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)

A 59 year old woman with insulin-dependent diabetes mellitus and chronic diarrhea was found to have mild steatorrhea, selective plasma IgA deficiency and adrenal insufficiency. Significant adrenal secretion of corticosteroids resulted only after prolonged stimulation with large doses of exogenous ACTH. Plasma ACTH levels were not elevated during clinical adrenal insufficiency or after metyrapone administration but did respond normally to vasopressin and insulin-induced hypoglycemia. These studies were interpreted as showing both primary adrenal insufficiency and impaired pituitary reserve for ACTH secretion in response to the feedback stimulus. No deficiency was found in secretion of other pituitary tropic hormones. Jejunal biopsy showed a lack of IgA-containing plasma cells. With cortisone replacement, diarrhea subsided and a malabsorption pattern on a film of the small bowel was no longer seen. IgA deficiency has been noted frequently with steatorrhea but rarely with diabetes and only once previously with adrenal insufficiency.
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PMID:Atypical adrenal insufficiency with failure of the pituitary feedback receptor. A case with associated diabetes mellitus and selective IgA deficiency with steatorrhea. 17 48

The effects of medroxyprogesterone acetate (MPA), administered im in a total weekly dose of 400, 700, or 1200 mg, on the pituitary-adrenal axis were studied in 12 cancer patients and 1 patient with diabetes mellitus. MPA reduced mean A.M. plasma cortisol concentrations by 76% and mean P.M. cortisol concentrations by 75%. The 24-hour production rate of cortisol was reduced by 67%. 41% of the individual A.M. cortisol determinations and 61% of the individual P.M. determinations were not significantly (p greater than .001) different from 0. Plasma ACTH levels were low throughout treatment, and the response to maximal ACTH stimulation was not pronounced. Evidence of adrenal insufficiency was not observed in any of the patients. The results demonstrate the corticosteroid replacement properties of MPA, and it is suggested that the suppression of adrenal function is most likely mediated by a negative feedback action on the hypothalamus or pituitary.
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PMID:The effect of medroxyprogesterone acetate on the pituitary-adrenal axis. 17 84

The widespread use of corticosteroids in clinical practice emphasises the need for a thorough understanding of their metabolic effects. In general, the actions of corticosteroids on carbohydrate, protein, and lipid metabolism result in increased hepatic capacity for gluconeogenesis and enhanced catabolic actions upon muscle, skin, lymphoid, adipose and connective tissues. Because of the morbidity associated with steroid therapy, the clinician must carefully consider in each case the gains that can reasonably be expected from corticosteroid therapy versus the inevitable undesirable side effects of prolonged therapy. Thus, it is important to remember that the enhanced anti-inflammatory activity of the various synthetic analogues of cortisol is not dissociated from the expected catabolic actions of glucocorticoid hormones. Replacement therapy with physiological doses of cortisol in primary or secondary adrenal insufficiency is intended to simulate the normal daily secretion of cortisol. Short term, high dose suppressive glucocorticoid therapy is indicated in the treatment of medical emergencies such as necrotising vasculitis, status asthmaticus and anaphylactic shock. With improvement of the underlying disorder, the steroid dosage can be rapidly tapered and then discontinued over a 2 to 3 day period. Long term, high dose suppressive therapy is often commonly used to treat certain diseases (see sections 4.7.2 and 4.7.3). In this setting, suppression of the hypothalamic-pituitary-adrenal axis may persist for as long as 9 to 12 months following steroid withdrawal if steroid doses are administered in the supraphysiological range for longer than 2 weeks. In general, higher doses, longer duration of usage, and frequent daily administration are all correlated with the severity of pituitary ACTH suppression. When steroid therapy is to be withdrawn, gradual tapering of the dosage is necessary; the steroid dosage should also be given as a single morning dose if possible. Rapid or total withdrawal of the steroid therapy may be associated with exacerbation of the underlying disease or with a steroid withdrawal syndrome. An additional important point to remember in any withdrawal programme is that the steroid dosage should be appropriately increased for an exacerbation of the underlying disease or for intercurrent major stress. Alternate day therapy is recommended as a steroid maintenance programme for patients requiring high dose glucocorticoid therapy over a prolonged period of time. Thus, it is usually employed to maintain a therapeutic benefit which had previously been extablished by daily steroid treatment. Complications resulting from corticosteroid therapy include: (1) proximal muscle weakness; (2) osteopenia; (3) unmasking of latent diabetes mellitus; (4) sodium retention and/or elevation of mean arterial blood pressure; (5) adverse psychiatric reactions; (6) development of glaucoma; and (7) reactivation of latent infections (such as tuberculosis).
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PMID:Corticosteroids: clinical pharmacology and therapeutic use. 20 58

The activity of microsomal drug-metabolizing enzymes is altered by several pathological or abnormal physiological states, such as changes in nutritional status, liver, heart or kidney diseases, hormonal disturbances, pregnancy, tumour-bearing state, adjuvant arthritis, changes in reticuloendothelial system and environmental factors (stress, irradiation, heavy metals). The activities of other metabolic pathways, such as glucuronidation, sulphate conjugation, acetylation and alcohol oxidation are generally affected to lesser extents. Rats are most commonly used in drug metabolism studies, and it is important to know that the activity of most of the microsomal drug-metabolizing enzymes is higher in males than in females through androgen action which is readily impaire drug-metabolizing enzymes in male rats are thus manifested by two mechanisms; one is by impairment of androgen action and the other is by depression of the basic enzymic activity. Therefore, those effects of pathological states, observed only in male rats but not in females, are generally not seen in other species of animals, including man. The effects of starvation, hyperthyroidism, adrenal insufficiency, diabetes and morphine administration are cases where changes in metabolism are due solely to impairment of androgen action. In other pathological cases, those drug-metabolizing enzymes showing sex differences are depressed more markedly in male rats than those showing no clear sex difference. The author therefore recommends the use of female rats in the evaluation of the effects of pathological states on hepatic microsomal drug-metabolizing enzymes. Generally, changes in activity of the hepatic enzymes reflect closely the changes in the rates of drug metabolism in vivo. However, the protein-binding of drugs, hepatic blood flow and renal function are also known to affect the rate of drug metabolism and excretion in vivo, and therefore changes of these factors in pathological states should also be taken into consideration.
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PMID:Drug metabolism under pathological and abnormal physiological states in animals and man. 32 97

Hyaline membrane disease is an important factor in the postnatal mortality of prematures. Its pathogenesis is examined. Prematurity, maternal diabetes, and caesarean section are seen as predisposing causes. Delayed biochemical maturation of the lung (shown by a low lecithin-sphyngomyelin ration in the amniotic fluid and probably caused by hypophyseal-adrenal insufficiency) results in an absence of surfactant. Labour stimulates its production by massive release of endogenous cortisol. The part played by betamethasone and other substances in prophylaxis is discussed. It is felt that, at present, the availability of preformed tensioactive factors alone can achieve the decidedly improved prognosis required in so serious a disease.
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PMID:[Recent acquisitions in hyaline membrane disease]. 33 Nov 43

Schmidt's syndrome (thyroid and adrenal insufficiency) and concurrent diabetes mellitus represent an intriguing multiple endocrinopathy in children. This report describes an eleven-year-old girl with diabetes of eight years' duration presenting in adrenal crisis. Serum thyroxine was undetectable, and antibodies to both thyroglobulin and adrenal tissue were found in high titer. The child's condition stabilized with hormonal replacement therapy, except for persistent growth failure. Approximately two years later she succumbed during a rapidly fulminant episode of ketoacidosis. The natural history of her illness supports recent speculation based on serologic data that juvenile diabetes mellitus may be an immunologic disorder in some children.
Diabetes Care
PMID:Schmidt's syndrome in a child with diabetes mellitus. 55 85

Hypoglycemia (h.) in the postneonatal period was predominantly observed in male infants and children. The incidence was 0,51/1000 hospitalizations. The majority of cases was found in the agegroup around 2 years. Concomitant diseases (mostly infections of the upper respiratory tract or gastrointestinal tract) were found in 30 out of 43 hospitalizations. Convulsions and coma were the most frequent symptoms which were found in 43%. In 30% some degree of somnolence was obvious. Hypoglycemia was not considered in the differential diagnosis in any case by the physician treating first. Only 7 out of 34 cases a complicated biochemical work up resulted in an etiological diagnosis: one leucininduced h.; one ketotic h,; one h. in dystrophy and bronchopneumonia with septicemia; one h. in meningococcic septicemia; one h. in adrenal insufficiency; one h. in isolated ACTH-deficiency; one ethyl-induced h.; one h. in polynesy of pancreas; one h. in insulinoma; one h. in diabetes mellitus under insulintherapy.
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PMID:[On the syndrome of childhood-hypoglycemia. II. Hypoglycemia in the postneonatal period (author's transl)]. 89 35

Addison's disease, when caused by idiopathic atrophy of the adrenal cortex, is frequently associated with other endocrine abnormalities. Primary hypothyroidism and hypogonadism have been reported in association with adrenal insufficiency; understandably, such cases may lead to diagnostic confusion with respect to possible pituitary disease. This case study concerns a woman who exhibited, in sequence and over a period of 17 years, hypogonadism, hypoadrenalism, diabetes mellitus and, finally, hypothyroidism. Originally misdiagnosed as having Sheehan's syndrome, she eventually became hyperpigmented. The true nature of her illness was then revealed to be primary insufficiency of multiple endocrine glands, with the demonstration of elevated levels of several pituitary hormones. Because multiple endocrine insufficiencies may coexist or develop with time, we suggest that a patient with a single documented endocrine deficiency be investigated initially and serially for additional glandular deficiencies.
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PMID:The syndrome of multiple endocrine gland insufficiency. 93 64

The unique combination of male hypogonadism with hypoparathyroidism, hypoadrenalism, hypothyroidism, diabetes mellitus, and alopecia totalis has been documented in a male patient who has been followed over the past 28 years. In this patient, first seen at the age of six for hypoparathyroidism alone, repeated clinical and laboratory endocrine evaluation detected the sequential development of the additional endocrine deficiencies. The presence of abnormal serum antibodies is consistent with an atuoimmune pathogenesis of this syndrome.
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PMID:Coexistence of primary endocrine deficiencies: a unique case of male hypergonadism associated with hypoparathyroidism, hypoadrenocorticism, and hypothyroidism. 100 83

Subnormal plasma 11-deoxycortisol (compound S) responses to metyrapone were found in patients with adrenal insufficiency or with Cushing syndrome caused by adrenal tumors and in those receiving long-term glucocorticoid or diphenylhydantoin sodium therapy. High normal or exaggerated responses were seen in women receiving oral contraceptives, patients with Cushing syndrome caused by adrenal hyperplasia, and those with untreated hypothyroidism. Diabetes mellitus, hypoglycemia, congestive failure, and obesity also were associated with exaggerated responses. Subnormal plasma S responses were observed in 15 patients who responded normally to a repeat test or to the standard metyrapone test. The abnormal response resulted from insufficient metyrapone, administration at the wrong time, or delay in obtaining the blood sample. The single-dose metyrapone test may be the procedure of choice in screening for adrenal insufficiency.
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PMID:Single-dose metyrapone test: review of a four-year experience. 105 66


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