Corticosteroids, urinary

Factors that can predispose patients to developing metabolic bone disease include deficiencies of phosphorus, calcium, and vitamin D vitamin D and/or aluminum toxicity amino acids and hypertonic dextrose infusions chronic metabolic acidosis corticosteroid therapy and lack of mobility.35,39 Calcium deficiency (due to decreased intake or increased urinary excretion) is one of the major causes of metabolic bone disease in patients receiving PN. Provide adequate calcium and phosphate with PN to improve bone mineralization and help to prevent metabolic bone disease. Administration of amino acids and chronic metabolic acidosis also appear to play an important role. Provide adequate amounts of acetate in PN admixtures to maintain acid-base balance. 

Close monitoring of 24-hour urinary free cortisol levels and serum cortisol levels are essential to identify adrenal insufficiency in patients with Cushing s syndrome. Steroid secretion should be monitored with all drug therapy and corticosteroid replacement given if needed. 

A rhythmic variation has been observed in levels of plasma hydroxy-corticosteroids (A9, B13, D9) and in the excretion of 17-ketosteroids (P7). As shown in Table 5, urinary excretions of potassium, sodium, chloride, 17-hydroxycorticosteroids and water have been reported to be greatest between 10 am to noon and lowest between 4 am and 6 am (S21). In this study it was shown that within 5 weeks subjects could acclimate to similar patterns for a 21-hour, rather than a 24-hour, day. Heilman and his associates reported that about half of the day s cortisol production is achieved in the early morning hours during sleep and that production is minimal between noon and 10 pm (H7). In one study the plasma cortisol in normal men was 24.6 5.5 /xg/100 ml at 7 am 13.1 3.4 fig/100 ml at 9 am 11.8 fig/100 ml at noon 9.1 2.3 jag/100 ml at 7 PM and 6.3 /ig/100 ml at 10 pm (A9). 

Drug/Lab test interactions Trans ent elevations of plasma 11-hydroxy-corticosteroid levels (Glenn-Nelson technique) may occur when IV calcium is administered, but levels return to control values after 1 hour. In addition, IV calcium gluconate can produce false-negative values for serum and urinary magnesium. 

Oral Treatment of hypokalemia in the following conditions With or without metabolic alkalosis digitalis intoxication familial periodic paralysis diabetic acidosis diarrhea and vomiting surgical conditions accompanied by nitrogen loss, vomiting, suction drainage, diarrhea, and increased urinary excretion of potassium certain cases of uremia hyperadrenalism starvation and debilitation corticosteroid or diuretic therapy. 

Special risk patients Administer cautiously to patients with decompensated cardiovascular, cirrhotic, and nephrotic disease circulatory insufficiency hypoproteinemia hypervolemia urinary tract obstruction CHF and to patients with concurrent edema and sodium retention those receiving corticosteroids or corticotropin and those retaining salt. 

Drug/Lab test interactions Plasma corticosteroid levels may be increased. Urinary steroid determinations may be altered by amphetamines. 

Drugs that may affect aspirin include activated charcoal, ammonium chloride, ascorbic acid or methionine, antacids and urinary alkalinizers, carbonic anhydrase inhibitors, corticosteroids, and nizatidine. Drugs that may be affected by aspirin include alcohol, ACE inhibitors, anticoagulants (oral), beta-adrenergic blockers, heparin, loop diuretics, methotrexate, nitroglycerin, NSAIDs, probenecid and sulfinpyrazone, spironolactone, sulfonylureas and exogenous insulin, and valproic acid. 

Echinacea (Echinacea purpurea) Uses immune system stimulant prevention/Rx of colds, flu as supportive th apy for colds chronic infxns of the resp tract lower urinary tract Action Stimulates phagocytosis cytokine production T resp cellular activity topically exerts anesthetic, antimicrobial, anti-inflammatory effects Efficacy Not established may X severity duration of URI Available forms Caps w/ powdered herb equivalent to 300-500 mg, PO, tid pressed juice 6-9 mL, PO, once/d tine 2-4 mL, PO, tid (1 5 dilution) tea 2 tsp (4 g) of powdered herb in 1 cup of boiling water Noles/SE Fever, taste p -version, urticaria, angioedema Contra w/ autoimmune Dz, collagen Dz, progressive systemic Dz (TB, MS, collagen-vascular disorders), HIV, leukemia, may interfere w/ immunosuppressive therapy Interactions t Risk of disulfiram-like reaction W/ disulfiram, metronidazole T risk of exacerbation of HIV or AIDS W/ chinacea amprenavir, other protease inhibitors X effects OF azathioprine, basiliximab, corticosteroids, cyclosporine, daclizumab, econazole vag cream, muromonab-CD3, mycophenolate, prednisone, tacrolimus EMS Possible immunosuppression... 

De Beilis MD, Baum AS, Birmaher B, Keshavan MS, Eccard CH, Boring AM, Jenkins FJ, Ryan ND (1999) A.E. Bennett Research Award. Developmental traumatology. Part 1 Biological stress systems [see comments]. Biol Psychiatry 45 1259-1270 de Kloet ER, Joels M, Oitzl M, Sutanto W (1991) Implication of brain corticosteroid receptor diversity for the adaptation syndrome concept. Methods Achiev Exp Pathol 14 104-132 Delahanty DL, Raimonde AJ, Spoonster E (2000) Initial posttraumatic urinary cortisol levels predict subsequent PTSD symptoms in motor vehicle accident victims. Biol Psychiatry 48 940-947... 

We studied by GC-MS the urinary excretion of a single patient with a documented mutation [49] and have found that the 5/3-reduced androgen metabolite excretion relative to 5a is decreased by about 80%, and 5/ -corticosteroid metabolite excretion is essentially absent [63]. To date there has no report of an adverse endocrine phenotype related to corticosteroid, mineralocorticoid, or androgen metabolism. 

Fink RS, Pierre LN, Daley-Yates PT, Richards DH, Gibson A, Honour JW. Hypothalamic-pituitary-adrenal axis function after inhaled corticosteroids unreliability of urinary free cortisol estimation. J Clin Endocrinol Metab 2002 87(10) 4541-6. 

Pal SB (1979) The pattern of urinary excretion of corticosteroids in Rhesus monkeys (Macaca mulatta). Endocrinology 73 359-62... 

Selective oxidative cleavage of the corticosteroid side chain sochum bismuthate was used as an analytical technique for the determination of urinary corticosteroids. Sodium bismudiate was chosen since it cleaves a-hydroxy acids readily (unlike periodic acid) and tolerates the water in urine samples (in contrast to LTA). 

Four children with the nephrotic syndrome developed transient hypercalciuria and intraluminal calcification in renal histopathological specimens without radiological evidence of renal calcification. These children were resistant to corticosteroids and were receiving furosemide plus albumin for the management of edema (10). This result stresses the pervasive effect of furosemide, and probably all loop diuretics, in increasing urinary calcium excretion, with resultant nephrocalcinosis. Whenever possible, steps should be taken to limit the hypercalciuric effect of loop diuretics. Such maneuvers could include limiting the sodium content of the diet and/or combining the loop diuretic with a thiazide diuretic. 

Beclomethasone dipropionate and budesonide Modulite formulations have been compared with equivalent chlorofluorocarbon products in small groups of healthy volunteers and asthmatic patients (18) there was no significant difference in morning serum cortisol or urinary cortisol excretion, suggesting that the systemic availability of the inhaled corticosteroids with different propellants is similar. Moreover, plasma profiles of beclomethasone dipropionate and B17MP were similar after inhalation of beclomethasone dipropionate Modulite and beclomethasone dipropionate-chlorofluorocarbon, suggesting that pulmonary delivery to the lung is comparable with the two propellants (18). 

Time of Administration The presence or absence of food in the gastrointestinal tract, corticosteroid secretion rhythm, circadian cycle, urinary excretion pattern, fluid intake, and drug-metabolizing enzyme rhythms all can influence the effect of the medication. 

Beetham R, Newman D, Urinary albumin and low molecular weight protein excretion in the nephrotic syndrome— sequential studies during corticosteroid treatment. Ann Clin Biochem 1992 29 450 3. 

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