Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The empty sella results from an extension of the subarachnoid space into an intrasellar position with subsequent remodeling of the sella turcica and the flattening of the pituitary gland. The sella turcica is usually enlarged causing the greatest diagnostic difficulty to distinguish it from a pituitary tumor. The most patients with this syndrome usually have normal pituitary function, while about 30% have varying degrees of hypopituitarism. The Authors describe a case report of a man with primary empty sella syndrome come to the medical observation for obesity and hyperglyccemia. The endocrine evaluation performed (TRH test, GN-RH test, T3, T4, FT3, FT4, Arginine test, metyrapone test) were normal. OGTT shows a maturity onset diabetes (glycemia = 160 mg%). This rare clinical association is not well understood. Probably this diabetes is to the interruption of the normal hypothalamo-pituitary neurovascular connection.
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PMID:[The primary empty sella syndrome. A case report study (author's transl)]. 747 Jan 79

Pituitary abscess is relatively rare. Only about 80 cases have been reported. Preexisting lesions in pituitary fossa, such as pituitary adenoma, craniopharyngioma and Rathke's cleft cyst, are inclined to be complicated by infection more than the normal pituitary glands are. We reported a case of pituitary abscess caused by infection of Rathke's cleft cyst. A 67-year-old male had general fatigue and loss of appetite 4 months before admission. On admission he was found to have diabetes mellitus, diabetes insipidus, and hypernatremia. These defects were controlled by medication but he gradually became comatose and febrile. CT and MRI revealed an intrasellar lesion with ring enhancement. Lumbar puncture demonstrated an increase of mononuclear cells and protein. Blood chemistry revealed a marked increase of CRP. He was operated on via the transsphenoidal approach, which revealed sphenoid sinusitis and abscess formation in the pituitary gland. Histological examination of the surgical specimen revealed infection of Rathke's cleft cyst but the fluid in the cyst was sterile. By the drainage of the cyst and the use of antibiotics the patient became alert and signs of infection disappeared. He was discharged with a slight hypopituitarism and returned to normal life. Mortality rate of pituitary abscess is decreasing but is still high because of hypopituitarism and severe infection. Accurate diagnosis and operation are necessary. Transsphenoidal surgery is preferable for postoperative drainage of the abscess.
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PMID:[A case of pituitary abscess caused by infection of Rathke's cleft cyst]. 747 22

MELAS syndrome is a form of mitochondrial myopathy with manifestations of seizure, stroke-like syndrome, lactic acidosis, ragged red muscle fibres and mitochondrial encephalopathy. The syndrome has been reported in association with a variety of endocrine and metabolic disorders including diabetes mellitus (DM), hypothalamo-pituitary hypofunction, hypothalamic growth hormone deficiency and delayed puberty. Mitochondrial DNA (mtDNA) point mutation may be the major pathological defect. However, association of MELAS syndrome with hyperthyroidism has not previously been reported. A case is reported from Taiwan of a 32-year-old woman suffering from MELAS syndrome with associated DM and hyperthyroidism. When the latter was diagnosed in April 1988, the patient underwent subtotal thyroidectomy. There was no family history of thyroid disease. Because of repeated seizures, she had computed tomography (CT) and magnetic resonance imaging (MRI) of the brain which showed focal, low-density lesions over the cerebral hemispheres. Both serum and cerebral spinal fluid lactic acid levels were elevated. Mild elevations of serum T4 and T3 and a high titre of TSH receptor antibody were still present. Hyperglycaemia was noted during hospitalization and DM confirmed by oral glucose tolerance test. Muscle biopsy showed ragged red fibres. DNA analysis showed an A-to-G transition at the 3243rd nucleotide position of the tRNA(Leu(UUR)) gene of the mtDNA from the patient. Quantitative polymerase chain reaction (PCR) and restriction analysis revealed that about 60% of the blood mtDNA was of mutant type. The patient received antithyroid drugs for hyperthyroidism, diet control for DM and anti-epileptic drugs for seizure.
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PMID:MELAS syndrome associated with diabetes mellitus and hyperthyroidism: a case report from Taiwan. 755 21

The authors established a means of effective gene transfer into human thyroid follicular cells via retroviral-mediated mechanisms. Using specific harvest and culture techniques, we investigated the selection of human thyroid cells in serum-free media. Normal adult human thyroid tissue was obtained after thyroidectomy from fresh specimens sent for frozen-section analysis. Follicular cells were harvested and grown in hormonally defined, serum-free media to prevent fibroblast growth with selection for differentiated function assessed by immunohistochemical staining for thyroglobulin. The efficiency of gene transfer into human thyroid cells was compared between the zen-beta-gal and LNL6 retroviral vectors. The zen-beta-gal retrovirus encodes the product beta-galactosidase, and gene expression was demonstrated by histochemical staining in 0.1% to 1% of the cells. An improved efficiency of 2% to 3% transduction was demonstrated using the LNL6 vector which carries the gene for neomycin resistance (NEO-R). Polymerase chain reaction (PCR) identification of the integrated proviral sequence (NEO-R gene) with Southern blot confirmation was used to quantitate LNL6 transductions and compare confluent versus actively dividing cell cultures. Follicular cell gene therapy has significant potential for treating congenital or acquired diseases of the thyroid as well as disorders of circulating proteins such as diabetes, hypopituitarism, and hemophilia. The ability to culture human follicular cells and perform effective gene transfer is paramount in the eventual realization of thyroid gene therapy.
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PMID:Gene transfer into human thyroid follicular cells. 796 61

Forty-one adults with established hypopituitarism and deficiency of growth hormone (GHD) were compared to an age and sex-matched group with another chronic metabolic disorder (diabetes mellitus) using standardized psychiatric rating and diagnostic measures. Nineteen (46%) of the GHD group were identified as definite psychiatric cases compared with 10 (24%) of the diabetics (odds ratio 1:9:1). The most frequent DSM III-R axis I psychiatric diagnoses were major depression (32% GHD patients and 10% of diabetic patients) and dysthymia. The risk of being a psychiatric case showed an association with duration of illness in the diabetic group, but not in the GHD group. Biochemical indices were not related to the risk of being a case in either group. Hypopituitarism is associated with a higher prevalence of psychiatric disturbance than can be attributed solely to the presence of a chronic disorder.
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PMID:Psychiatric morbidity in adults with hypopituitarism. 774 79

The changes in normal endocrine physiology which accompany pregnancy result in changes in normal ranges of hormone levels and in specific changes in the course and management of endocrine diseases. This review presents information about the various endocrine diseases and their management in pregnant adolescents. Normal pituitary function during pregnancy is described as is the effect of pregnancy on pituitary tumors such as microadenomas and prolactinomas. The effects of bromocriptine therapy in cases where tumor enlargement occurs during pregnancy are tabulated. Methods of distinguishing placental growth hormone secretion and pituitary growth hormone secretion in patients with acromegaly are presented (with the note that acromegalic patients rarely become pregnant). TSH-secreting, gonadotropin, and nonsecreting tumors are rare in this age group, and there is no evidence that they enlarge during pregnancy. The discussion of the pituitary covers chronic hypopituitarism, Sheehan's Syndrome, lymphocytic hypophysitis, and diabetes insipidus. After reviewing normal changes in thyroid physiology during pregnancy, hyperthyroidism (usually due to Graves' disease), thyroid storm, and hypothyroidism are considered. The adrenal is the next subject, with a brief description of normal changes during pregnancy followed by comments on Cushing's Syndrome, adrenal insufficiency, congenital adrenal hyperplasia, and primary hyperaldosteronism. The symptoms, diagnosis, and treatment of pheochromocytomas, which are uncommon during pregnancy but are associated with high fetal and maternal mortality, are the next topics. After a review of changes in calcium metabolism during pregnancy and hypercalcemia, this report ends with a consideration of diabetes mellitus which includes alterations in maternal carbohydrate metabolism during pregnancy, effects of diabetes on the fetus, and management of insulin-dependent diabetes mellitus during pregnancy (the most likely type to be present in adolescents).
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PMID:Endocrine problems of adolescent pregnancy. 824 53

Growth retardation is a common feature in children with end-stage renal failure (ESRF). Medical management of renal insufficiency rarely normalizes growth and optimistic reports on the effect of rhGH treatment on growth velocity may presage more extensive use of rhGH in pediatric nephrology. Ample evidence has shown beneficial effects of GH replacement therapy in both childhood and adolescent hypopituitarism. However, the remarkably few side effects of treatment reported in these conditions cannot necessarily be extrapolated to children with ESRF. Uremia is associated with a wide range of metabolic and hormonal derangements including decreased glucose tolerance. This is mainly due to impaired insulin-stimulated glucose disposal in peripheral tissues and insufficient insulin-induced suppression of hepatic glucose production. Insulin-stimulated glucose uptake in skeletal muscle in ESRF is reduced by 30-50% as compared to that in healthy subjects, and a reduction may be detected even in subjects with a more moderate reduction in renal function (GFR around 25 ml/min). Dialysis therapy improves the disturbed insulin action significantly. The cause of the insulin resistance in ESRF is multifactorial. Impaired physical fitness, accumulation of uremic toxins, raised levels of GH and glucagon, metabolic acidosis, dyslipidemia and the medication applied may all contribute. If exogenous GH administration is added to the already marked uremic insulin resistance, insulin action may be severely disturbed and the secondary hyperinsulinism further magnified. However, frank diabetes mellitus does not develop unless the beta cells fail to meet the enhanced demands. This will probably occur only in patients with a beta-cell genotype pivotal for the phenotypic expression of non-insulin dependent diabetes mellitus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucose metabolism in chronic renal failure with reference to GH treatment of uremic children. 837 90

The authors investigate the in vitro component of an ex situ strategy for gene transfer into the thyroid gland using DNA complex and retroviral vectors. Canine follicular cells harvested by unilateral lobectomy and grown in low-serum media proliferated in culture and retained their differentiated state as evidenced by morphology and thyroglobulin expression. Transient and "stable" gene transfer in thyroid cells were evaluated by comparing DNA and retroviral transduction techniques. Effective gene transfer and expression was demonstrated by histochemical staining for the marker gene product beta-galactosidase. The efficiency of transduction was assessed using an amphotropic retroviral vector carrying the neomycin resistance gene and semiquantitative polymerase chain reaction (PCR) identification of integrated proviral sequences. This analysis demonstrated a proviral frequency in transduced cultures of 10% to 30%. Transduced cells showed no change in morphology or growth patterns and maintained differentiated function as assessed by antibody staining for thyroglobulin. The thyroid gland is an attractive target for somatic gene therapy because of its large protein-synthetic capacity, sensitivity to hormonal regulation, and proportionately high blood flow. Follicular cell gene therapy may be useful not only for treating congenital or acquired diseases of the thyroid, but also disorders of circulating proteins such as hypopituitarism, hemophilia, and diabetes.
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PMID:DNA- and viral-mediated gene transfer in follicular cells: progress toward gene therapy of the thyroid. 841 42

A patient developed insulin-dependent diabetes mellitus at the age of 9 years, complicated by a sensory/autonomic polyneuropathy which presented with a respiratory arrest at the age of 41 years. The neuropathy increased in severity over the subsequent two decades. At the age of 52 years she had hypopituitarism, hypothyroidism and low normal adrenal function. Autopsy at the age of 59 years revealed loss of pituitary tissue with evidence of hypophysitis, a lymphocytic thyroiditis and severe adrenal atrophy with lymphocytic infiltration of the medulla. The pancreas showed reduced numbers and size of the islets of Langerhans with total loss of immunoreactivity for insulin but intact glucagon-producing cells. These features are consistent with a type 2 autoimmune polyendocrine syndrome, in which lymphocytic hypophysitis has not previously been recorded. There was severe loss of myelinated nerve fibres in the sural nerve and rostrally accentuated fibre degeneration in the gracile fasciculi, but only mild cell loss in the dorsal root ganglia. This combination suggests the presence of a central-peripheral distal axonopathy. The cervical sympathetic ganglia were severely atrophic. Minor inflammatory infiltration was observed in the dorsal root and sympathetic ganglia. Significant vascular abnormalities were not present in the peripheral nerves. This, and the pattern of nerve fibre degeneration, suggest that in this case the neuropathy was likely to have been related to metabolic rather than vascular causes. The inflammatory infiltrates in sensory and sympathetic ganglia raise the possibility of an autoimmune inflammatory contribution to the neuropathy.
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PMID:Severe sensory-autonomic neuropathy and endocrinopathy in insulin-dependent diabetes. 854 64

In order to investigate whether the ubiquitous signalling peptide endothelin might also act as a neuromodulator in the stimulation of the hypothalamic-pituitary-adrenal axis, 15 patients (4 female, 11 male, aged 35-67 years) with hypopituitarism were investigated and the results were compared to those of 8 healthy male volunteers (aged 24-31 years). Patients and controls received double-blind in random order either 0.1 IE per kg body weight regular insulin (insulin induced hypoglycemia) or 1 ml 0.9% sodium chloride (placebo) on 2 separate days. Control subjects only received on an additional day 0.1 IE per kg body weight regular insulin plus glucose 10% (euglycemic hyperinsulinemic glucose clamp). In control subjects hypoglycemia resulted in a significant increase in adrenocorticotropin (ACTH) and cortisol which was preceded by an increase in circulating endothelin levels (p < 0.01 vs placebo and euglycemic clamp) while endothelin, ACTH and cortisol remained unchanged both after placebo and in the euglycemic hyperinsulinemic clamp. In contrast, patients with hypopituitarism showed neither changes in circulating endothelin levels nor a stimulation of the hypothalamic-pituitary-adrenal axis during insulin-induced hypoglycemia. These data demonstrate that 1) endothelin levels are enhanced by metabolic stress 2) the responsiveness of endothelin levels to metabolic stress is linked to the presence of an intact pituitary gland and 3) endothelin might be involved in the stimulation of the hypothalamic-pituitary-adrenal axis.
Exp Clin Endocrinol Diabetes 1997
PMID:Clinical evidence for a neuromodulator action of endothelin in the hypothalamic-pituitary-adrenal axis in man. 908 94


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