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

Abnormalities in sodium homeostasis and in atrial natriuretic peptide (ANP) behavior could play a role in determining and accelerating the development of glomerular hypertension, hypertension, and microalbuminuria in insulin-dependent diabetes. The aim of the present study was to investigate in 32 hypertensive insulin-dependent diabetic patients (HD) with an altered albumin excretion rate the natriuretic response and ANP release to saline load (2 mmol/kg 90 min, and the effects angiotensin converting enzyme inhibitor therapy 2.5 to 5.0 mg cilazapril, once daily), and calcium antagonists (sustained release verapamil: 120 to 240 mg Isoptin Press, once daily, and long acting nifedipine: 20 to 40 mg Adalat AR, twice daily) on sodium homeostasis and albumin excretion rate. Eight normal subjects matched for sex, age, and weight served as controls. The 32 HD patients showed a blunted response in ANP release and sodium excretion during saline infusion in comparison with controls. The cilazapril and verapamil treatments were tested in 16 of the 32 HD patients and were both effective in ameliorating natriuretic and ANP response to saline load and in decreasing albumin excretion rate. The combined cilazapril and verapamil treatment further improved both these parameters in these patients, although blood pressure levels were comparable. The other 16 HD patients underwent sequential verapamil and nifedipine treatment. Verapamil was more effective than nifedipine in improving natriuresis and ANP release to saline load and in lowering the albumin excretion rate. The results of the present study demonstrate that sodium homeostasis and ANP release are altered in hypertensive nephropathic patients, and both cilazapril and verapamil are more effective than nifedipine in ameliorating natriuresis, ANP release, and albumin excretion rate.
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PMID:Effects of angiotensin converting enzyme inhibitors and calcium antagonists on atrial natriuretic peptide release and action and on albumin excretion rate in hypertensive insulin-dependent diabetic patients. 145 87

The TEAM trial investigated the effectiveness and tolerance of a fixed combination of the ACE inhibitor and calcium channel blocker (2 mg trandolapril and 180 mg verapamil retard) (preparation Tarka) in an open multicentre prospective study of treatment of moderately severe hypertension (diastolic pressure at the end of the two-week wash-out period 100-115 mm Hg). The trial comprised 163 patients who were treated first for four weeks by a monotherapy with 2 mg trandolapril. After these four weeks patients who attained normal blood pressure proceeded with trandolapril treatment. Hypertensive patients who did not attain normal diastolic pressure levels were treated for another four weeks by a fixed combination of trandolapril and verapamil SR. After four weeks of treatment with trandolapril 62 patients of 163 (37%) had a diastolic blood pressure of less than 90 mm Hg. The fixed combination of trandolapril and verapamil SR reduced the diastolic blood pressure to less than 90 mm Hg in 71.6% of the patients resistant to treatment with 2 mg trandolapril and in another 15.6% of patients it reduced the diastolic blood pressure by 10 mm Hg or more. After two months of treatment 60 patients had a normal blood pressure due to trandolapril (37%) and another 73 patients (45%) treated by a combination of trandolapril and verapamil SR, i.e. a total of 133 patients (82%) who originally suffered from moderately severe hypertension, attained a normal diastolic blood pressure. The mean decrease of diastolic pressure after two months of treatment was 19.5 mm Hg in "non-respondents" to trandolapril monotherapy and 23.6 mm Hg in "respondents". The mean decrease of systolic pressure in "non-respondents" and "respondents" after trandolapril treatment was 19.5 mm Hg and 35.0 mm Hg resp. The fixed combination of trandolapril and verapamil was not only effective but was associated with a minimum of undesirable effects. The incidence of headaches declined significantly. The combination of the above preparations is useful also because both preparations have a cardio- and nephroprotective effect and do not affect the lipid and carbohydrate metabolism. Treatment with a fixed combination of trandolapril and verapamil SR is indicated in moderately severe hypertension not responding to monotherapy, in particular when associated with diabetes, hyperlipoproteinaemia, ischaemic heart disease or left ventricular hypertrophy.
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PMID:[The TEAM study--a study of the effectiveness and tolerance of treatment of essential hypertension with a fixed combination of trandolapril and verapamil]. 982 54

The article focuses on the action of isoptin as a monotherapy and in the complex with mildronat in 67 patients with non-insulindependent diabetes mellitus (NIDM) and supraventricular arrhythmia. Isoptin has been shown to be a very effective drug in patients with atrial disorders of cardiac rhythm suffering from diabetes mellitus and ischemic heart disease, especially so in a complex therapy with mildronat. The results obtained permit recommending isoptin as an antiarrhythmic drug in NIDM patients.
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PMID:[Isoptin in the therapy of supraventricular arrhythmia in patients with diabetes mellitus, non-insulin dependent, concurrent with ischemic heart disease]. 1188 47

Gingival enlargement is common among patients and can be caused by a variety of etiological factors. The most common reason is poor oral hygiene and high bacterial load that leads to gingival inflammation and enlargement. Other implicated factors include systemic drugs, such as phenytoin (Dilantin) taken by epileptic patients, calcium channel blockers such as nifedipine (Procardia) and verapamil (Calan) for the treatment of hypertension, arrhythmia and angina. Another class of medication associated with gingival enlargement is immunosuppressive agents given to organ-transplant patients to prevent rejection of the new element such as cyclosporine. Some enlargements could be associated with other conditions such as puberty, pregnancy or diabetes or be a symptom of a systemic disease (leukemia, Wegener's granulomatosis or sarcoidosis). In rare cases the cause for the enlargement is genetic and termed hereditary gingival fibromatosis (HGF). HGF is a genetic disorder characterized by a progressive enlargement of the gingiva. Histologically, the gingiva is characterized by an accumulation of dense fibrous connective tissue. This is believed to be due to an imbalance between synthesis and degradation of extracellular matrix composed mainly of collagen molecules or due to an alteration in fibroblast proliferation. Different pathogenic mechanisms have been proposed and examined over the years but no precise process has been identified. The main objective of this paper is to discuss this genetic anomaly and support it with clinical cases of a mother and her two children. It will focus on the clinical and histologic characteristics of HGF as well as known biologic and genetic features and treatment modalities.
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PMID:Gummy smile: could it be genetic? Hereditary gingival fibromatosis. 2287 May 49

Gingival enlargement is common among patients and can be caused by a variety of etiological factors. The most common reason is poor oral hygiene and high bacterial load that leads to gingival inflammation and enlargement. Other implicated factors include systemic drugs, such as Phenytoin (Dilantin) taken by epileptic patients, Calcium Channel Blockers such as Nifedipine (Procardia) and Verapamil (Calan) for the treatment of hypertension, arrhythmia and angina. Another class of medication associated with gingival enlargement is immunosuppressive agents given to organ-transplant patients to prevent rejection of the new element, such as Cyclosporine. Some enlargements could be associated with other conditions such as puberty, pregnancy or diabetes or be a symptom of a systemic disease (leukemia, Wegener's granulomatosis or sarcoidosis). In rare cases the cause for the enlargement is genetic and termed Hereditary Gingival Fibromatosis (HGF). HGF is a genetic disorder characterized by a progressive enlargement of the gingiva. Histologically, the gingiva is characterized by an accumulation of dense fibrous connective tissue. This is believed to be due to an imbalance between synthesis and degradation of extracellular matrix composed mainly of collagen molecules or due to an alteration in fibroblast proliferation. Different pathogenic mechanisms have been proposed and examined over the years but no precise process has been identified. The main objective of this paper is to discuss this genetic anomaly and support it with clinical cases of a mother and her two children. It will focus on the clinical and histologic characteristics of HGF as well as known biologic and genetic features and treatment modalities.
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PMID:Gummy smile: could it be genetic? Hereditary gingival fibromatosis. 2334 94