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PubMed2000

Leptin production in adipocytes from morbidly obese subjects: stimulation by dexamethasone, inhibition with troglitazone, and influence of gender.

This study examined the regulation of leptin production by dexamethasone and troglitazone. Subcutaneous and omental adipose tissue was obtained during bariatric surgical procedures (30 women and 16 men; body mass index, 52.5 +/- 1.7 kg/m2, age, 39 +/- 2 yr), and adipocytes were cultured in suspension. Subcutaneous adipocytes from females released significantly more leptin than did omental cells from the same subject (P < 0.05), but basal leptin release was not different in adipocytes from these depots in males. Dexamethasone (0.1 micromol/L) significantly increased leptin release within 24 h from sc (135 +/- 13% of control) and omental (227 +/- 53%) adipocytes of females, but not males. Dexamethasone-stimulated leptin production at 48 h was significantly greater in the omental adipocytes of females (398 +/- 64% of control) than in sc adipocytes of females (207 +/- 21%) or the omental (211 +/- 33%) and sc (180 +/- 23%) adipocytes of males. Troglitazone (10 micromol/L; 48 h) significantly inhibited dexamethasone-stimulated leptin release in sc (57 +/- 10.7% inhibition) and omental adipocytes (134 +/- 26% inhibition). There was no gender-related difference in the effect of troglitazone to inhibit dexamethasone-stimulated leptin release. Troglitazone significantly inhibited basal leptin production from omental adipocytes by 15.0 +/- 5.2%. The effect of dexamethasone and troglitazone to regulate leptin release was mediated through changes in ob gene expression, but did not involve changes in glucose uptake or metabolism to lactate. The data suggest that adipocytes from females are more responsive to the stimulatory effect of dexamethasone in vitro than are adipocytes from males. If adipocytes from females are more responsive to relevant in vivo stimuli for leptin secretion such as insulin or glucose, this could contribute to the gender difference in serum leptin. The data also suggest that leptin release from omental adipocytes may be more responsive to hormonal and nutrient regulation in vivo than are sc adipocytes.

Adipocytes↗
PubMed1996

Dexamethasone stimulation of rat insulin-like growth factor binding protein-1 promoter activity involves multiple cis-elements.

Insulin-like growth factor binding protein-1 (IGFBP-1) modulates the mitogenic actions of IGF-I and IGF-II. Dexamethasone increases IGFBP-1 mRNA abundance and gene transcription in rat liver and in H4-II-E rat hepatoma cells. A glucocorticoid response element (GRE) located at nucleotide (nt) -91/-77 is required for dexamethasone to stimulate rat IGFBP-1 promoter activity in transient transfection assays in H4-II-E cells. Mutagenesis of nt -108/-99 (the M4 region of the insulin response element), however, decreased dexamethasone-stimulated promoter activity despite the presence of an intact GRE, suggesting that regulatory sites in addition to the GRE were required for optimal dexamethasone stimulation. To identify these sites, we introduced 5'-deletion and substitution mutations into rat IGFBP-1 promoter fragments coupled to a luciferase reporter gene and transfected these constructs into H4-II-E cells. Three sites are required for optimal basal promoter activity: a site (nt -62/-50) that binds the liver-enriched transcription factor, hepatocyte nuclear factor-1 (HNF-1), the M4 site, and a putative binding site for transcription factor AP-2 (nt -293/-286). The HNF-1 and M4 sites and an upstream site (nt -252/-236) are also involved in dexamethasone stimulation under some, but not all, circumstances. Mutation of either the HNF-1 site or the M4 site decreased dexamethasone stimulation by more than 80% in constructs whose 5'-end was at nt -92, -135, or -235 but not if the 5' -end was at nt -278 or -327. These results suggest that the nt -278/-236 region can compensate for the loss of the HNF-1 site or the M4 site but that the HNF-1 and M4 sites do not compensate for each other in constructs whose 5'-end was at nt -135 or -235, which lack the nt -278/-236 region. The site within the nt -278/-236 region was localized to nt -252/-236 by deoxyribonuclease I protection and transfection assays. Thus, several cis-elements in the rat IGFBP-1 promoter cooperate, in varying combinations, with the low-affinity GRE to allow optimal dexamethasone-stimulated promoter activity.

Animals↗
PubMed2004

A dose ranging study of dexamethasone for preventing patient-controlled analgesia-related nausea and vomiting: a comparison of droperidol with saline.

UNLABELLED: We designed this study to determine the minimum dose of dexamethasone for preventing nausea and vomiting associated with the use of morphine by patient-controlled analgesia (PCA). Two hundred forty female patients were randomly assigned to receive dexamethasone 2, 4, 8, or 12 mg IV immediately before induction of anesthesia. Droperidol (0.1 mg/mL with morphine 1 mg/mL in PCA pump) and saline were used as controls. The complete response (no postoperative nausea and vomiting and no need for rescue antiemetic for a 24-h postoperative period) rates for dexamethasone 8 mg (72.2%) and 12 mg (78.9%) were significantly more than for saline (42.9%) (P < 0.05). Patients who received dexamethasone 12 or 8 mg also reported higher patient satisfaction than those who received saline (P < 0.05). These results were as effective as adding droperidol 0.1 mg/mL to the morphine PCA without causing drowsiness, restlessness, or arrhythmias. Smaller doses of dexamethasone (4 or 2 mg) were not effective for this propose. The results suggest that dexamethasone 8 mg IV is the minimum effective dose for the reduction of PCA morphine-related nausea and vomiting. IMPLICATIONS: Morphine administration by patient-controlled analgesia (PCA) is often associated nausea and vomiting. In this double-blind study, the minimum effective dose of dexamethasone for reducing this complication was 8 mg. This was as effective as adding droperidol 0.1 mg/mL to the morphine PCA without causing drowsiness, restlessness or arrhythmias.

Aged↗
PubMed2004

Dexamethasone has a central antiemetic mechanism in decerebrated cats.

Dexamethasone is an effective antiemetic drug, but its mechanism of action is unclear. We designed this study to investigate the direct antiemetic action of dexamethasone in the medulla of cats. By using an oscillographic vomiting model, decerebrated cats received microinjections of dexamethasone 100 nL (1 microg, n = 7; 0.1 microg, n = 7) into the bilateral nuclei tractus solitarii, which led to a significant prolongation of the latency (1 microg, 6.4 +/- 1.1 min versus 28.2 +/- 4.9 min, P < 0.05; 0.1 microg, 6.7 +/- 1.1 min versus 27.1 +/- 5.0 min, P < 0.05) of the first emetic episode and significantly decreased the frequency of emetic episodes (1 microg, 2.7 +/- 0.8 versus 0.1 +/- 0.4, P < 0.05; 0.1 microg, 2.9 +/- 0.9 versus 0.3 +/- 0.5, P < 0.05) induced by xylazine. Pretreatment with mifepristone, a glucocorticoid receptor antagonist, blocked the antiemetic effect of dexamethasone in the bilateral nuclei tractus solitarii. However, microinjection of dexamethasone into the unilateral nucleus tractus solitarius alone did not alter the latency of the first emetic episode or the frequency of emetic episodes induced by xylazine. Local application of dexamethasone into the area postrema had no effect on the latency of the first emetic episode or the frequency of emetic episodes induced by xylazine. These results suggest that dexamethasone exerts its central antiemetic action through an activation of the glucocorticoid receptors in the bilateral nuclei tractus solitarii in the medulla.

Animals↗
PubMed1993

Dexamethasone decreases the delivery of tumor-specific monoclonal antibody to both intracerebral and subcutaneous tumor xenografts.

The effect of dexamethasone on the delivery of monoclonal antibody L6 IgG to intracerebral and subcutaneous LX-1 small cell lung carcinoma xenografts was evaluated in nude rats (n = 157). Dexamethasone (0, 8, or 24 mg/m2) was given 18 hours before infusion of L6 IgG, with or without osmotic disruption of the blood-brain barrier. Compared with controls, the 8 mg/m2 dose decreased delivery of L6 IgG (12-37%) to all tissues, but the only significant decrease (P < 0.001) was in the subcutaneous tumor (37%). In the 24 mg/m2 group, L6 IgG delivery was significantly (P < 0.001) decreased to all tissues (37-60%). Dexamethasone had no effect on plasma levels. Barrier disruption significantly (P < 0.0001) increased L6 IgG delivery to intracranial tumor and surrounding brain, but not to subcutaneous tumor or plasma. The percentage of decremental effect of dexamethasone on L6 IgG delivery was the same with and without barrier disruption and was not associated with the time the animals were killed (P > 0.05). Compared with controls, the ratio of intracranial tumor to normal brain showed no change with dexamethasone, but the ratios of both intracranial and subcutaneous tumors to plasma significantly (P < 0.002) decreased with both doses. The in vitro cell binding capacity of L6 IgG to LX-1 cells remained unchanged after incubation of cells with dexamethasone over a 3-log concentration for 4 days, demonstrating no effect on antigen expression. This study suggests that dexamethasone has a clinically relevant generalized (i.e., central nervous system and systemic) vascular effect on permeability to L6 IgG monoclonal antibody.

Animals↗
PubMed1985

Effect of dicyclomine on intestinal absorption, disposition and biliary excretion of dexamethasone.

The effect of dicyclomine, a cholinergic blocking agent, on the in situ intestinal absorption, plasma clearance, biliary excretion of dexamethasone was examined in rats. The plasma concentrations and area under the plasma concentration-time curve (AUC) of dexamethasone after both a single and repeated oral coadministration with dexamethasone phosphate (4 mg/kg) and dicyclomine (4 mg/kg) were significantly reduced compared with those after dexamethasone alone, without the alteration of elimination rate. The in situ absorption study also indicated that the absorption of dexamethasone was reduced to about a half after repeated coadministration of the two drugs. The renal plasma flow (RPF) in coadministration group was significantly enhanced compared with that of dexamethasone alone. The biliary excretion of dexamethasone was reduced, in proportion to the plasma concentrations, by dicyclomine. Therefore, dicyclomine should be administered taking much care in the corticosteroid treatment, because of producing the decrease in absorption.

Administration, Oral↗
PubMed2000

Detrimental effects of high-dose dexamethasone in severe, refractory, HIV-related thrombocytopenia.

OBJECTIVE: To report a case of HIV-related thrombocytopenia in which high-dose dexamethasone was ineffective and immunologically detrimental. CASE SUMMARY: A 39-year-old white man with persistent, severe, HIV-1-related thrombocytopenia was admitted for epistaxis, bleeding gums, petechiae, and bruising. Previous unsuccessful attempts to reverse the thrombocytopenia included zidovudine, prednisone, vincristine, interferon alfa, and intravenous immune globulins. Based on previous anecdotal reports of the effectiveness of high-dose dexamethasone in refractory, HIV-related thrombocytopenia, we instituted treatment with intravenous dexamethasone 40 mg/d for four sequential days every 28 days. After three cycles of therapy, the platelet count remained < 15 x 10(9)/L; however, the CD4+ lymphocyte count decreased progressively from 1447 x 10(6)/L at baseline to 560 x 10(6)/L three months after the third cycle. Due to persistent, severe thrombocytopenia and bleeding, the patient underwent splenectomy, resulting in normalization of the platelet count. DISCUSSION: High-dose dexamethasone has been proposed as treatment for patients with immune thrombocytopenia as an alternative to chronic oral corticosteroids and claimed to be associated with better effectiveness and fewer adverse effects. The results of this treatment in our patient show that this regimen may not only be ineffective, but may also be immunologically detrimental in HIV-infected patients. Although the deterioration of the immunologic status of our patient cannot be fully attributed to high-dose dexamethasone based on the Naranjo scale, the previous long-lasting stability of CD4+ cells and the temporal relationship of a decrease in the CD4+ cell count coinciding with administration of high-dose dexamethasone suggest a causative role of the treatment. CONCLUSIONS: A possible cause-effect relationship between the treatment and the decrease in the CD4+ cell count suggests that the use of high-dose dexamethasone may not be justified in patients with severe, HIV-related thrombocytopenia.

Adult↗
PubMed1985

[A comparative study of the accelerated metabolism of cortisol, prednisolone and dexamethasone in patients under rifampicin therapy].

Although rifampicin (RFP) is known to be one of the potent hepatic microsomal enzyme inducers, little has been reported about the detailed pharmacokinetics of glucocorticoids in patients under RFP therapy. In this paper, the metabolism of cortisol, prednisolone and dexamethasone were investigated comparatively by simultaneous injection of these glucocorticoids. Eleven patients under RFP therapy, including 7 with tuberculosis together with collagen diseases and 4 with tuberculosis alone, were studied. Sixteen normal volunteers and 4 patients with collagen diseases not under RFP therapy were also examined as controls. After 1 mg of betamethasone was administered orally on the previous night for the suppression of endogenous cortisol, a mixed solution of 1 mg each of cortisol, prednisolone and dexamethasone was given intravenously. Plasma steroid levels of periodically collected blood samples were determined by respective radioimmunoassay after extraction with dichloromethane and purification by paper chromatography. Half-times of plasma disappearance (t 1/2), metabolic clearance rates (MCR) and total apparent distribution volumes (V) of these glucocorticoids were calculated using the single compartment model. The mean values of t 1/2 of cortisol, prednisolone and dexamethasone in patients with collagen diseases under RFP therapy were 1.8 +/- 0.3 (Mean +/- SD) (p less than 0.05), 1.4 +/- 0.2 (p less than 0.001) and 1.3 +/- 0.3 hours (p less than 0.001), respectively, which were significantly shortened when compared with normal subjects (cortisol, 2.1 +/- 0.2; prednisolone, 2.5 +/- 0.7; dexamethasone, 3.5 +/- 1.0 hours). The MCR of cortisol, prednisolone and dexamethasone in these patients were 139 +/- 57, 141 +/- 53 (p less than 0.01) and 722 +/- 137 l/day/m2 (p less than 0.001), respectively, which were increased when compared with normal subjects (cortisol, 114 +/- 20; prednisolone, 75 +/- 25; dexamethasone, 153 +/- 45 l/day/m2). The metabolism of these glucocorticoids in patients with collagen diseases under RFP therapy were also accelerated when compared with those in patients with collagen diseases not under RFP therapy. The t 1/2 of cortisol, prednisolone and dexamethasone in patients with tuberculosis alone under RFP therapy were 1.3 +/- 0.3 (p less than 0.001), 1.4 +/- 0.5 (p less than 0.01) and 1.2 +/- 0.3 hours (p less than 0.001), respectively, which were significantly shortened when compared with normal subjects.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1983

Up-regulation of insulin receptors with dexamethasone in cultured human urinary bladder carcinoma cells.

Cultured human urinary bladder carcinoma cells ( JTC -32) were used to investigate the regulation of insulin receptors by dexamethasone. When the cells were preincubated with dexamethasone at 37 degrees C, insulin binding sites increased up to 24 h. A large increase in insulin binding sites took place for 14 h of preincubation with dexamethasone. At lower concentrations of dexamethasone (less than 1 nM), no significant increase in insulin binding sites was observed, but the maximal increase was observed at more than 10 nM. Scatchard plots showed that dexamethasone increased the number of high affinity insulin binding sites (2.8 fold) without any change in the apparent equilibrium constant in JTC -32 cells. In addition, this steroid hormone also increased the number of low affinity insulin binding sites (1.6 fold) with a small change in the apparent equilibrium constant. Although insulin and dexamethasone did not affect the number of cells or the amount of cellular proteins per dish, dexamethasone plus insulin slightly increased them.

Cells, Cultured↗
PubMed1976

The insulin tolerance test after pre-treatment with dexamethasone.

The plasma 11-hydroxycorticosteroid and serum GH responses to insulin-induced hypoglycaemia were studied in 25 healthy volunteers. The results of a control insulin tolerance test were compared with those of 2 similar tests which were performed after pre-treatment with dexamethasone 0.5 and 1.0 mg, respectively. The GH response to hypoglycaemia was significantly lower in women than in men in all 3 tests. In men, but not in women, the GH response was lower after pre-treatment with 1 mg dexamethasone than in the other 2 tests. The plasma 11-hydroxycorticosteroid response was significantly greater after pre-treatment with 0.5 mg dexamethasone than in the control test, and was at least as good after 1 mg dexamethasone. After pre-treatment with dexamethasone the subjects experienced less discomfort and a shorter duration of sweating than in the control insulin tolerance test. Pre-treatment with 1 mg dexamethasone also has other advantages. Thus, the basal plasma cortisol level is low and stable, which facilitates estimation of the magnitude of the cortisol response. Furthermore, information is obtained about the dexamethasone suppression response.

11-Hydroxycorticosteroids↗
PubMed1987

Effects of dexamethasone on ovarian activity in rats.

Rats with 5-day ovarian cycles were treated with dexamethasone (0.025 to 0.4 mg per rat per day) to examine its effects on ovarian activity. All doses of dexamethasone markedly suppressed endogenous secretion of ACTH as evidenced by decrease in weight of the adrenal glands after 7-23 days of treatment. Treatment with 0.4 mg of dexamethasone from the day of ovulation appeared to induce pseudopregnancy in more than 90% of the rats studied: pseudopregnancies lasted for 14-22 days. Induction of pseudopregnancy occurred less, in a dose-dependent fashion, when the lower doses of dexamethasone were administered. However, prolonged treatment with these lower doses resulted also in pseudopregnancy albeit after 1 or more cycles of 5 to 7 days. The effects of large doses of glucocorticoids on ovarian activity in rats, and possibly in humans as well, may be mediated predominantly through a stimulatory action of such drugs on prolactin secretion. Treatment with 0.4 mg per day of dexamethasone from the day before pro-oestrus did not interfere with ovulation and pseudopregnancy ensued this ovulation in all rats studied. Occasionally, unexpectedly large numbers of eggs per ovulating animal were found during treatment with dexamethasone. The data indicate failure of large doses of dexamethasone to interfere with ovulation and, possibly, induction of an increase in numbers of maturing follicles: this latter action deserves further analysis.

Animals↗
PubMed1989

Study on clinical and endocrine characteristics of dexamethasone-suppressible hyperaldosteronism compared with those in primary aldosteronism owing to aldosterone-producing adenoma.

The clinical and endocrine characteristics of 12 Japanese patients with dexamethasone-suppressible hyperaldosteronism were compared with those in 49 Japanese patients with primary aldosteronism due to aldosteronoma. The results were as follows: 1. Most of the laboratory data in the two groups were almost the same. 2. The grade of vascular damage in both uncontrolled (3) and well-controlled (9) patients with dexamethasone-suppressible hyperaldosteronism did not correlate with blood pressure response. 3. The responsiveness of plasma aldosterone to exogenous ACTH in 6 patients with dexamethasone-suppressible hyperaldosteronism was not different from that in 9 patients with aldosteronoma. Even in 3 well-controlled patients in the former group, the plasma aldosterone response was as low as in all the 3 patients with small aldosteronomas. 4. In 4 patients with small aldosteronomas, plasma aldosterone was continuously suppressed with daily dexamethasone to the same degree as in dexamethasone-suppressible hyperaldosteronism. 5. The blood pressure, however, did not improve even in the patients with small aldosteronomas. The possible indistinguishable mechanism in dexamethasone-suppressible hyperaldosteronism and primary aldosteronism with small adenomas and the role of unknown hypertensinogenic steroid(s) other than aldosterone in inducing hypertension in dexamethasone-suppressible hyperaldosteronism are discussed.

Adenoma↗
PubMed1990

Inhibition by dexamethasone of arginine vasopressin and ACTH responses to insulin-induced hypoglycemia and cigarette smoking in normal men.

Glucocorticoids are known to inhibit the AVP response to osmotic and hemodynamic stimuli in humans. In the present study, we examined whether the AVP response to other primary stimuli, such as insulin-induced hypoglycemia and cigarette smoking was sensitive to inhibition by dexamethasone. The plasma ACTH responses were also measured. Twenty-four normal men were randomly divided into 3 groups of 8 subjects. One group was tested with insulin (0.15 IU/kg in an iv bolus) and another group with cigarette smoking (2 non-filter cigarettes smoked in succession within 10 min) with and without pretreatment with dexamethasone (2 or 4 mg in an iv bolus 10 min before insulin or smoking). The third group was tested with dexamethasone alone (2 or 4 mg in an iv bolus). The administration of dexamethasone (2 or 4 mg) alone did not modify the circulating levels of AVP and ACTH at any time during the next hour. The hypoglycemic response to insulin was similar regardless of dexamethasone treatment. AVP rose sharply in response to both hypoglycemia and smoking, reaching mean peak levels at 45 and 30 min, respectively. After both stimuli, the mean peak levels of AVP were 2.25 times higher than baseline. Pretreatment with dexamethasone (2 or 4 mg) significantly decreased the AVP responses to both hypoglycemia and cigarette smoking. Following pretreatment with dexamethasone (2 or 4 mg) the AVP increments in response to hypoglycemia or cigarette smoking were only 1.7 times higher than baseline. The plasma concentrations of ACTH were strikingly increased by hypoglycemia. The mean peak level was 3.5 times higher than baseline and was reached at 45 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1995

Dexamethasone therapy is associated with a rise in urinary epidermal growth factor concentrations in the preterm infant.

The effect of glucocorticoid hormones on epidermal growth factor (EGF) concentrations has not been described in the premature infant. We examined this relationship in a group of infants treated with dexamethasone for airway edema (three to five doses) or chronic lung disease (six weeks of a tapering protocol). We collected urinary samples in 45 infants (25 for airway edema, 20 for chronic lung disease) before, during and after the use of dexamethasone. The EGF values were unchanged in infants that were given dexamethasone for airway edema. In contrast, all infants treated for chronic lung disease increased their EGF values by 1 week of therapy. At the end of the dexamethasone taper, ten of the infants had recovered successfully from ventilatory support. This group of infants had post-therapy EGF values that were significantly higher than pretherapy values. In the ten infants that were still ventilator dependent at the end of therapy, EGF values were not different from pretherapy values. We conclude that dexamethasone therapy was associated with an increase in urinary EGF values in the preterm infant treated for at least 1 week. The positive correlation of tapering from ventilatory support with increases in EGF values suggests that EGF may be a marker of dexamethasone effect or an effector of dexamethasone action.

Adrenocorticotropic Hormone↗
PubMed1999

Randomized placebo-controlled trial of a 42-day tapering course of dexamethasone to reduce the duration of ventilator dependency in very low birth weight infants: outcome of study participants at 1-year adjusted age.

OBJECTIVE: Ventilator-dependent preterm infants are often treated with a prolonged tapering course of dexamethasone to decrease the risk and severity of chronic lung disease. The objective of this study was to assess the effect of this therapy on developmental outcome at 1 year of age. METHODS: Study participants were 118 very low birth weight infants who, at 15 to 25 days of life, were not weaning from assisted ventilation and were then enrolled in a randomized, placebo-controlled, double-blind trial of a 42-day tapering course of dexamethasone. Infants were examined at 1 year of age, adjusted for prematurity, by a pediatrician and a child psychologist. A physical and neurologic examination was performed, and the Bayley Scales of Infant Development were administered. All examiners were blind to treatment group. RESULTS: Groups were similar in terms of birth weight, gestational age, gender, and race. A higher percentage of dexamethasone recipients had major intracranial abnormalities diagnosed by ultrasonography (21% vs 11%). Group differences were not found for Bayley Mental Development Index (median [range] for dexamethasone-treated group, 94 [50-123]; for placebo group, 90 [28-117]) or Psychomotor Development Index Index (median [range]) for dexamethasone-treated group, 78 (50-109); for placebo-treated group, 81 [28-117]). More dexamethasone-treated infants had cerebral palsy (25% vs 7%) and abnormal neurologic examination findings (45% vs 16%). In stratified analyses, adjusted for major cranial ultrasound abnormalities, these associations persisted (OR values for cerebral palsy, 5.3; 95% CI: 1.3-21.4; OR values for neurologic abnormality 3.6; 95% CI: 1.2-11.0). CONCLUSIONS: A 42-day tapering course of dexamethasone was associated with an increased risk of cerebral palsy. Possible explanations include an adverse effect of this therapy on brain development and/or improved survival of infants who either already have neurologic injury or who are at increased risk for such injury.

Cerebral Palsy↗
PubMed1999

Early dexamethasone therapy and blood cell count in preterm infants.

OBJECTIVE: To assess the effects of early postnatal dexamethasone therapy on hematologic values in preterm infants. MATERIALS AND METHODS: We reviewed the hematologic data of 179 preterm infants who participated in a double-blind clinical trial of early postnatal dexamethasone therapy (<12 hours after birth) for the prevention of chronic lung disease. One group (86 infants) received saline and the other group (93 infants) received dexamethasone. Dexamethasone was given intravenously every 12 hours in tapering doses: 0.25 mg/kg on days 1 to 7, 0.12 mg/kg on days 8 to 14, 0.05 mg/kg on days 15 to 21, and 0.02 mg/kg on days 21 to 28. Blood samples were obtained on days 0, 3, 7, 10, 14, 21, and 28. None of the infants received prenatal steroid therapy. RESULTS: Multiple regression analysis revealed significant differences in the values versus time curves of the white blood cell, neutrophil, lymphocyte, basophil, and eosinophil counts between the two groups. The white blood cell count was significantly higher in the dexamethasone group on days 7 through 14, and this was associated with significantly higher numbers of segmented neutrophils and band forms and significantly lower numbers of lymphocytes and eosinophils. The hematocrit and platelet counts were similar in the two groups throughout most of the trial. Except for platelet count, steroid therapy did not alter the hematologic values for infants with bacteremia. CONCLUSION: Dexamethasone affects white blood cell, segmented neutrophil, lymphocyte, basophil, and eosinophil counts in neonates. This should be taken into consideration when evaluating preterm infants who are receiving dexamethasone.early dexamethasone therapy; neonatal blood count; preterm infant; respiratory distress syndrome.

Bacteremia↗
PubMed2004

Antibody response to diphtheria-tetanus-pertussis immunization in preterm infants who receive dexamethasone for chronic lung disease.

OBJECTIVE: To study the effect of dexamethasone in preterm infants with chronic lung disease (CLD) on antibody response to routine immunization against diphtheria, tetanus, and pertussis (DTP). METHODS: Serum samples were obtained before and after immunization with DTP (Trivax-AD) from an unselected cohort of 93 preterm infants in the United Kingdom. Antibodies to diphtheria and tetanus and to 4 pertussis antigens (pertussis toxin, filamentous hemagglutinin, pertactin, and fimbrial agglutinogens 2 + 3) were measured by an enzyme-linked immunosorbent assay. Linear regression models were fitted to the natural log of antibody titers to compare the dexamethasone-treated and -untreated infants adjusting for potential risk factors. RESULTS: Sixty-seven (72%) of 93 infants received dexamethasone. Preimmunization geometric mean titers (GMTs) were comparable in both groups for all antibodies. The rise in GMT after immunization was reduced in the dexamethasone-treated group. Final GMT was significantly lower for tetanus, diphtheria, pertussis toxin, and fimbrial agglutinogens 2 + 3 but not for filamentous hemagglutinin or pertactin. Using the minimum protective titer of 0.01 IU/mL, there was no significant reduction in protection for diphtheria and tetanus in the dexamethasone-treated infants. Using the higher reference titer of 0.1 IU/mL, there was a 16% reduction in protection for diphtheria (95% confidence interval: 3%-27%) and a 9% reduction in protection for tetanus (95% confidence interval: -7% to 20%). CONCLUSIONS: The use of dexamethasone for CLD in preterm infants is associated with a reduction in antibody titer to routine immunization against diphtheria and tetanus. Antibody responses to 2 of 4 pertussis antigens are reduced, but the clinical significance of this observation is unclear. Protection against tetanus and diphtheria is not impaired when the lower reference value for protective antibody is used. On the basis of this study of UK preterm infants who were treated with dexamethasone for the management of CLD, we conclude that the current DTP immunization schedule is adequate and do not recommend additional booster protection against tetanus or diphtheria during early infancy. When diphtheria prevalence is increased, however, additional protection should be considered.

Antibodies, Bacterial↗
PubMed2006

Low-dose dexamethasone facilitates extubation among chronically ventilator-dependent infants: a multicenter, international, randomized, controlled trial.

OBJECTIVE: Postnatal corticosteroid therapy is controversial. The aim of this study was to determine the short-term effects of low-dose dexamethasone treatment among chronically ventilator-dependent neonates. METHODS: Very preterm (gestational age: <28 weeks) or extremely low birth weight (birth weight: <1000 g) infants who were ventilator dependent after the first 1 week of life were eligible and were assigned randomly to receive masked dexamethasone (0.89 mg/kg over 10 days) or saline placebo. Data on ventilator and oxygen requirements and deaths were recorded. RESULTS: Seventy infants were recruited from 11 centers, at a median age of 23 days. More infants were extubated successfully by 10 days of treatment in the dexamethasone group (60%, 21 of 35 patients) than in the control group (12%, 4 of 34 patients) (odds ratio [OR]: 11.2; 95% confidence interval [CI]: 3.2-39.0). Ventilator and oxygen requirements improved substantially, and the duration of intubation was shorter. There was little evidence for a reduction in either the mortality rate (dexamethasone group: 11%; control group: 20%; OR: 0.52; 95% CI: 0.14-1.95) or the rate of oxygen dependence at 36 weeks (dexamethasone group: 85%; control group: 91%; OR: 0.58; 95% CI: 0.13-2.66). There were no obvious effects of low-dose dexamethasone on blood glucose concentrations, blood pressure, or other complications. No infant experienced intestinal perforation. CONCLUSIONS: Low-dose dexamethasone treatment after the first 1 week of life clearly facilitates extubation and shortens the duration of intubation among ventilator-dependent, very preterm/extremely low birth weight infants, without any obvious short-term complications. Combined with recent evidence that infants at very high risk of bronchopulmonary dysplasia may benefit in the long term, our study reopens debate regarding the role of low-dose, late postnatal, corticosteroid therapy.

Bronchopulmonary Dysplasia↗