Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article deals with the use of oral contraceptives and IUDs by chronically ill adolescent females. Results of controlled studies of contraceptive choices and problems are reviewed for teenagers with cardiac disease, epilepsy, multiple sclerosis, migraine headaches, asthma, cystic fibrosis, inflammatory bowel disease, hepatitis, diabetes mellitus, thyroid disease, oligomenorrhea and amenorrhea. If oral contraceptives (OC) are prescribed for use in teens with cardiac disease, a contraceptive with 35ug or less of estrogen and the equivalent of 1 mg or less of norethindrone should be used. The low-dose progestin only pill can be prescribed, but should be used in conjunction with a back-up barrier method. Reports to date have failed to reveal increased seizure activity in epileptic pattients on OCs, and there is no significant evidence to date that OCs alter the course of multiple sclerosis. Although the evidence is inconclusive, the physician should use extreme caution in prescribing OCs for teens with prior migraines. Regarding asthmatic patients, no problems have been reported with IUD use except in regard to steroid therapy and its possible effect on reducing IUD effectiveness. No adverse effects 2ndary to the use of OCs in asthmatic patients have been reported. OCs should be avoided or used with extreme caution in the cystic fibrosis patient. Teens with active inflammatory bowel disease should be advised that OCs may be ineffective or dangerous; there are no reports available on the effects of the IUD on the disease. The pill is contraindicated during active liver disease or cirrhosis. The IUD is not highly recommended for contraception in diabetic teenagers, whereas a low-dose combined OC can be used with extreme caution. However, OCs should be avoided in the diabetic patient with nephropathy, vascular complications or retinopathy. There is at present no contraindication for contraceptive use by women with thyroid disease. Finally, patients with prolonged post pill amenorrhea and infertility are generally females with amenorrhea or oligomenorrhea before pill use.
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PMID:Contraceptive use in the chronically ill adolescent female: Part I. 351 58

The metabolism and disposition of buspirone have been studied in the rat, the monkey, and in more than 150 human subjects. Buspirone is well absorbed, but is subject to first-pass metabolism. The mean systemic availability is approximately 4 percent. Buspirone is eliminated primarily by oxidative metabolism, which produces several hydroxylated metabolites, including 5-hydroxy-buspirone and 1-pyrimidinylpiperazine. The latter metabolite is from 1 to 20 percent as potent as buspirone in a variety of pharmacologic tests; 5-hydroxybuspirone is essentially inactive. In humans, the systemic exposure to buspirone increases linearly in relation to the oral dose. Food increases the bioavailability of buspirone by decreasing first-pass metabolism; absorption is not markedly altered. The pharmacokinetics of buspirone were not significantly different in men and women or in individuals 21 to 40 years old compared with those over 65 years of age. Half-life values observed in healthy volunteers ranged from two to 33 hours. Mean half-life values observed in healthy volunteers in the 14 studies conducted to date ranged from 2 +/- 1 to 11 +/- 3 hours. The half-life in women tended to be slightly longer than in men, but the difference was not significant. Hepatic cirrhosis resulted in a marked decrease in the clearance of buspirone, which correlated with serum alkaline phosphatase activity. Renal disease produced a modest decrease in buspirone clearance, which could not be correlated with an objective clinical measurement reflecting the severity of renal impairment. Buspirone was not removed by hemodialysis. Buspirone is highly protein bound (more than 95 percent), interacting with both albumin and alpha-acid glycoprotein. However, buspirone did not displace dilantin, propranolol, digoxin, or warfarin from plasma proteins. In rats, buspirone neither inhibited nor induced hepatic mixed-function oxidases. Co-administration of buspirone with amitriptyline or diazepam did not alter the disposition of these agents or their demethylated metabolites.
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PMID:Metabolism and disposition of buspirone. 351 29

Carnitine (beta-hydroxy-gamma-N-trimethylaminobutyric acid) is required for transport of long-chain fatty acids into the inner mitochondrial compartment for beta-oxidation. Widely distributed in foods from animal, but not plant, sources, carnitine is also synthesized endogenously from two essential amino acids, lysine and methionine. Human skeletal and cardiac muscles contain relatively high carnitine concentrations which they receive from the plasma, since they are incapable of carnitine biosynthesis themselves. Since the discovery of a primary genetic carnitine deficiency syndrome in 1973, carnitine has become the subject of extensive research. It is now recognized that carnitine deficiency may also occur secondary to genetic disorders of intermediary metabolism as well as to a variety of clinical disorders, including renal disease treated by hemodialysis, the renal Fanconi syndrome, cirrhosis, untreated diabetes mellitus, malnutrition, Reye's syndrome, and certain disorders of the endocrine, neuromuscular, and reproductive systems. Administration of the anticonvulsant valproic acid and total parenteral nutrition may also induce hypocarnitinemia. In many instances, the physiological implications of secondary carnitine deficiency have not been resolved. However, evidence for a specific carnitine requirement for the newborn, especially if preterm, is accumulating. Moreover, carnitine administration may have a favorable effect on some forms of hyperlipoproteinemia. Carnitine, now recognized as a conditionally essential nutrient, is a significant factor in preventive medicine.
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PMID:Carnitine: an overview of its role in preventive medicine. 353 87

The calcium antagonists diltiazem, nifedipine and verapamil are widely used in the treatment of coronary heart disease, arterial hypertension, certain supraventricular tachyarrhythmias and obstructive hypertrophic cardiomyopathy. During recent years their pharmacokinetic properties and metabolism have been studied in more detail. Although these 3 calcium antagonists exhibit great diversity in chemical structure, they exhibit common pharmacokinetic properties. These drugs are extensively metabolised and only traces of unchanged drugs are eliminated in urine. Their systemic plasma clearances are high and dependent on liver blood flow. Therefore, their bioavailabilities (diltiazem 40 to 50%; nifedipine 40 to 50%; verapamil 10 to 30%) are low despite almost complete absorption following oral administration. During long term treatment, oral clearance decreases and bioavailability increases due to saturation of hepatic first-pass metabolism. Pronounced intra- and inter-individual variations in clearance and bioavailability are observed. In patients with liver cirrhosis the various pharmacokinetic parameters are grossly altered. Clearance decreases, elimination half-life is substantially prolonged, and bioavailability more than doubles. In addition, the volume of distribution increases. Whereas renal disease has no impact on the pharmacokinetics of diltiazem and verapamil, elimination half-life of nifedipine increases in relation to the degree of renal impairment due to an increase in volume of distribution. Systemic clearance, however, remains unchanged. The data so far available indicate that the plasma concentrations of these drugs correlate with both their electrophysiological and haemodynamic effects. However, no effective therapeutic plasma concentration range has been firmly established. As reliable clinical end-points are available for dose titration of calcium antagonists, it is doubtful whether therapeutic drug monitoring will be of great value. Calcium antagonists are often administered in combination with a variety of other drugs. Thus, the potential for both pharmacodynamic and pharmacokinetic drug interaction exists. The interaction between digoxin and these drugs is of clinical importance. Verapamil and diltiazem cause a significant increase in plasma digoxin concentrations. In contrast, nifedipine does not lead to a significant increase in the plasma digoxin concentration. The mechanism responsible for this interaction is inhibition of both renal and non-renal digoxin clearance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical pharmacokinetics of verapamil, nifedipine and diltiazem. 354 36

A method to calculate unbound cortisol from total cortisol (measured by competitive protein binding) and CBG (measured by radial immunodiffusion) based on the binding equilibrium has been evaluated. The calculated results (y) correlate well with those (x) obtained by centrifugal ultrafiltration at 37 degrees C (y = 1.04 x - 2.11 ng/ml; r = 0.975; n = 150). The concentration of CBG is similar in normal men (37.7 +/- 3.5 (SD) micrograms/ml; n = 12) and women (39.5 +/- 3.7 (SD) micrograms/ml; n = 7) and shows no diurnal variation, but marked diurnal variation is observed for total cortisol (193.7 +/- 35.0 (SD) ng/ml at 08.00 h vs 43.2 +/- 23.3 (SD) ng/ml at 22.00 h; n = 19) and particularly for unbound cortisol (16.5 +/- 5.6 (SD) ng/ml at 08.00 h vs 2.3 +/- 1.8 (SD) ng/ml at 22.00 h; n = 19). The concentration of CBG (89.1 +/- 11.2 (SD) micrograms/ml) and of total cortisol (395.6 +/- 103.3 (SD) ng/ml at 08.00 h; 110.3 +/- 16.6 (SD) ng/ml at 22.00 h) are clearly elevated in estrogen treated women (n = 11) but unbound cortisol levels (17.2 +/- 7.7 (SD) ng/ml at 08.00 h; 2.5 +/- 0.5 (SD) ng/ml at 22.00 h) are similar to the control group. The concentration of CBG is significantly decreased in patients with Cushing's syndrome (33.2 +/- 5.6 micrograms/ml; n = 17) and unbound cortisol is relatively more elevated than total cortisol in these patients. In adrenal insufficiently CBG is normal, but total and unbound cortisol are markedly decreased. There is a significant decrease of CBG in hyperthyroidism (35.7 +/- 5.5 micrograms/ml; n = 22), in cirrhosis (32.0 +/- 8.0 micrograms/ml; n = 14) and in renal disease and a significant increase in patients treated with antiepileptic drugs (47.5 +/- 6.3 micrograms/ml; n = 14), but total and unbound cortisol are normal in all these conditions. We conclude that unbound cortisol can be calculated in a simple and reliable way from total cortisol and CBG and permits a better evaluation of adrenal function, particularly in patients with altered CBG concentrations.
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PMID:Clinical use of unbound plasma cortisol as calculated from total cortisol and corticosteroid-binding globulin. 356 Sep 36

Basing on the data obtained at 10433 autopsies performed from 1972 to 1981, cases of secondary kidney cirrhosis (chronic pyelonephritis, glomerulonephritis and interstitial nephritis) and renal pelvis cancer were thoroughly analysed. Analgetic nephropathy was found in 13.5% of all chronic interstitial and tubulo-interstitial inflammatory renal diseases, and in cases of bilateral lesions--in 17.2%. The conclusion was made on the basis of morphologic criteria ("chronic" papillary necroses and capillarosclerosis of renal pelvis). There was 41 patient with analgetic nephropathy, who died of chronic renal insufficiency, i.e. 10.6% out of the total number of patients deceased of the same reason for the period mentioned. In the biopsy material reviewed for the same period, that mainly consisted of cases with renal pelvis cancer, analgetic nephropathy was found in 15.7%.
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PMID:[Morphology of analgesic nephropathy and its incidence in Czechoslovakia]. 356 46

Necropsy findings of hepatobiliary system from 78 patients with end-stage renal disease maintained on hemodialysis are reported. Ninety percent of the patients exhibited some abnormalities. Multiple abnormalities often coexisted in each patient. Hepatomegaly was found in 50% of the patients and could be attributed to a discernible cause in all but two of the affected patients who had isolated hepatomegaly. Hepatic congestion was also prevalent and was complicated by fibrosis, cardiac cirrhosis, and centrilobular necrosis and hemorrhage in some patients. This was associated with chronic fluid overload, hypertension, and/or cardiovascular disease in the affected patients indicating the importance of adequate control of these factors. Mild periportal hepatic fibrosis, fatty metamorphosis, triaditis, hemosiderosis, and cystic changes were also seen with some frequency--the latter were associated with polycystic kidney disease and were complicated by massive intracystic hemorrhage and abscess formation, each in one patient. Chronic active hepatitis was found in three patients and was associated with chronic HBs antigenemia in one patient and presumed non-A, non-B infection in two. Nearly 22% of the patients showed either cholelithiasis at autopsy or before cholecystectomy due to complications. Significant negative findings included lack of acute viral hepatitis, silicone hepatosis, and recently described focal anoxic lesions associated with erythrocyte sludging. In conclusion, the present study has demonstrated the spectrum of hepatobiliary pathology in a large group of patients with end-stage renal disease maintained on hemodialysis.
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PMID:Hepatobiliary pathology in hemodialysis patients: an autopsy study of 78 cases. 375 41

Resistance to loop diuretics is often encountered clinically. Studies in healthy subjects have shown that overall response to loop diuretics depends upon the interplay between the total amount of drug reaching the urine, the time course of its entry into urine and the pharmacodynamics of response to diuretic in the urine. The mechanism by which diuretic resistance occurs has been elucidated in several clinical conditions. Treatment with inhibitors of prostaglandin synthesis has no effect on diuretic appearance in urine but blunts response by blocking the increase in renal blood flow produced by loop diuretics. In the elderly and in patients with moderate renal insufficiency, the mechanism of resistance appears to be purely pharmacokinetic, involving altered access of diuretic into the urine. In contrast, patients with nephrotic syndrome and hepatic cirrhosis manifest a purely pharmacodynamic form of resistance: in nephrosis, diuretic may bind to protein in the urine; in cirrhosis the mechanism of resistance is unclear. Lastly, in patients with congestive heart failure, with intravenous administration, resistance represents a pharmacodynamic phenomenon. With oral administration, however, the time course but not the extent of absorption is altered; consequently, in this setting, both pharmacokinetic and pharmacodynamic changes may contribute to the subnormal response. Strategies for overcoming resistance to loop diuretics in patients receiving NSAIDs or those with renal disease, hepatic cirrhosis or congestive heart failure include one or more of: increasing the dose size; administering frequent 'small' (but effective) doses; continuous intravenous infusion of the diuretic; or concomitant administration of another diuretic such as metolazone or hydrochlorothiazide.
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PMID:Resistance to loop diuretics. Why it happens and what to do about it. 390 37

A clinical and electrophysiological study of neuropathy in 215 unselected Ethiopian diabetics and 100 healthy controls was carried out at the Tikur Ambassa Teaching Hospital, Addis Ababa. The prevalence in diabetics was 54%, in controls 8%. The prevalence was significantly related to the duration of diabetes: 42%, 60% and 80% for a duration of respectively less than 5 years, 5 to 14 years, and 15 years and longer. There was no relationship of the prevalence to age. Diabetics with retinopathy (15%), nephropathy (12%) and liver cirrhosis (13%) had prevalences of respectively 70%, 76% and 71%; much higher figures than in patients without these complications. A higher prevalence of neuropathy was detected by nerve conduction studies than by clinical methods. The mean conduction velocity diminished in direct relation to the duration of the diabetes. The prevalence of neuropathy in our patients is similar to the prevalence reported from other countries in Africa. Poor nutritional background, inadequate control of the diabetes and the high prevalence of associated diseases such as liver cirrhosis may be partly responsible for the high prevalences of neuropathy in African diabetics.
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PMID:Neuropathy in Ethiopian diabetics: a correlation of clinical and nerve conduction studies. 401 53

Measurements of total body potassium (T.B.K.) were made by whole-body counting in four groups of patients receiving oral frusemide for one year. Patients in group 1 had essential hypertension and normal renal function and received 40 mg frusemide daily without potassium supplements. Patients in group 2 were similar but received oral potassium supplements for the first four months of treatment. Patients in group 3 had hypertension associated with renal disease and received 120 mg frusemide daily without potassium supplements. Patients in group 4 also had hypertension and renal impairment and in addition to 120 mg frusemide daily they received oral potassium supplements for four months. No evidence of depletion of T.B.K. was found in any of the groups after continuous treatment with frusemide for one year. It is questioned whether potassium supplementation in long term diuretic therapy with frusemide is necessary unless there is evidence of pre-existing potassium depletion or of some other factor such as cardiac failure, cirrhosis of the liver, or the nephrotic syndrome.
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PMID:Total body potassium in long-term frusemide therapy: is potassium supplementation necessary? 421 34


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