitis, it may be considered a syndrome including heterogeneous disorders, of which the pathogenesis remains to be elucidated.
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5/24. Case report: plasma adrenalin in a child with ketotic hypoglycemia and calcifications of the suprarenal glands.

    Urinary excretion of adrenalin has been reported to be reduced during insulin-induced hypoglycemia in a significant proportion of children having ketotic hypoglycemia. By employing a sensitive double-isotope derivative technique, plasma adrenalin and plasma noradrenalin were determined in a boy 6 years 9 months old who had had ketotic hypoglycemia with intermittent hypoglycemic symptoms from the age of 10 months. Bilateral calcifications of the suprarenal glands were present. The adrenocortical function was normal. The plasma adrenalin response to hypoglycemia were practically absent, being only 4% of the value obtained in healthy children. The results were related to previous findings of a low plasma adrenalin response in patients with ketotic hypoglycemia without adrenal calcifications and support the assumption that ketotic hypoglycemia is associated with hypoadrenalinemia.
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6/24. Polyglandular endocrine failure in a patient with amyloidosis secondary to familial mediterranean fever.

    familial mediterranean fever (FMF) is 1 of the major causes of secondary amyloidosis. Renal involvement is the main clinical complication and it mostly presents with nephrotic syndrome and chronic renal failure. Although deposition of amyloid has been reported in several endocrine glands such as the adrenal, thyroid, and testes, clinically significant functional impairment is uncommon. Herein, we describe a patient in whom the diagnosis of FMF was based on molecular screening and who presented with recurrent hypoglycemic attacks and extensive amyloid deposition affecting various organ function including adrenal, thyroid, parathyroid, testes, intestinal system, and the heart.
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7/24. Primary antiphospholipid syndrome associated with acute adrenal failure.

    We describe a 48-year-old woman with primary antiphospholipid syndrome who developed acute adrenal failure after an operation for a uterine myoma. After surgery, she developed a preshock state with hypotension, hypoglycemia, and hyponatremia. A diagnosis of primary antiphospholipid syndrome was made based not only on her past history of skin ulceration and recurrent spontaneous abortions but also on the presence of anticardiolipin antibodies. An abdominal computed tomography showed a bilateral enlargement of the adrenal glands but no high-density region in either gland. The patient recovered from the shock-like syndromes after the administration of glucocorticoids. Because it is possible that patients with antiphospholipid syndrome have acute or chronic adrenal failure caused by repeated hemorrhage or thrombosis, it may be important to monitor adrenal function in patients when the presence of this antibody is detected.
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8/24. hyponatremia and hypoglycemia in acute Sheehan's syndrome.

    We report the case of a 23-year-old Saudi Arabian woman who presented to the medical intensive care unit with severe hyponatremia and hypoglycemia following a cesarean section delivery complicated by hemorrhage due to disseminated intravascular coagulopathy. She was treated successfully for adrenal insufficiency acutely, and was later discharged on hormone replacement therapy. To our knowledge, this is the first case report of acute Sheehan's syndrome presenting with both hyponatremia and suggestive hypoglycemia. Pituitary necrosis is an uncommon complication of peripartum hemorrhagic shock. Since the initial description by Sheehan in 1937, the incidence of the syndrome has gradually declined through improved management of hemodynamic complications leading to the infarction of the gland. There are many studies describing complications of late Sheehan's syndrome; however, relatively few contain descriptions of the acute phase. In addition, the diagnosis of this syndrome is often determined after resolution of the acute process with resultant lack of data regarding immediate endocrine and imaging abnormalities. In this report, we describe the complete endocrine and imaging assessment of a patient presenting in critical condition due to necrosis of the pituitary gland in the immediate postpartum period.
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9/24. Neonatal identification of pituitary aplasia: a life-saving diagnosis. review of five cases.

    BACKGROUND: Neonatal onset hypopituitarism is a life-threatening, potentially treatable endocrine disease. A possible cause is congenital absence of the anterior pituitary gland, a condition very rarely reported in the literature. methods: A series of 5 cases of children with pituitary aplasia referred to the Centre of Paediatric endocrinology 'Rina Balducci', Tor Vergata University, Rome, is presented. RESULTS: Major clinical features in our patients were respiratory distress on the first day of life, in spite of uneventful pregnancy, labour and delivery, metabolic acidosis, non-cholestatic jaundice, hypotonia, severe hypoglycaemia, hypogenitalism, and midline defects. diagnosis was established by endocrine tests during hypoglycaemia and hypothalamic-pituitary MRI scan. Symptoms disappeared soon after replacement therapy was started. CONCLUSION: We stress the importance of performing baseline endocrine tests as soon as possible during hypoglycaemia and MRI of the brain aimed at visualizing the hypothalamic-pituitary area in neonates with hypogenitalism and severe unexplained hypoglycaemia, so that the irreversible neurological and developmental consequences of panhypopituitarism can be prevented by adequate replacement therapy.
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10/24. pregnancy in a woman suffering from type 1 diabetes associated with Addison's disease and Hashimoto's thyroiditis (fully developed Autoimmune Polyglandular Syndrome Type 2).

    In this article the pregnancy of a woman suffering from the complete triad typical of Autoimmune Polyglandular Syndrome Type 2 (Addison's disease type 1 diabetes Hashimoto's thyroiditis) is reported. By using insulin pump therapy with insulin lispro, it was possible to balance diabetes control with changes of steroid replacement therapy. pregnancy was uneventful until week 27, when signs of preeclampsia occurred. The boy was born without difficulty at gestational age 37 weeks by planned cesarean section but signs of diabetic fetopathy (macrosomia, hypoglycaemia and hypocalcaemia) were expressed. He required a short course of hydrocortisone therapy. He made a good and rapid recovery. The mother made a good post-operative recovery too, but 4 months after the delivery microalbuminuria as well as mild hyperuricemia are still present. Interdisciplinary approach and very careful observation of the mother as well as of the child enabled successful outcome of this highly risky pregnancy.
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