Gene/Protein Disease Symptom Drug Enzyme Compound
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Estrogenic compounds are the most important group of drugs that can induce hypertension. Studies have shown an incidence of significant hypertension amounting to less than 1% after 1 year of taking oral contraceptives and about 2% after 5 years. The ratio of the incidence of hypertension among ''takers'' to that of ''nontakers'' has been assessed at 1.8 by 1 study and 2.6 by another. Small but significant increments in systolic and diastolic pressures can be discerned during the first 2 years of treatment. Cessation of treatment has resulted in pressures returing to pretreatment levels within 3 months. In those previously normal the highest readings during oral contraceptive use were only 155/90 mm of Hg. Severe hypertension is more likely to occur in the predisposed, and malignant hypertension has been reported. Previous hypertension, toxemia of pregnancy, obesity, and nephropathy are predisposing conditions. Although progestagens, used alone, do not cause clinical hypertension the incidence of hypertension associated with an estrogen-progestogen combination was directly related to the dose of progestagen used. Weight gain is often observed in oral contraceptive users and is occasionally accompanied by edema and hypertension. There is a marked increase in the circulating level of renin substrate (angiotensinogen) which is caused by the estrogen component of the pill. The increase in renin substrate is associated with increase in plasma levels of renin activity, angiotensin 2, and aldosterone, together with a fall in plasma renin concentration. The suppression of plasma renin concentration can persist for weeks after stopping the pill. The factors responsible for hypertension are probably intrinsic and may be either neural, vascular, or renal. Patients taking oral contraceptives should have blood pressure checks at 6-month intervals, and more frequently in high risk cases. In the management of those with only mild blood pressure elevation, such patients should change to a preparation with the lowest available estrogen dosage, 30 mcg of ethinyl estradiol, or reserve the method for use during crucial periods of family planning. With moderate hypertension the oral contraceptive should be suspended for 3-6 months. If the blood pressure falls, oral contraceptives should not be resumed but another method recommended. Continuing hypertension requires further study and possibly elective sterilization. Severe hypertension requires withdrawal of the pill, urgent investigation, and treatment. Other drugs may cause hypertension. Management of these patients is outlined. Structural formulae of progesterone, norethisterone acetate, medroxyprogesterone acetate, and norgestrel are shown.
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PMID:Drug-induced hypertension: pathogenesis and management. 18 40

The application of programmable pocket calculators to clinical dietetics is described. The development of programs for the HP-67 and 97 for the evaluation of nutritional intakes of patients with obesity, renal disease, etc. and for the calculation and interpretation of food intakes in nutritional surveys is given in detail. The calculators simplify the practical work, shorten the calculation time substantially and allow direct incorporation of newly published data into analysis.
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PMID:The use of a programmable pocket calculator in clinical dietetics. 43 45

113 cases of pancreatic and renal disease studied by both ultrasound and computed tomography (CT) were analyzed retrospectively. CT provided a diagnosis when pancreatic ultrasound was unsuccessful due to overlying bowel gas or obesity and when renal ultrasound was unsuccessful due to obesity, reverberations from ribs, small lesions, or multiple lesions. Conversely, ultrasound provided a diagnosis when CT was unsuccessful due to lack of fat planes or respiratory motion. CT usualy distinguished carcinoma from pancreatitis when ultrasound showed a focal echogenic mass. CT resolved renal cyst from neoplasm when ultrasound showed a mixed echo pattern mass.
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PMID:Complementary use of ultrasound and computed tomography in studies of the pancreas and kidney. 61 98

The natural history of patients with glucose intolerance was observed in 334 patients during a period of 18 years. Glucose tolerance testing (100 g orally) was characterized by measurement of induced insulin secretion. Diabetic complications of retinopathy, sensory neuropathy, and renal disease developed only in the group of patients in whom the induced serum insulin peak fell below 60 mu U/ml. Preservation of an insulin secretory reserve that permitted serum insulin peaks of 60 muU/ml or greater was not associated with development of these complications or symptoms of insulin deficiency despite the presence of an equal degree of fasting hyperglycemia and glucose intolerance. A critical amount of insulin secretory reserve distinguishes between two qualitatively distinct clinical syndromes: true diabetes mellitus (the development of signs and symptoms of insulin deficiency) and the syndrome of pure resistance to insulin (signs and symptoms of hyperglycemia in the setting of adequate or excessive insulin secretion, frequently with obesity, but without diabetic complication).
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PMID:Insulin secretion in the diagnosis of adult-onset diabetes mellitus. 67 27

We studied the prevalence and the risk factor among the patients of gout in Mexico. Research was conducted in the National Institute of Cardiology and in our private practice. Prevalence of hiperuricemia and gout in the Institute of Cardiology was of 1% (970 out of nearly 100,000 patients). We divided those cases of two subgroups: Reumatology patients (333) and Cardiovascular patients (529). In the first group primary gout was (96.3), and (50.32% in the second. Risk factor was quite different too: nephropathy 9.9%, lithiasis 9.3%, pyelonephritis 2.7%, cardioangiosclerosis 12.9%, aortosclerosis 6.6%, coronary insufficiency 6.3%, myocardial infarction 0.9%, arterial hypertension 24.6% obesity 56.1% and diabetes 9.9% in the Reumatology group; in the Cardiovascular one, nephropathy 14.3%, lithiasis 12.2%, pyelonephritis 7.1%, cardioangiosclerosis 62.7%, aortosclerosis 31.7%, coronary insufficiency 24.9%, myocardial infarction 29%, arterial hypertension 51%, obesity 54.8% and diabetes 20.4%. Among the private practice patients prevalence was of 10.1% (961). In an early age (39 years) in men and a later one for women (53 years). Other characteristics of epidemiology and risk factor are: primary gout 89%, atherosclerosis 5%, coronary disease 4.6%, lithiasis 4.7%, nephropathy 2%, pyelonephritis 1%, obesity 43%, and diabetes 4.6%. In an small group of patients of our private practice we made an exhaustive study of risk factor and the metabolic disorder of lipids. We found the following frequency: 9.3 of nephropathy, 31.2% of lithiasis, 18.7% of pyelonephritis, 68.9% of cardioangiosclerosis, 46.8% de coronary insufficiency, 9.3% of myocardial infarction, 68.7% of arterial hypertension, 68.7% of obesity and 18.7% of diabetes. In the lipid profile we found an increase in triglicerids and prebeta lipoprotein. We have amply discussed the relation between hiperuricemia and pathology considered as a risk factor from the genetic point of view as well as the metabolic and circumstancial aspect. From all that we concluded that risk is multifactorial.
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PMID:[Various epidemiological aspects of hyperuricemia and gout in Mexico: incidence and the cardiovascular risk factor]. 72 44

Fasting serum triglyceride and cholesterol measurements, and lipoprotein characterization by ultracentrifugation, were performed in four groups of patients with chronic renal disease (uraemic, short- and long-term haemodialysis and renal transplant recipients) and the results compared with those obtained from age- and sex-matched control subjects. Basal insulin and growth hormone levels, and serum creatinine and albumin concentrations were measured in, and detailed dietary histories taken from patients in each group. The predominant lipid abnormalities were hypertriglyceridaemia and increased very low density lipoproteins (type IV hyperlipoproteinaemia) in both uraemic and haemodialysis patients. Following renal transplantation, a different pattern of hyperlipidaemia was found. Hypercholesterolaemia was more common and hypertriglyceridaemia less common than in the uraemic and haemodialysis group. The lipoprotein abnormalities were increased low density and/or very low density lipoproteins, with types IIa IIb and IV hyperlipoproteinaemia occurring equally frequently. In uraemic and haemodialysis patients, the proportion of carbohydrate in the diet was high, and may have played a role in the genesis of hypertriglyceridaemia. There was a positive correlation between relative body weight and serum triglyceride in the long-term dialysis group. In renal allograft recipients hypertriglyceridaemia could be attributed, at least in part, to obesity, prednisone dosage and the degree of impairment of graft function. The aetiology of hypercholesterolaemia in the transplant recipients was unclear. Neither basal insulin nor growth hormone levels were elevated in any patient group. Uraemic hypertriglyceridaemia is a clearly defined and well documented metabolic abnormality which is not corrected by dialysis. Post-transplantation hyperlipidaemia however, is a condition of variable presentation and multifactorial aetiology.
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PMID:Studies on the nature and causes of hyperlipidaemia in uraemia, maintenance dialysis and renal transplantation. 110 47

The relationship between arterial blood pressure and clinically apparent diabetes mellitus was examined by measuring blood pressure, under standardised conditions, in 735 ambulant diabetic patients attending St. Mary's and King's College Hospital, London. Other biometric, clinical and family data were also systematically collected. A large proportion of first degree relatives of the diabetics and a control group of first degree relatives of non-diabetics were also seen and examined; they were also tested for the presence of unsuspected diabetes. Blood pressure in diabetics was evaluated in two ways. Mean pressures (systolic and diastolic) were calculated by age and sex and compared with similar data from two British non-diabetic populations. In addition, age and sex adjusted blood pressure "scores" were derived for each of the diabetic propositi and for the relatives by calculating the degree to which their pressures deviated from the mean of a corresponding age/sex group of non-diabetics. These deviations were then made comparable by standardising them for the systematic change in variance with age and sex. Using both "raw pressures" and "adjusted scores" the influence of age, sex, obesity, arm girth, response to diagnosis and ethnic, obstetric and anamnestic features were examined. Analysis of the influence of various characteristics of the diabetic state on blood pressure was made; this included mode of presentation, known duration; insulin dose and degree of metabolic control. Finally the relationship of blood pressure levels to the long-term sequels of diabetes was analysed with special reference to renal disease, eye changes, neuropathy and arterial disease. No systematic difference between arterial blood pressure in diabetics and a suitable control population was detected. Younger patients, females more than males, tended to have somewhat higher mean diastolic pressures but these were balanced by rather lower mean pressures in older diabetics. There was evidence of raised pressure levels at the time of diagnosis of diabetes, particularly in older patients, which "settled" with time for reasons which were not clear. The relationship of arterial pressure with adiposity was comparable to that in non-diabetics. After allowance for age and sex, blood pressures and scores were not related to the mode of onset of the diabetes. In the youngest onset group, however, known duration of diabetes appeared to correlate positively with arterial pressure in excess of the effect of age. Insulin dose and metabolic characteristics of the diabetes showed little clear association with arterial pressure but, as expected, patients with evidence of renal disease had higher mean pressures. However, cause-effect relationship between raised pressure and renal disease in diabetics may operate in both directions. Some elements of retinopathy were positively correlated with blood pressure; others were not. The role of co-existing renal disease in determining this association was examined...
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PMID:Arterial pressure in clinically apparent diabetics. 123 79

Points of agreement: (1) In IDDM, hypertension occurs in patients who have already developed nephropathy, probably in the microalbuminuric phase. (2) Hypertension is an important accelerator of the development of diabetic nephropathy. (3) Hypertension, obesity and NIDDM are often associated, and insulin resistance is commonly observed in all three states. (4) Antihypertensive therapy retards the development of diabetic nephropathy in IDDM and reduces proteinuria in NIDDM. (5) The choice of antihypertensive agent in the diabetic patient must be based upon the efficacy of the drug as well as avoidance of side effects including deleterious influence on glucose, insulin and lipid levels and renoprotection. (6) Carefully conducted long-term comparative trials between different classes of antihypertensive drugs in microalbuminuric IDDM and NIDDM patients are essential. Points of major controversy: (1) Detection of IDDM patients prone to the development of diabetic nephropathy can be performed by measuring specific parameters such as erythrocyte Na(+)-Li+ countertransport activity. (2) Insulin resistance is a pathogenic mechanism rather than purely an association with hypertension and obesity. (3) A certain class of antihypertensive agents--ACE inhibitors--confers a specific renoprotective effect in diabetic nephropathy, in addition to its effects upon systemic blood pressure. (4) Reduction of blood pressure should be considered in the normotensive microalbuminuric diabetic patient. (5) Microalbuminuria is a sufficient 'surrogate endpoint' for the progression of renal failure.
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PMID:Meeting report of the International Society of Hypertension Conference on Hypertension and Diabetes. 131 6

Four patients of pure gouty nephropathy are presented. Gout was of over five years duration and asymptomatic nephropathy manifested as non-oliguric acute renal failure. Diseases commonly associated with it like uric acid stones, urinary tract infections, hypertension, diabetes mellitus, hyperlipidemid, obesity and nephrosclerosis were absent. Reduction in serum uric acid level resulted in prompt improvement in renal functions. Early detection and control of hyperuricemia may help in restoration of renal functions.
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PMID:Non-oliguric acute renal failure in gout. 139 13

The goal of this review was to assess the magnitude of coronary artery disease (CAD) mortality and its determinants in insulin-dependent diabetes mellitus (IDDM) patients with persistent proteinuria. By reanalyzing data from two previously published studies of patients with nephropathy, it was found that these patients had extremely high CAD mortality rates in comparison with IDDM patients without proteinuria, but only after the age of 35 yr. In addition, the risk of CAD death was associated with high serum cholesterol levels but was unrelated to systemic blood pressure, smoking habits, and obesity. Further studies of the determinants of CAD in patients with IDDM and proteinuria are urgently needed. Except for efforts to lower serum cholesterol, it is not known whether any other measure can be undertaken to reduce the extremely high mortality due to CAD that afflicts IDDM patients with persistent proteinuria, in particular those patients whose renal failure might have been "successfully" postponed by antihypertensive therapy.
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PMID:Coronary artery disease is the major determinant of excess mortality in patients with insulin-dependent diabetes mellitus and persistent proteinuria. 145 52


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