rifampin and Addison-Disease

Topics: Acute Disease; Addison Disease; Adrenal Insufficiency; Adult; Antibiotics, Antitubercular; Drug Therapy, Combination; Female; Humans; Rifampin; Tuberculosis, Pulmonary

We herein report a rare occurrence of Addison's disease caused by acute adrenal gland tuberculosis occurring in association with miliary tuberculosis and the administration of rifampicin. An 82-year-old woman with miliary tuberculosis was treated with antituberculous chemotherapeutic agents including rifampicin (RFP), but she still demonstrated general malaise in addition to hyponatremia. Abdominal CT showed an enlargement of the right adrenal gland. However, after discontinuing RFP, the patient's symptoms improved. We carefully reinitiated the administration of RFP. The patient's condition thereafter did not worsen, and the treatment could thus be maintained. It is extremely important to immediately recognize adrenal crisis precipitated by the administration of RFP.

Topics: Acute Disease; Addison Disease; Adrenal Gland Diseases; Aged; Aged, 80 and over; Antibiotics, Antitubercular; Female; Humans; Rifampin; Tomography, X-Ray Computed; Tuberculosis, Endocrine; Tuberculosis, Miliary

We submit the case of a male patient, suffering from a tuberculous ethiology adrenal primary insufficiency, showing a dermal lesion, in which necrotizing granulomas were found, and from which bacterial culture growth yielded mycobacterium bovis. Given the clinical findings, and awaiting for the bacterial culture result, a triple treatment with tuberculostatics was started, but had to be discontinued because of hepatic toxicity. After culture of cutaneous biopsy yielded micobaterium tuberculosis, treatment with streptomycin, rifampicin and etambutol was restarted. Three weeks later, in spite of increasing hydrocortisone dose to 40 mg, adrenal insufficiency reappeared. Under the circumstances, we chose to continue rifampicin and double hydrocortisone dose. The case is of concern because of the concurrency of three nowadays infrequent disorders: tuberculous ethiology adrenal insufficiency, cutaneous tuberculosis due to mycobacterium bovis and primary adrenal insufficiency due to rifampicin treatment, the latter resolved after increasing hydrocortisone dose.

Topics: Addison Disease; Adrenal Gland Diseases; Aged; Antibiotics, Antitubercular; Humans; Hyperpigmentation; Male; Mycobacterium bovis; Rifampin; Tuberculosis, Cutaneous; Tuberculosis, Endocrine

Topics: Addison Disease; Aged; Antitubercular Agents; Chemical and Drug Induced Liver Injury; Female; Humans; Isoniazid; Pyrazinamide; Rifampin; Tuberculosis, Miliary

Topics: Addison Disease; Adult; Antitubercular Agents; Ethambutol; Germany; Humans; Hydrocortisone; Hyperpigmentation; Isoniazid; Male; Pyrazinamide; Rifampin; Tuberculosis, Endocrine

Topics: Addison Disease; Aged; Antitubercular Agents; Cortisone; Diagnosis, Differential; Female; Humans; Lymph Nodes; Neck; Rifampin; Tuberculosis, Lymph Node

The patient was a 76 year-old female with tuberculous tendonitis, treated with anti-tuberculous drugs including rifampicin (RFP). About two weeks after the start of RFP, she noticed general malaise and started vomiting, and the laboratory data showed severe hyponatremia. Because of mild liver dysfunction, RFP was discontinued and her symptoms gradually improved. Abdominal X-ray and CT showed swellings and calcifications of adrenal glands bilaterally. Serum ACTH level was high and cortisole, 17-OHCS, and 17-KS levels were normal. Her response to rapid ACTH stimulation was blunted significantly. After another trial of RFP, she started to vomit and complain general malaise again. We diagnosed her as partial Addison's disease and administered hydrocortisone with RFP. After this treatment her improvement was rapid. It has been known that RFP causes induction of enzymes in hepatic microsomes which increase the catabolism of glucocorticoids. To avoid the risk of adrenal insufficiency, patients with insufficient adrenal hormone reserve should receive compensatory hydrocortisone while they are taking RFP.

Topics: Addison Disease; Aged; Antibiotics, Antitubercular; Female; Humans; Hydrocortisone; Rifampin; Tendinopathy; Tuberculosis

Tuberculosis of the adrenal glands is a common cause of Addison's disease in developing countries. We conducted a study to determine if treatment of such patients with modern anti-tuberculous chemotherapy would lead to an improvement in plasma cortisol and aldosterone levels.. Prospective study.. 5 patients with Addison's disease secondary to tuberculosis.. Basal and ACTH stimulated plasma cortisol and aldosterone levels were measured prior to instituting anti-tuberculous chemotherapy, as well as one month after its conclusion. Four patients were again studied over the next 2-5 years.. Peak plasma cortisol levels prior to treatment were markedly reduced (range, < 14-110 mumol/l). There was no improvement one month (< 14-143 mumol/l) or 2-5 years (< 14-69 mumol/l) after completing anti-tuberculous chemotherapy. Peak plasma aldosterone at diagnosis was < 56-210 pmol/l; it was undetectable in 4 patients. No improvement was observed one month (< 56-210 pmol/l), or 2-5 years (< 56-389 pmol/l) after stopping anti-tuberculous chemotherapy. Plasma aldosterone levels at both these time points were far lower than those in control subjects (median 736 pmol/l, 560-1512 pmol/l; p < 0.01). One patient had an increase in peak aldosterone from < 56 pmol/l to 389 pmol/l, though peak cortisol actually declined in this subject (from 110 mumol/l to 69 mumol/l).. Treatment of tuberculous Addison's disease with anti-tuberculous chemotherapy does not lead to normalization of ACTH stimulated plasma cortisol or aldosterone levels during the 2-5 year period of study. However, prolonged follow up with regular adrenal function tests is warranted in all such patients.

Topics: Addison Disease; Adrenal Cortex; Adrenal Cortex Function Tests; Adrenal Gland Diseases; Adrenocorticotropic Hormone; Adult; Aldosterone; Anti-Inflammatory Agents; Antitubercular Agents; Drug Therapy, Combination; Fludrocortisone; Humans; Hydrocortisone; Isoniazid; Male; Middle Aged; Prednisolone; Prospective Studies; Pyrazinamide; Rifampin; Tuberculosis, Endocrine

Adrenal computed tomographic (CT) scanning was conducted in twelve patients with Addison's disease during the clinical course. In tuberculous Addison's disease (n = 8), three of four patients examined during the first two years after disease onset had bilaterally enlarged adrenals, while one of four had a unilaterally enlarged one. At least one adrenal gland was enlarged after onset in all six patients examined during the first four years. Thereafter, the adrenal glands may atrophy bilaterally, in contrast to adrenal glands in idiopathic Addison's disease, which atrophy bilaterally from disease onset (n = 2). Adrenal calcification was a less sensitive clue in tracing pathogenesis, i.e., adrenal calcification was observed in five of eight patients with tuberculous Addison's disease, but not in idiopathic patients. Thus, adrenal CT scanning could show the etiology of Addison's disease (infection or autoimmunity) and the phase of Addison's disease secondary to tuberculosis, which may be clinically important for initiating antituberculous treatment.

Topics: Addison Disease; Adrenal Glands; Adult; Aged; Atrophy; Female; Humans; Hydrocortisone; Isoniazid; Male; Middle Aged; Rifampin; Streptomycin; Tomography, X-Ray Computed; Tuberculosis, Pulmonary

To investigate the effect of rifampicin on the metabolism of hydrocortisone, we measured serum sodium level and blood glucose concentration before lunch in a patient with Addison's disease when treated with hydrocortisone 30 mg/day alone and together with rifampicin 450 mg/day for more than two weeks. We also studied the area under the plasma cortisol curve (AUC), half-life (T 1/2) and clearance rate (CLs) of hydrocortisone after both oral ingestion and intravenous injection of 20 mg hydrocortisone. The results showed that rifampicin increased the metabolism of cortisol by shortening of its T 1/2, increasing its CLs and decreasing its AUC. It decreases the blood sodium level and glucose concentration and makes the patient liable to have hypoglycemic symptoms before lunch. We conclude that the increase of metabolism of cortisol after simultaneous taking of rifampicin may induce adrenal crisis in Addison's disease.

Topics: Addison Disease; Adult; Blood Glucose; Female; Humans; Hydrocortisone; Prospective Studies; Rifampin; Sodium

A patient with spinal tuberculosis and subclinical adrenal tuberculosis who developed acute Addisonian crisis on starting anti-tuberculosis therapy including rifampicin is reported. The possibility that many patients with tuberculosis have adrenal involvement with limited hormonal reserve and that they may develop incipient adrenal failure on commencing treatment is discussed.

Topics: Addison Disease; Adrenal Gland Diseases; Antitubercular Agents; Humans; Male; Middle Aged; Rifampin; Tuberculosis, Endocrine; Tuberculosis, Spinal

Topics: Addison Disease; Adrenal Cortex Hormones; Adrenal Insufficiency; Humans; Male; Middle Aged; Rifampin; Tuberculosis, Male Genital

Topics: Addison Disease; Aged; Aged, 80 and over; Female; Humans; Rifampin; Tuberculosis, Pulmonary

Topics: Addison Disease; Adrenal Glands; Humans; Rifampin; Tomography, X-Ray Computed; Tuberculosis

Treatment of tuberculosis with rifampicin in patients with pre-existing adrenal failure has been reported to induce adrenal crisis due to alteration of cortisol metabolism by induction of hepatic mixed liver oxygenase enzymes. To determine whether mineralocorticoid metabolism is altered by rifampicin treatment, we established the pharmacokinetics of immunoreactive aldosterone. The metabolic clearance rate (MCR) and plasma half-life of this material were measured before and after 6 days of rifampicin treatment (600 mg/day) in seven patients with Addison's disease due to tuberculosis. Antipyrine clearance and urinary 6-beta-hydroxycortisol excretion was determined to demonstrate induction of the cytochrome P450 dependent enzymes. Infusion of aldosterone at a constant rate of 0.17 mg/h over 4.5 h produced steady state concentrations after 2 h, with no difference before and after rifampicin treatment (mean +/- SD, 1649 +/- 144 vs 1586 +/- 80 pg/ml, respectively). The disappearance curve of IR-aldosterone from plasma was biexponential. No change could be observed in the plasma half-lives (alpha-phase 29 +/- 1.9 min vs 30 +/- 1.5 min, beta-phase 129 +/- 3.2 min vs 126 +/- 4.3 min), the MCR (1.47 +/- 0.1 l/h/kg vs 1.46 +/- 0.1 l/h/kg), and the volume of distribution (9.9 +/- 1.9 vs 10.2 +/- 0.3 l). The antipyrine half-life decreased significantly from 12.2 +/- 2.6 h to 7.6 +/- 0.9 h (P less than 0.05) with a rise in antipyrine clearance from 0.38 +/- 0.07 to 0.80 +/- 0.23 ml/min/kg (P less than 0.05) and no change in the volume of distribution.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Addison Disease; Adult; Aldosterone; Antipyrine; Female; Humans; Hydrocortisone; Male; Middle Aged; Rifampin; Tuberculosis

Topics: Addison Disease; Adrenal Insufficiency; Glucocorticoids; Humans; Male; Middle Aged; Rifampin; Tuberculosis, Renal

Two patients with Addison's disease related to urogenital tuberculosis had enlargement of one or both adrenal glands detected with computed tomographic scanning. Review of reports of adrenal size on computed tomographic examination suggests that adrenal enlargement in the presence of Addison's disease demands further investigation about the cause of the adrenal insufficiency.

Topics: Addison Disease; Adrenal Glands; Adrenocorticotropic Hormone; Aged; Cortisone; Drug Therapy, Combination; Fludrocortisone; Humans; Isoniazid; Male; Middle Aged; Prednisone; Rifampin; Tomography, X-Ray Computed; Tuberculosis, Male Genital

Rifampicin induced profound alterations in cortisol metabolism when administered to three patients with primary adrenal failure receiving adequate corticosteroid replacement therapy. In one patient, adrenal crisis was precipitated after the institution of rifampicin therapy for treatment of coexistent tuberculosis and in another, profound asthenia, decrease in blood pressure, hyperkalemia, and hyponatremia developed during the hydrocortisol kinetic study. The clinical symptoms subsided and the electrolyte abnormalities were corrected approximately 7 days after rifampicin withdrawal. The half-life of hydrocortisol and the area under the curve were decreased by 35% and 23%, respectively, whereas the systemic clearance was increased by 35% during rifampicin administration. It appears, that the effectiveness of glucocorticoids and mineralocorticoids were greatly impaired by rifampicin administration due to induction of liver steroid-metabolizing enzymes. It is strongly recommended that in patients with compromised adrenal function, treatment with rifampicin must be accompanied by doubling or tripling the dose of adrenal steroids to maintain adequate steroid replacement therapy.

Topics: Acute Disease; Addison Disease; Adrenal Cortex Hormones; Adult; Dexamethasone; Drug Interactions; Enzyme Induction; Female; Fludrocortisone; Humans; Hydrocortisone; Kinetics; Liver; Male; Prednisolone; Rifampin

Topics: Addison Disease; Adrenal Insufficiency; Drug Therapy, Combination; Female; Humans; Isoniazid; Middle Aged; Rifampin

Deviation of cortisol metabolism in favour of its 6 beta-hydroxylated derivative was demonstrated in two patients with adrenal failure receiving substitution corticosteroid therapy and rifampicin. The existence of a frank increase in the metabolic clearance antipyrin was in favour of an hepatic enzyme induction. After rifampicin treatment was stopped, the 24 hour urinary excretion of 6 beta-OH-F returned to normal, demonstrating the responsability of the drug. This enzyme induction results in a need to increase the dose of hydrocortisone substitution therapy in patients with Addison's disease treated with rifampicin.

Topics: Addison Disease; Adrenal Cortex Hormones; Adrenal Insufficiency; Adult; Aged; Antipyrine; Enzyme Induction; Humans; Hydrocortisone; Hydroxycorticosteroids; Liver; Male; Metabolic Clearance Rate; Rifampin; Steroid Hydroxylases; Tuberculosis

Topics: Addison Disease; Cortisone; Cytochrome P-450 Enzyme System; Enzyme Induction; Humans; Rifampin

Topics: Addison Disease; Aged; Cortisone; Drug Interactions; Female; Humans; Isoniazid; Recurrence; Rifampin; Streptomycin; Tuberculosis

A patient with Addison's disease required increased corticosteroid dosage whilst receiving rifampicin. The pharmacological half-life of cortisol was reduced, but returned to normal when rifampicin was stopped. Cortisolproduction rates in four patients with pulmonary tuberculosis rose during treatment with rifampicin, as did urinary D-glucaric-acid excretion, an index of liver microsomal-enzyme activity. The alteration of the corticosteroid requirement in the patient with Addison's disease and the elevation of the cortisol-production rates were attributed to increased cortisol catabolism following hepatic macrosomal-enzyme induction by rifampicin.

Topics: Addison Disease; Adipates; Adrenal Glands; Adult; Cortisone; Dose-Response Relationship, Drug; Drug Antagonism; Drug Therapy, Combination; Fludrocortisone; Half-Life; Humans; Hydrocortisone; Isoniazid; Male; Rifampin; Streptomycin; Sugar Acids; Tuberculosis, Pulmonary