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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty children with diabetes inspidus, 19 children and adolescents and one baby of 2 months, were treated with DDAVP. The drug was very effective, the average urine volume being 1.7 L/24 hours. The control of the diuresis in the baby was very satisfactory. There were no secondary effects and the only episode of water intoxication occurred in a girl with corticosteroid deficiency which was not well controlled. The effects of this drug are discussed in the light of the biochemistry and pharmacology and the activity compared with that of Lysine vasopressin (LVP). Plasma levels of DDAVP and LVP showed that DDAVP persists for longer which may explain its greater potency and duration of action.
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PMID:[Treatment of ADP responsive diabetes insipidus in children with DDAVP (1-desamino-8-D-arginine-vasopressin)]. 61 Jun 62

The physiologic factors involved in vaseopressin (ADH) release and action are reviewed with emphasis on the interaction between osmotic and volume stimuli to the discharge of ADH. Abnormalities in reception of stimuli to ADH release, and in the impaired synthesis and release of ADH, are reviewed in relation to the causes of diabetes insipidus, and information on the biochemical changes which have been described in patients with nephrogenic diabetes insipidus is also discussed. We summarize the pathologic lesions and associated diseases found in 54 of our patients with diabetes insipidus. Criteria for establishing the diagnosis of diabetes insipdus are reviewed with emphasis on the dehydration test, including the importance of measuring plasma osmolality at the conclusion of water deprivation. Treatment of diabetes insipidus is briefly discussed with emphasis on the use of DDAVP and oral agents. The syndrome of inappropriate ADH secretion (SIADH) is reviewed including our experience with 39 patients. The differential diagnosis of SIADH, including the value of water loading and the measurement of ADH levels, is discussed. We comment on treatment of these patients including the use of investigational drugs. Lastly, we review the pharmacologic features and clinical relevance of some drugs which alter the release and action of ADH.
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PMID:Pathophysiologic and pharmacologic alterations in the release and action of ADH. 81 77

Four Sudanese children with DIDMOAD syndrome (diabetes insipidus, diabetes mellitus, optic atrophy and deafness) are reported. They were two boys (aged 15 and 16 years) in one family and a boy and a girl (aged 16 and 6 years, respectively) in another family. Diabetes mellitus was first to appear (at 3-8 years) followed by deafness and visual failure; and the disease ended fatally in one patient (aged 20 years). In the other three, diabetes insipidus was confirmed using water deprivation test for 8 hours. The maximum urine osmolality ranged between 131-523 mOsm/kg, whereas the corresponding plasma osmolality ranged between 315-332 mOsm/kg. Slight further improvement in urine concentration was observed in 2 of the patients following the use of desmopressin (DDAVP, 20 micrograms intranasally). Intravenous pyelography, voiding cystourethrography and ultrasound revealed severe bilateral hydronephrosis, dilated ureters and distended bladder without vesicoureteral reflux in the three patients. With the high rate of consanguinity prevalent in North Africa and the Middle East, we recommend examining children who present with diabetes mellitus in this region for features of DIDMOAD syndrome.
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PMID:Diabetes insipidus, diabetes mellitus, optic atrophy and deafness (DIDMOAD syndrome). A clinical study in two Sudanese families. 187 84

We report three Libyan children from one family with the syndrome diabetes insipidus, diabetes mellitus, optic atrophy and deafness, (DIDMOAD). Two children presented with diabetic ketoacidosis while one was discovered during screening of the family. All three children are alive, two of them on desmopressin (DDAVP) and insulin therapy and one on DDAVP only.
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PMID:DIDMOAD syndrome in a Libyan family. 242 93

Tissue plasminogen activator (t-PA), tissue plasminogen activator inhibitor, (PAI), and von Willebrand factor (vWF) were measured in 30 diabetics and 17 control subjects. These studies were performed to clarify the role of obesity in causing abnormalities of the fibrinolytic system in diabetics. The t-PA antigen response measured after the infusion of desmopressin acetate (DDAVP) was similar in all groups. Peak responses to DDAVP for controls, type I diabetics, and type II diabetics were 21.2 +/- 9.5 ng/mL, 27.5 +/- 9.0 ng/mL, and 28.8 +/- 11.0 ng/mL (NS), respectively. These responses did not correlate with the body mass index (BMI) or any other of the indices examined. A significant decrease of t-PA activity as contrasted with t-PA antigen following DDAVP occurred in type II diabetics only. The decrease of t-PA activity strongly correlated with greater basal levels of plasminogen activator inhibitor in these same subjects. The plasma level of plasminogen activator inhibitor correlated with BMI but with no other index examined. In contrast to t-PA activity and PAI, vWF responses to DDAVP inversely correlated to basal vWF concentration in all groups. Basal concentrations of vWF were increased in both type I and II diabetics and showed no relationship to degree of obesity. In summary, these results suggest that type II diabetic subjects have decreased t-PA activity, which is best explained by increased levels of PAI. The increased PAI appears related to obesity and not diabetes per se.
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PMID:Fibrinolytic capacity following stimulation with desmopressin acetate in patients with diabetes mellitus. 250 17

A 22 year-old woman with diabetes insipidus on chronic therapy with desmopressin acetate (DDAVP) developed recurrent venous thromboembolism and transient thrombocytopenia temporally related to the administration of DDAVP. Large increases in plasma von Willebrand factor (vWF), vWF-activity, and relative increases in the concentrations of the larger multimeric forms of vWF-antigen were observed, as well as a plasma factor which sensitized normal platelets to undergo spontaneous aggregation in vitro. Additional studies showed that the patient's plasma retained the platelet aggregation inducing activity after selective removal of vWF by immunoabsorption. The nature of the platelet activating factor and the relationship of this factor and the excessively increased and transiently abnormal vWF to the recurrent venous thromboembolism in this patient remain uncertain. Although the findings do not implicate definitively DDAVP in the elevation of vWF in this patient, it is suggested that its use be considered with caution in patients with diabetes mellitus and increased levels of vWF.
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PMID:Venous thromboembolism and transient thrombocytopenia in a patient with diabetes insipidus treated with desmopressin acetate (DDAVP). 326 97

In this longitudinal study we measured beta-TG, PF4, fibrinolytic activity (extrinsic and euglobulin fraction), fibrinogen, FVIII RAg and FVIII Rcof before and after i.v. DDAVP (FPA was only measured before DDAVP) in 20 patients with diabetes mellitus. These parameters were measured on three occasions: phase I: during disregulation, phase II: after three weeks of strict control, phase III: after nine weeks of good control. Twenty-two healthy volunteers served as normal controls. No significant differences related to metabolic control were found for beta-TG, PF4, FPA and fibrinogen. There was no change after i.v. DDAVP administration. Fibrinolytic activity showed a significant increase after i.v. DDAVP. Baseline values and post-DDAVP increase were not significantly different from our normal controls. FVIII RAg and FVIII Rcof were both significantly elevated in diabetes mellitus. Both increased significantly after DDAVP. The FVIII RAg release (delta FVIII RAg) was significantly less in the diabetics. Fibrinolytic activity, FVIII RAg and FVIII Rcof are independent of the degree of metabolic control in patients with diabetes.
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PMID:The effect of diabetes regulation on platelet release, fibrinolysis and coagulation tests, before and after stimulation with DDAVP. 392 75

The renal glycoprotein hormone erythropoietin (Epo) is the key element in the feedback control of the production of red blood cells (RBC) in bone marrow. Excess of antidiuretic hormone (ADH) increases the RBC mass by increasing the synthesis of Epo. The mechanism of the Epo stimulating effect of ADH is not fully understood. Rats were treated with ADH with or without prior injection of a V1a-receptor antagonist. Additional experiments were carried out by stimulating the V2-receptor by desmopressin (DDAVP). Epo level in plasma was doubled following injections of ADH. Blockade of the V1a-receptor completely abolished the Epo stimulating effect of ADH. Neither ADH alone nor the combined giving of V1a-antagonist and ADH had an influence on the glomerular filtration rate or the renal plasma flow. Therefore, the increased Epo synthesis after application of ADH cannot be explained by a constriction of renal blood vessels with consecutive ischemic hypoxia. There is rather a direct stimulation of Epo synthesis by ADH via its receptors. Since a selective stimulation of the V2-receptor by DDAVP did not increase to Epo level in plasma, the observed increase of Epo is mediated by the V1a-receptor.
Exp Clin Endocrinol Diabetes 1995
PMID:Increased production of erythropoietin after application of antidiuretic hormone. A consequence of renal vasoconstriction? 853 59

Desmopressin (DDAVP), an AVP.V2-receptor agonist, evokes endothelium-dependent relaxation (EDR) due to nitric oxide (NO), EDR factor (EDRF) in the systemic vasculature, and glomerular afferent arterioles via AVP receptor(s). Glyceryl trinitrate (GTN) causes endothelium-independent (nonreceptor-mediated) vasodilation. We elucidated the possible involvement of EDRF in early non-insulin-dependent diabetes mellitus (NIDDM) and glomerular hyperfiltration (GHF) by DDAVP and GTN infusions. Patients with advanced DM nephropathy (DM.Np) (n = 7) were also examined. DDAVP and GTN decreased the mean blood pressure in DM with GHF (DM + GHF) and without GHF (DM-GHF) greater than that in normal subjects (N), without any difference in the heart rate changes in any group. Plasma levels of cGMP, a cellular messenger of NO, were significantly increased by DDAVP and GTN with a similar increment in each group. DDAVP caused a significant increase in urinary cGMP excretion in each group with a similar increment in each group. However, it caused a transient increase in creatinine clearance only in DM + GHF although GTN did not, and an exaggerated excretion of urinary albumin in early NIDDM, especially in DM+GHF, without a change in beta 2-microglobulin excretion. In contrast, in DM.Np GTN caused a decrease in blood pressure and an increase in plasma cGMP levels, but DDAVP did not. In conclusion, in peripheral vasculature and kidney, an enhanced sensitivity of vascular smooth muscle to NO is present in early NIDDM. The exaggerated dilation of glomerular afferent arterioles by preferentially produced NO in in situ, which causes a rise in PGC, might be partly responsible for the glomerular hyperfiltration and subsequently the increase in the glomerular protein permeation of DM+GHF. However, in peripheral blood vessels of DM.Np EDR is impaired. Thus, EDR seems to change with the development of NIDDM.
J Diabetes Complications
PMID:Endothelium-dependent relaxation in peripheral vasculature and kidney of non-insulin-dependent diabetes mellitus. 857 27

Tissue-type plasminogen activator (tPA) is an endothelium-derived vasoactive substance which is released to the blood stream by exercise, blood occlusion, and desmopressin (DDAVP). The increased capacity of the plasma tPA level raised by these factors is thought to reflect in vivo endothelial function. On the other hand, endothelial dysfunction has been reported in patients with hypercholesteremia as well as in those with diabetes mellitus. Therefore, diabetic patients with hypercholesteremia were administered 5 mg of simvastatin daily for one month and plasma tPA responses evoked by DDAVP were examined before and after treatment for hypercholesteremia. While the treatment of simvastatin for one month significantly reduced serum cholesterol levels from 257 +/- 12 mg to 206 +/- 10 mg (no change in HbA1c was observed during the study), plasma tPA levels and % delta vWF (von Willebrand factor) following DDAVP infusion significantly increased from 11.4 +/- 1.2 ng/ml to 13.4 +/- 1.4 ng/ml and from 69.3 +/- 23.4% to 126.5 +/- 47.4%, respectively. However, neither increase in plasma levels of guanosine 3', 5'-cyclic monophosphate (cGMP) nor change in the depressive response of blood pressure was observed following DDAVP infusion after the treatment of simvastatin. In addition, no change in urinary albumin excretion rate was observed with the treatment of hypercholesteremia. Therefore, it was suggested that improvement in hypercholesteremia may ameliorate vascular endothelial dysfunction in diabetic patients with hypercholesteremia and that hypercholesteremia may enhance endothelial dysfunction in these patients.
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PMID:[Effect of hypercholesteremia on vascular endothelial function and albumin excretion rate in patients with diabetes mellitus]. 895 5


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