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PubMed2004

[Inhibition of human lung fibroblast proliferation and the mitogen activated protein kinase pathway by dexamethasone].

OBJECTIVE: To investigate the effects of dexamethasone on human lung fibroblast cell proliferation, cell cycles, and cell mitogen-activated protein kinases (MAPKs) passway. METHODS: Dexamethasone was used at various concentration in culture medium. Cell number was counted using a hemacytometer. Whole cell propidium iodide staining and flow cytometric analysis were performed to determine cellular DNA content. MAPK proteins and activation were tested by Western blot analysis with antibodies to c-Jun N-terminal kinase (JNK), phospho-JNK, extracellular signal-regulated kinase (ERK), phospho-ERK, p38 and phospho-p38. RESULTS: 1x10(-7) mol/L and 1x10(-6) mol/L dexamethasone suppressed the proliferation of lung fibroblast cells by 34% and 72%, respectively, than that of control. This suppression was dose-dependant. Dexamethasone suppressed cell cycle with accumulation of cells in G1/G0 stage. It increased from 81.9% to 90.1% compared with that of control. We did not find any apoptosis induced by dexamethasone for lung fibroblast cells. Using Western blot analysis, we found that dexamethasone resulted in decreased activity of ERK, but had no effects on JNK and p38. CONCLUSIONS: Dexamethasone may suppresses the proliferation of lung fibroblast cells, which is partly resulted from the facts that it can inhibit ERK activation in MAPK-signaling pathway but has little effect on JNK and p38 pathway. Dexamethasone may not induce lung fibroblast cell apoptosis directly.

Cell Cycle↗
PubMed2004

Antinociceptive synergy between dexamethasone and the B vitamin complex in a neuropathic pain model in the rat.

The combination of dexamethasone and B-vitamins is widely used in Mexico to treat neuropathic pain in human beings. However, so far there is no evidence in preclinical models about the efficacy of this combination. The purpose of this study was to assess the possible synergistic interaction between dexamethasone and the B-vitamin complex in a neuropathic pain model in the rat. Neuropathic pain was induced by ligation of the left L5 and L6 spinal nerves in female Wistar rats. Tactile allodynia was determined by measuring paw withdrawal in response to probing with a series of calibrated von Frey filaments. Dexamethasone (4-32 mg/kg), B-vitamins (75-600 mg/kg), or a combination of dexamethasone and B-vitamins (100:100:1 of vitamin B1, B6 and B12, respectively) was administered subcutaneously and the antiallodynic effect was determined. Isobolographic analyses were used to define the nature of the functional interactions between dexamethasone and B-vitamins (0.5:0.5). Dexamethasone (ED30 5.4+/-1.2 mg/kg), B-vitamins (ED30 181.1+/-2.6 mg/kg), and fixed-dose ratio dexamethasone-B-vitamins combinations dose-dependently reduced tactile allodynia in the rat. Theoretical ED30 value for the combination estimated from the isobologram was 128.2+/-5.8 mg/kg. This value was significantly higher than experimental ED30 value which was 21.8+/-2.3 mg/kg. Results indicate that subcutaneous administration of dexamethasone and B-vitamins interacted synergistically to reduce tactile allodynia in the rat and suggest the use of this combination to reduce neuropathic pain in humans.

Animals↗
PubMed2005

Apoptotic efficacy and inhibitory effect of dexamethasone on matrix metalloproteinase.

BACKGROUND: There is now accumulating evidence that matrix metalloproteinases and apoptosis may play an important role in inflammation processes. This study was undertaken to determine the effect of dexamethasone on apoptosis and matrix metalloproteinase 2 (MMP-2) activity compared with two nonsteroidal anti-inflammatory drugs (NSAIDs), piroxicam and diclofenac. MATERIAL/METHODS: A fibrosarcoma (WEHI-164) cell line was used for evaluating tolerability, MMP-2 activity, and apoptosis. Dexamethasone, piroxicam, and diclofenac were used at concentrations of 10-200 microg/ml in triplicate, two-fold dilutions. MMP-2 activity was assessed using zymography. For assessment of apoptosis, terminal deoxyribonucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) was used. RESULTS: Cytotoxicity analysis of dexamethasone showed a greater tolerability than diclofenac at concentrations of 10-100 microg/ml, whereas the cytotoxic effect of dexamethasone and piroxicam were parallel at doses of 5-80 microg/ml. The dose-dependent inhibitory effect of dexamethasone on MMP-2 activity was significantly less than that of the tested NSAIDs at concentrations of 10-80 microg/ml, while it increased at doses of >100 microg/ml compared with piroxicam. Moreover, the rate of apoptosis for dexamethasone-treated cells was 20.92%, the values for diclofenac and piroxicam being 78% and 28.15%, respectively. CONCLUSIONS: Our findings suggest that dexamethasone is able to induce apoptosis and suppress MMP-2 activity. Collectively, dexamethasone might be assumed as an agent which could be recommended for chemopreventive purposes.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1980

Mechanism underlying the inhibitory effect of dexamethasone on in vivo erythropoiesis.

The time-response curve for RBC-59Fe uptake following i.p. injection of 5 mg of dexamethasone into normal, non-polycythemic mice, shows a maximal depression (50% of normal) at 3 days after dexamethasone with return to almost normal values by 5 days. The effect is dose-related showing a plateau with doses of dexamethasone above 3 mg. The shape of the time-response curve indicates that the more mature cells in the erythron are not affected by dexamethasone and that the major effect of the steroid must be on earlier erythroid cells. Intravenous injection of dexamethasone 33 and 48 h after i.v. injection of erythropoietin in post-hypoxic polycythemic mice has no effect on the response to erythropoietin, suggesting that the early and late erythroblasts develop normally into erythrocytes. Injection of dexamethasone 13 h after erythropoietin is also ineffective, suggesting that the final steps of differentiation from erythropoietin responsive cells (ERC) to proerythroblasts are not affected. On the contrary, injection of dexamethasone 1 h after erythropoietin reduces by 60% the effective erythropoiesis, which can be attributed to a decrease in differentiation of ERC into proerythroblasts. These results indicate that the inhibitory action of dexamethasone on erythropoiesis is exerted on cells of the erythroid line before the stage of proerythroblast is reached.

Animals↗
PubMed2005

[Effective combination therapy of bortezomib and dexamethasone for two patients with refractory multiple myeloma].

We describe 2 cases of conventional therapy-resistant multiple myeloma (MM) that responded to bortezomib and dexamethasone therapy. Case 1: A 62-year-old woman with MM (IgG, kappa-type, stage IIIA) resistant to DMVM-IFN (dexamethasone, ranimustine, vincristine, melphalan, interferon-a), VAD (vincristine, doxorubicin, dexamethasone), high-dose melphalan with autologous peripheral blood stem cell transplantation (PBSCT) and thalidomide, received 2 courses of bortezomib treatment. In the first course, bortezomib alone was administered and then in the second course bortezomib was given in combination with dexamethasone. The patient's serum IgG level decreased from 8040 to 1020 mg/dl and the level of plasma cells in bone marrow was 1.2% after the treatments. Adverse reactions including rash, anemia, and thrombocytopenia occurred in the first course; however, they were milder in the second course combined with dexamethasone. Case 2: A 43-year-old man with MM (IgD, gamma-type, stage IIA) resistant to conventional and high-dose chemotherapy with PBSCT as well as thalidomide therapy, received treatment with bortezomib alone and then in combination with dexamethasone. His serum IgD level decreased from 2140 to 623 mg/dl. He suffered adverse reactions such as fatigue, anemia, and thrombocytopenia in the first course, which were relieved in the second course. These results indicate that the combination of bortezomib and dexamethasone is effective in the treatment of refractory MM and that dexamethasone can reduce the adverse reactions of bortezomib.

Adult↗
PubMedDate not supplied

[Hypothalamo-pituitary axis: effects of physical training in rats administered with dexamethasone].

AIM: To investigate the effects of physical training associated to dexamethasone administration in carbohydrate metabolism and adrenocorticotrophic hormone (ACTH) release. MATERIALS AND METHODS: Young Wistar rats were divided into four groups: sedentary control (CS), sedentary dexamethasone (DxS), trained control (CT) and trained dexamethasone (DxT). The rats were submitted to swimming training associate to administration of dexamethasone for ten weekends. Before sacrifice the rats received subcutaneous insulin to calculate the maximum decreased in blood glucose. Venous blood was sampled obtained at the end experiment period to determine glucose, insulin, free fatty acids (FFA) and ACTH. Gastrocnemius and liver tissue samples were used to determination glycogen, and adipose epididymal tissue was used to measured the weight. RESULTS: Dexamethasone administration provoke insulin resistance and the physical training reverted this aspect. Training promoted increase in muscle and liver glycogen store and a high utilization of FFA. Moreover, the dexamethasone provoke decreased of ACTH release in response to acute exercise, showing marked differences in the functioning of the hypothalamy-pituitary-adrenal (HPA) axis between groups of rats. CONCLUSIONS: a) Low-dose of dexamethasone promote several side effects in metabolism intermediary and chronic exposure to steroid was associated with insulin resistance; b) The regular swimming exercise promoted increased insulin sensitivity. Therefore, exercise can override the dexamethasone negative feedback of the HPA axis activation in rats.

Adrenocorticotropic Hormone↗
PubMed1988

The glucocorticoid dexamethasone inhibits synthesis of interferon by decreasing the level of its mRNA.

Human fibroblasts were induced to secrete interferon (IFN) by treatment with the double-stranded RNA poly(inosinic).poly(cytidylic) acid or by infection with Newcastle disease virus. Treatment with 0.1-1 microM dexamethasone reduced the amount of IFN secreted by approximately 40-70%, respectively. A similar decrease in secretion of human IFN-beta was detected in dexamethasone-treated murine C127 cells that carry an IFN expression vector. These cells transcribe constitutively human IFN-beta under the control of a viral thymidine kinase promotor. Secretion of murine IFN induced by double-stranded RNA was also reduced in dexamethasone-treated C127 cells. The amount of IFN-beta mRNA present in fibroblasts and C127 cells was measured by hybridization to complementary RNA. Treatment with dexamethasone markedly reduced the level of IFN-beta mRNA present in both cells. The time course of this decrease was measured in C127 cells; 50 and 80% loss of IFN mRNA was observed after approximately 7.5 and 12 h, respectively. Murine IFN mRNA was also decreased in dexamethasone-treated C127 cells induced with double-stranded RNA. However, the rate of transcription of human IFN mRNA measured by run-on assays in isolated nuclei of dexamethasone-treated C127 cells was found to be comparable to that of control untreated cells. The finding that dexamethasone reduces the level of IFN mRNA transcribed under the control of both its own promotor and an unrelated promotor, together with the observation that dexamethasone does not apparently alter the rate of transcription of this mRNA, suggest that glucocorticoids may regulate IFN production by decreasing the level of its mRNA.

Animals↗
PubMedDate not supplied

Compensatory adrenal growth in dexamethasone treated male and female hamsters.

The aim of the study was to investigate the unilateral adrenalectomy - induced compensatory adrenal growth in dexamethasone treated male and female hamsters (Mesocricetus auratus Waterhouse). Animals were treated for 5 days with 25 micrograms dexamethasone/animal/day or with 0.2 ml 0.9% NaCl. The first injection was made 0.5-1 h after monolateral adrenalectomy or sham operation. In three sets of experiments male and female hamsters received no injection. Only in one of three experiments was the relative adrenal weight of monoadrenalectomised male and female hamsters receiving no injections higher than in sham operated groups. In the case of NaCl treatment, only in one group of monoadrenalectomised males was the relative weight of the right adrenal higher than in the control group. On the contrary, in all three experiments with dexamethasone treatment the relative weight of the solitary adrenal was higher than in sham operated animals, while there was no difference among appropriate groups of females. In monoadrenalectomised dexamethasone-treated male hamsters, volume of the glomerulosa and reticularis zones was higher than in sham operated group. Neither the average cell volume in particular adrenocortical zones nor the number of parenchymal cells in the zones and in the entire cortex were changed due to adrenalectomy in dexamethasone treated males. There was no difference in all stereologic parameters studied when monoadrenalectomised and sham operated dexamethasone treated females were compared. Plasma cortisol level was lower in hemiadrenalectomised dexamethasone-administered males, while 3H-thymidine incorporation was higher in both male and female dexamethasone-treated hemiadrenalectomised hamsters. The obtained results demonstrate the evident sex-dependent response of the hamster adrenal gland to monoadrenalectomy and dexamethasone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1985

Effects of multiple intramuscular injections and doses of dexamethasone on plasma cortisol concentrations and adrenal responses to ACTH in horses.

Adrenocortical function was assessed in horses given multiple IM doses of dexamethasone to determine the duration of adrenocortical suppression and insufficiency caused by 2 commonly used dosages of dexamethasone (0.044 and 0.088 mg/kg of body weight). Dexamethasone was administered at 5-day intervals for a total of 6 injections. Daily blood samples were collected. The plasma was frozen and later assayed for cortisol. An ACTH response test was determined 2 days before the first injection of dexamethasone and again 8 days after the last dexamethasone injection. Maximum suppression of plasma cortisol was observed in horses given both dosages of dexamethasone (0.044 and 0.088 mg/kg). Plasma cortisol concentrations returned to base-line values in all horses by 4 days after dexamethasone injection. Normal ACTH responses observed after 6 dexamethasone injections given at 5-day intervals indicated that measurable adrenal atrophy did not develop under the conditions of this study.

Adrenal Cortex↗
PubMed1988

Hemodynamic and sympathoadrenal responses to altitude in humans: effect of dexamethasone.

Altitude exposure alters hemodynamics and sympathoadrenal function and elicits acute mountain sickness (AMS). Since dexamethasone prevents AMS and influences responsiveness to catecholamines, we studied hemodynamic and sympathoadrenal responses to 4,570 m simulated altitude in 8 subjects treated with dexamethasone or placebo. Mean pulse rates were less at altitude with dexamethasone (96.1 for placebo and 84.1 for dexamethasone; treatment-altitude interaction, p = 0.0045). Altitude led to a postural decline in mean arterial pressure (posture-altitude interaction, p = 0.0026), but this was not affected by dexamethasone. Dexamethasone reduced urinary epinephrine to a greater extent during altitude exposure (from 9.41 ng.mg-1 creatinine with placebo to 4.16 with dexamethasone) when compared with sea level (from 3.24 to 3.08). Urinary excretion of norepinephrine was unchanged at altitude. We conclude that acute altitude exposure is associated with stimulation of the adrenal medulla and not the sympathetic nervous system. Dexamethasone blocks the adrenal medullary response and blunts the pulse rate increase at altitude.

Adrenal Medulla↗
PubMed1986

Effect of dexamethasone on vascular function in RIF-1 tumors.

The present series of experiments was conducted to determine the effect of dexamethasone on vascular function and cell proliferation in s.c. RIF-1 tumors. 125I-BSA, 51Cr-EDTA dilution techniques were used to evaluate dexamethasone induced changes in tumor plasma water, capillary permeability, and extracellular water volumes, while 59Fe and 51Cr labeled erythrocyte techniques were used to assess changes in tumor exchangeable erythrocyte volumes. 86RbCl distribution studies were also conducted to evaluate vascular perfusion in RIF-1 tumors after dexamethasone treatment. In this corticosteroid receptor containing tumor model, dexamethasone had profound effects on all of the measured parameters of vascular function. Reduced tumor cell proliferation after dexamethasone treatments was accompanied by reduced capillary permeability, reduced interstitial water volumes, increased plasma volumes, and reduced vascular perfusion. Serial studies after dexamethasone treatments indicated that increases in vascular perfusion preceded proliferative recovery. Intervals of maximal [3H]thymidine labeling after dexamethasone were characterized by transient increases in capillary permeability, interstitial water volumes, and tumor erythrocyte exchange with the general circulation. At intervals of maximal cell proliferation (36-48 h after dex) 86RbCl distribution in tumors was about 3 times that seen in untreated controls. The results seem to indicate that, as in edematous normal tissues, dexamethasone can have profound effects on vascular function and water compartmentalization in RIF-1 tumors.

Animals↗
PubMed1986

Modulation of hybridoma formation by dexamethasone.

In an effort to determine the effect of dexamethasone on hybridoma formation, spleen cells from BALB/c mice hyperimmunized with sheep red blood cells (SRBC) were fused with mouse plasmacytoma cells (P3U1) in the presence of polyethylene glycol (PEG). Dexamethasone was added in decreasing doses (10(-3) to 10(-9) mM) to the hypoxanthine-aminopterin-thymide (HAT) medium immediately after the PEG-mediated cell fusion. 10(-3) mM of this steroid was found to inhibit markedly the number and size of hybridoma clones generated, while 10(-5) mM dexamethasone was shown to enhance hybridoma formation. The effect of 10(-3) mM dexamethasone was most pronounced when added immediately after fusion. When this dose was given 48 or 120 h after cell fusion, the extent of the inhibitory effect was less pronounced. High concentration of dexamethasone may also inhibit monoclonal antibody production by hybridomas once generated. An increase in the number of clones formed was observed when 10(-5) mM dexamethasone was added to HAT medium as well as an increase in the average colony size. Large clones were also observed with lower dexamethasone doses ranging from 10(-7) to 10(-9) mM. Possible mechanisms on the effect of dexamethasone on hybridoma formation are discussed.

Animals↗
PubMed1987

[Time course of the cerebroprotective effect of dexamethasone in experimental head injury].

Despite the widespread use of glucocorticoids in patients with severe head injury, the usefulness is still controversial. In the past, the effect was investigated only in terms of dose-response relationship. We have, however, studied the time factor for the administration of dexamethasone to obtain maximal beneficial effect together with investigating the influence of actinomycin-D, an inhibitor of messenger RNA synthesis, before dexamethasone treatment. Awake male mice of dd-strain were restrained and subjected to head injury using a bakelite weight of 30 g dropped from a height of 17.8 cm above the skull. This injury resulted in immediate loss of consciousness in 100%, convulsive seizure in about 70% and death in about 30% of animals. The severity of consciousness disturbance was evaluated by a pair of indices in time interval: time required for the recovery of righting reflex (RR) and for the recovery of spontaneous movement (SM). 4 mg/kg of dexamethasone phosphate was given intraperitoneally 0.5, 4, 6, 12, 18 or 24 hours before injury. Actinomycin-D of 0.5 mg/kg was injected intravenously 1 h before each dexamethasone treatment in separate animals. In the other group of animals, dose was changed with varying time course of dexamethasone pretreatment, e.g., 2, 4, 6 or 8 mg/kg given 0.5, 2 or 4 h before injury. It was found that dexamethasone of 4 mg/kg pretreatment 4-12 hours significantly improved the recovery from consciousness disturbance and death rate. Actinomycin-D given before dexamethasone treatment completely abolished the protective effect of dexamethasone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Stages of hyperadrenocorticism: response of hyperadrenocorticoid dogs to the combined dexamethasone suppression/ACTH stimulation test.

A study was designed to evaluate the response of blood cortisol content in dogs tentatively diagnosed as having hyperadrenocorticism by using the combined dexamethasone suppression/ACTH stimulation test procedure. Four groups of abnormal responses were identified in 54 dogs. In group I (14.8% of the dogs with abnormal responses), the only abnormality was partial suppression with dexamethasone (clinically normal dogs suppressed to less than 10 ng/ml). In group II (29.6%), 2 abnormalities were found: partial suppression with dexamethasone and hyperreactivity to the ACTH stimulation test. In group III (typical pituitary-dependent hypercortisolism, 48.1%), 3 abnormalities were found: base-line hypercortisolemia, partial suppression with dexamethasone, and hyperreactivity to the ACTH stimulation test. In group IV (7.4%), 2 abnormalities were found: base-line hypercortisolemia and partial suppression with dexamethasone. Base-line blood cortisol content was normal in 44.4% of the adrenopathic dogs. A normal response to ACTH stimulation was seen in 25.9% of the dogs, and 74.1% of the dogs hyperreacted to the ACTH stimulation test. All of the adrenopathic dogs were found to suppress partially with dexamethasone. Failure to suppress the adrenal gland completely (less than 10 ng/ml) with dexamethasone was the most consistent finding in adrenopathic dogs when using the combined dexamethasone suppression/ACTH stimulation test procedure. It was concluded that the test procedure is feasible, flexible, and convenient for clinical situations. Also, these results suggested that there may be several stages in the negative feedback failure associated with hyperadrenocorticism in dogs.

Adrenal Cortex Function Tests↗
PubMed1982

Effect of dexamethasone on hexamethylene bisacetamide-induced Friend cell erythrodifferentiation.

Friend erythroleukemic cells can be induced to differentiate by chemicals such as dimethyl sulfoxide and hexamethylene bisacetamide (HMBA) in a dose-dependent manner. Others have shown that dexamethasone and other steroid hormones can inhibit the differentiation induced by dimethyl sulfoxide. We show here that dexamethasone has a dual mode of action on the HMBA-induced differentiation of a Friend cell line, DS19. At concentrations above 10(-10) M, dexamethasone inhibits the HMBA-induced differentiation in DS19 cells. We further found that as the concentration of HMBA is reduced, the amount of dexamethasone required to inhibit differentiation increases. Such inhibition seems to act primarily by decreasing the probability that a cell will become committed to differentiate. Besides, dexamethasone does not inhibit hemoglobin synthesis of cells which are committed in its absence. In addition, we show that sensitivity to the inhibition by dexamethasone is inversely related to the inducibility of cell populations. The second action of dexamethasone, observed at concentrations between 10(-10) and 10(-13) M, is to increase the proportion of hemoglobin-containing cells relative to that for cells cultured in its absence. The degree of this synergistic effect for induced differentiation is inversely related to the level of induction in the absence of dexamethasone and thus is best observed in the cells cultured at low levels of HMBA. We present evidence that this synergistic effect may be due to an increased viability of the induced cells and possibly an increase in the proliferative capacity of these cells.

Acetamides↗
PubMed1984

Dexamethasone inhibition of rat hepatoma growth and alpha-fetoprotein synthesis.

The effect of dexamethasone on hepatoma growth and differentiation, as well as the production of alpha-fetoprotein (AFP) and albumin, was investigated. Treatment of rats with dexamethasone strongly reduced (by 83 to 98%) the serum levels of AFP in rats bearing Morris hepatomas 7777, 8994, 7288c , and 9618A2 . Reduced AFP levels were due in part to a large reduction in tumor load in dexamethasone-treated rats. Hepatoma weights, on the average, were reduced by 64 to 90% relative to controls, while a large bowel transplantable tumor was affected only slightly. Lower serum AFP levels in rats with hepatomas 7777, 8994, and 9618A2 also resulted from reduced AFP synthesis, as indicated by lower cytoplasmic AFP levels. Cytoplasmic albumin levels were higher in dexamethasone-treated rats bearing hepatomas 7777, 8994, and 7288c than they were in rats which did not receive dexamethasone. RNA dot hybridization also indicated that dexamethasone reduced the amount of AFP mRNA in hepatoma 7777 while increasing albumin mRNA. Two-dimensional gel electrophoresis of tumor cytosol proteins showed that dexamethasone reduced synthesis of all AFP variants which could be detected by this technique. A number of abundant hepatoma-associated and liver-associated proteins were not significantly affected by dexamethasone.

Animals↗
PubMed1982

Clomiphene and dexamethasone in women unresponsive to clomiphene alone.

Twelve oligomenorrhic women with polycystic ovary syndrome (PCO) in whom clomiphene (250 mg daily for 5 days) and 10,000 IU human chorionic gonadotropin had failed to induce ovulation were treated with clomiphene and dexamethasone. Eight of the 12 women underwent complete hormonal assessment during treatment. Six of the 12 ovulated and 1 conceived. Serum total and unbound estradiol and testosterone (T), serum dehydroepiandrosterone sulfate (DHEA-S), sex hormone binding-globulin binding capacity (SHBG-BC), luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) were measured during clomiphene and dexamethasone therapy. SHBG-BC increased in response to clomiphene whether or not ovulation occurred. After treatment with clomiphene and dexamethasone there was a significant decrease in serum T, unbound T, and DHEA-S 2 weeks after dexamethasone administration, but there were no change in LH, FSH, or PRL. In patients who ovulated after clomiphene and dexamethasone, T and unbound T increased again after clomiphene was begun despite the continuation of dexamethasone. The women who ovulated after clomiphene and dexamethasone treatment had significantly higher pretreatment levels of DHEA-S than those who did not ovulate. Clomiphene and dexamethasone treatment may be beneficial to women who have elevated levels of DHEAS and who fail to ovulate with maximum doses of clomiphene.

Anovulation↗
PubMed1984

Dexamethasone: pharmacokinetics in neurological patients.

A high performance liquid chromatographic assay has been used to measure the time courses of plasma dexamethasone concentrations in patients with various neurological disorders being treated with this steroid. The pharmacokinetics of the drug in these circumstances differed from the kinetics in healthy volunteers. In particular whole body clearances were higher, causing a substantially impaired mean oral bioavailability of the drug with considerable interindividual variation in bioavailability. The clearance of dexamethasone was increased by concurrent phenytoin therapy, and dexamethasone and phenytoin are often given together in neurosurgical practice. The previously unrecognized bioavailability limitation of oral dexamethasone may explain individual instances of apparent steroid-resistant neurological disease, and suggests the desirability of monitoring plasma dexamethasone levels when using the steroid therapeutically. Some preliminary evidence has been obtained suggesting that it may be possible to avoid adrenal suppression from long-term high-dosage dexamethasone therapy, if plasma dexamethasone levels can be allowed to fall to zero between consecutive dexamethasone doses.

Adult↗