Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The MCR of prednisolone (11 beta,17,21-trihydroxypregn-1,4-diene-3,20-dione) and the absorption of prednisone (17,21-dihydroxypregn 1,4-diene-3,11,20-trione) were studied in five normal subjects and four patients. Plasma and urinary prednisolone were measured by a competitive radioassay. The MCR was determined after iv administration of 30 mg nonisotopic prednisolone using one-compartment (MCR1) and two-compartment (MCR2) analyses. These values were compared with the MCR determined after oral administration of nonisotopic prednisone (MCR0). MCR1 and MCR2 were closely correlated, indicating the applicability of first order kinetics to the study of prednisolone metabolism. In subjects with normal gastrointestinal function, MCR0 was consistently lower than MCR2 (mean MCR2 = 0.175 liters/h.kg; MCR0 = 0.145 liters/h.kg). In two patients with steroid malabsorption, the MCR0 was significantly greater than MCR2. Knowledge of the expected relationship between MCR0 and MCR2 allowed quantitation of the degree of malabsorption. With or without impaired absorption, the absorptive process was essentially complete by the time of the peak plasma concentration. Estrogen therapy lowered the MCR0, and high prednisone dose increased the MCR0. Those effects and the effects of iv prednisolone administration on the MCR are explained by the effects of plasma protein binding of prednisolone. These studies demonstrate the usefulness of the oral MCR determination in the evaluation of steroid absorption and metabolism.
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PMID:Studies comparing the metabolic clearance rate of 11 beta,17,21-trihydroxypregn-1,4-diene-3,20-dione (prednisolone) after oral 17,21-dihydroxypregn-1,4-diene-3,11,20-trione and intravenous prednisolone. 42 20

Experimental evidence is presented which suggests that age-induced changes in the collagenous matrix, the main constituent of the organic portion of bones, are at least partially responsible for age-induced physiological osteoporotic changes in the skeleton. In particular, there seems to be a labile fraction of recently synthesized collagen in bones, which loses its metabolic activity rapidly with advancing age. Experimental and clinical hormonal disorders and disturbances in calcium metabolism also cause changes in skeletal metabolism; these changes seem to be largely mediated through changes in the collagenous matrix. In experimental hyperthyroidism and hyperparathyroidism, the rate of degradation of the collagenous matrix appears to act as a moderator or "final messenger" in hormone-induced bone resorption. In conditions with altered calcium metabolism, such as malabsorption associated with hypocalcemia, altered bone metabolism may be due to osteomalacia or hypocalcemia-induced hyperparathyroidism. An increase in the rate of bone destruction in relation to the rate of bone formation is probably also the cause of postmenopausal osteoporosis. At present there is no optimal form of hormonal treatment for age-induced or post menopausal osteoporosis. Estrogen replacement therapy may be the best available treatment for postmenopausal osteoporosis, but slowing down the already low rate of bone catabolism in elderly subjects by estrogen or other therapeutic means requires long periods of treatment before pronounced increases in the total mass of bones take place and prophylactic administration of estrogen may produce better results.
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PMID:Relation to osteoporosis of age- and hormone-induced changes in the metabolism of collagen and bone. 97 17

Estrogen treatment improves calcium malabsorption induced by surgical or natural menopause, but the mechanisms involved are still under debate, with both increased production of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] and improved peripheral responsiveness to the steroid having been proposed. To address this issue, we studied the effect of short term administration of 1,25-(OH)2D3 (1 microgram/day for 7 days) on intestinal fractional absorption of 47Ca (47Ca FA) and vertebral bone density, measured by dual photon absorptiometry, in 14 premenopausal women (aged 31-50 yr) before and 6 months after oophorectomy. After surgery, patients were randomly allocated to a 6-month treatment with either conjugated estrogens (0.625 mg/day; n = 7) or placebo (n = 7). Oophorectomy caused a decrease in both basal 47Ca FA (-40.8 +/- 23.4%; P = 0.004) and vertebral bone density (-7.21 +/- 1.20%; P less than 0.001) in the placebo group. Estrogen replacement prevented these changes and increased basal serum 1,25-(OH)2D3 (+10.3 +/- 10.9%; P = 0.047), whereas a detectable but not significant decrease was observed in the control group (-8.8 +/- 10.5%; P = 0.07). Assessment of 47Ca FA before and after 1,25-(OH)2D3 administration revealed a similar degree of responsiveness to the steroid in the estrogen-treated women before and at the end of the study period (45.8 +/- 6.9% vs. 42.9% +/- 14.9% from basal, respectively; P = 0.142), but a blunted response to 1,25-(OH)2D3 was observed in the placebo group at 6 months (27.9 +/- 17.7%) compared to the result obtained before surgery (36.7 +/- 9.1%; P = 0.032). Multifactor analysis of variance revealed that the effects of estrogen and 1,25-(OH)2D3 on 47Ca FA were independent of basal serum 1,25-(OH)2D3 levels. On the other hand, calcitriol administration increased serum 1,25-(OH)2D3 to a similar extent before and 6 months after surgery in the placebo group (24.2 +/- 18.3% vs. 34.7 +/- 16.7% from basal, respectively; P = 0.484) as well as in the estrogen-treated women (34.2 +/- 17.2% vs. 26.6 +/- 15.45%; P = 0.302). The significant impairment of 1,25-(OH)2D3 stimulation of 47Ca FA in spite of increased levels of circulating 1,25-(OH)2D3 in the untreated women is suggestive of an end-organ resistance to the vitamin D metabolite in a hypoestrogenic condition, which can be prevented by hormone replacement, and supports the hypothesis of a vitamin D-independent action of estrogen on intestinal calcium absorption.
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PMID:Estrogen preserves a normal intestinal responsiveness to 1,25-dihydroxyvitamin D3 in oophorectomized women. 222 86

Even though the oral contraceptive (OC) pill is the most effective reversible contraceptive, many OC users still conceive. Common reasons for OC failure are missed pills, drug interactions, and malabsorption caused by vomiting or diarrhea. The first report of OC failure linked to simultaneous use of another drug was in 1971. The drug was rifampicin, which was used to treat tuberculosis. Broad-spectrum antibiotics may inhibit OC efficiency through several mechanisms. Antibiotics destroy the bacteria which hydrolyse sulphate and glucuronide conjugates (metabolites of ethinyl estradiol). Thus, the enterohepatic recirculation of ethinyl estradiol that normally occurs is prevented, resulting in a reduction in plasma concentration of ethinyl estradiol. Antibiotic-induced diarrhea may increase urinary or fecal excretion of the OC. The antibiotic (e.g., rifampicin) may increase liver degradation of the OC hormones. There may even be other possible mechanisms. Experimental evidence for many of the commonly accepted mechanisms is lacking. Drug interactions are more common in users of the low dose estrogen OCs. In a review of drug interactions during 1968-1984, penicillins and tetracyclines were associated with 70% of cases. OCs with 30 mcg ethinyl estradiol comprised the greatest number of reports. Less than 10% of adverse drug reactions are reported to the Committee on Safety of Medicines via the yellow card plan. Dentists should advise female patients using OCs about reduced efficiency of the OCs while taking an antibiotic. They should follow the recommendations of the UK Family Planning Association. Dentists could routinely provide all female patients prescribed an antibiotic an information pamphlet that provides detailed advice and recommendations on the use of alternative methods. They have a professional obligation to know the physiology of reproduction, the pharmacology of drug interactions with the OC, and contraceptive methods.
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PMID:Oral contraceptives and antibiotics: important considerations for dental practice. 780 51

After the development of monophasic combined oral contraceptives (COCs), containing a fixed dose of estrogen and progestogen, biphasic and triphasic COCs were introduced in the 1980s; in these the dose of ethinyl estradiol and progestogen changes during the pill cycle. In the so-called every day pills, the 21 pills of active steroid combination are followed by 7 inactive pills containing starch, iron, or bran. Method failures of OCs are among the lowest ranging from 0.2-1/100 woman-years. User failures can be as high as 6.2/100 women-years. The individual difference in peak plasma levels of estrogens in women taking identical OCs can be 10-fold. Conditions that affect the bioavailability of contraceptive steroids are: 1) drug interaction (vitamin C, drugs that induce liver enzymes, and antibiotics); 2) vomiting; 3) vegetarianism; 4) missing pills; and 5) malabsorption. Metabolic effects of COCs pertain to carbohydrate metabolism, lipid metabolism, hemostasis, and vitamins. Prescribing of COCs involves counseling clients about contraindications to COCs, starting routines, and the pill-free interval, as well as follow-up and monitoring, the problem of missing pills, and selection criteria for OC use. Medical conditions in which COC use requires special consideration are sickle cell disease, trophoblastic disease, HIV disease, gallstones, epilepsy, valvular heart disease, oligomenorrhea/amenorrhea, inflammatory bowel disease, and surgery. Side effects of COCs may include depression, nausea, vomiting, headaches, urinary tract infection, and lower genital tract infections. 6 months after stopping the OC 1% of users become amenorrheic. Many of the common causes of amenorrhea, such as weight loss amenorrhea and polycystic ovarian disease, may be treated with the COC until the couple desires to have a baby. The new progestogens desogestrel, norgestimate, and gestodene are highly selective compared to first and second generation progestogens.
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PMID:Combined oral contraceptives: acceptability and effective use. 832 4

3 conditions may be responsible for absence of menstruation in women taking the minipill: pregnancy, extrauterine pregnancy, or endometrial atrophy which is the most frequent cause but should be treated only after the other 2 possibilities are excluded. The most frequent cause of pregnancy while taking minipills is error in pill consumption due to forgetting, but malabsorption due to vomiting less than 2 hours after taking the pill or an interaction with some other medication may be responsible. The possibility of extrauterine pregnancy should be systematically considered, and the possibility that a micropill and not a minipill is involved should be ruled out. With a sequential minipill contraceptive efficacy does not reach 100% but iatrogenic amenorrhea is infrequent because of the strong dose of ethinyl estradiol. In the case of a preexisting amenorrhea that does not respond to the estrogen or progestin dose, a prolactin adenoma may be suspected. After 2 consecutive beta tests of pregnancy 8 days apart have been negative, it may be concluded that endometrial atrophy is the cause of the amenorrhea. Unprotected sexual relations should be avoided and the patient should be given a fast-acting combined oral contraceptive such as Lutestral to induce bleeding, after which the minipill can be resumed. If unprotected intercourse occurs there is a risk of pregnancy since amenorrhea and anovulation are not synonymous. A morning after pill can be used if the unprotected sexual relations occurred within the last 72 hours. If a pill was forgotten or probably forgotten before the emenorrhea, the most prudent attitude would be to consider the pill to have been ineffective during the preceding 21 days and to test for pregnancy. Unprotected intercourse should be avoided, a fast-acting combination pill should be prescribed to induce bleeding, and the minipill should then be resumed. Amenorrhea in the 1st month of use after an abortion is not significant. This secondary effect of the minipill should be explained to the patient to avoid unnecessary worry.
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PMID:[Do's and don'ts in treating amenorrhea in women taking the minipill]. 1226 2