Methyldopa-Induced Syndrome of Inappropriate Antidiuretic Hormone Secretion and Bone Marrow Granulomatosis (original) (raw)
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Growth hormone and cortisol secretion after oral and intravenous administration of methyldopa
Acta pharmacologica et toxicologica, 1975
The effect of oral administration of methyldopa for two to three weeks on growth hormone and cortisol secretion was studied in untreated hypertensive patients in an insulin stimulation test. In addition, the effect of an acute intravenous infusion of methyldopa on these hormones was studied in norrnotensive patients. In an insulin-hypoglycaemia test the levels of serum growth hormone did not differ significantly after treatment with methyldopa (750 mg daily) from the levels obtained before treatment. The levels of plasma cortisol tended to be slightly lower after the treatment than before treatment up to 90 minutes, although the difference was statistically significant only at 30 minutes. The decrease in blood pressure after treatment was significant. An acute infusion of methyldopa (250 mg intravenously) induced no significant changes in blood pressure in normotensive patients. The concentration of plasma cortisol decreased slightly but significantly after the infusion. However, there were no significant changes in the secretion of growth hormone after the infusion. It is concluded that treatment of hypertension with methyldopa does not cause any clinically important alterations in the anterior pituitary function.
Increases in Methyldopa Absorption and Renal Excretion After Multiple Doses
The Journal of Clinical Pharmacology, 1992
A retrospective analysis of previous studies examining met hyldopa absorption suggested the possibility that the absorption of methyldopa might increase on repeat methyldopa ingestion. A prospective study was undertaken to determine the effect of repeated oral doses of met hyldopa on met hyldopa absorption. Thirteen healthy subjects ingested single 250 mg methyldopa doses on days 0, 7, 14, 28, 56, and 112; 24 urine samples were collected and analyzed for methyldopa and its major metabolites on each study day and methyldopa plasma levels were measured over 8 hours at days 0 and 56. There were significant increases in the absorption of methyldopa (as estimated by the urinary excretion of methyldopa and the measured metabolites over 24 hours) at day 56(33.4 ± 8.9%, P <.025) compared with day 0(26.0 ± 10.8%). There was also a significant increase in renal clearance of unmetabolized methyldopa (62.7 ± 13.6 vs. 99.3 ± 29.1 mL/min, P < .01) and a decrease in the plasma half-life of methyldopa at day 56 (2.22 ± 0.91 vs. 1.56 ± 0.68 hr. P <.05). There was a tendency toward increases in methyldopa absorption at day 7, 14, 28, and 112. Several possible explanations for the changes in methyldopa disposition are discussed.
Hepatic injury and drug metabolism in patients with alpha-methyldopa-induced liver damage
European Journal of Clinical Pharmacology, 1977
The clinical picture and drug metabolism in 36 consecutive patients with alpha-methyldopa-induced hepatic injury were investigated. The diagnosis was based on case history and biochemical, histological and follow-up studies after withdrawal the drug. Alpha-methyldopa-induced liver damage was found to occur in two phases, acutely within months and chronically within years after beginning treatment. Differences were also found in clinical symptoms and the results of liver tests on the patients if they were divided on the basis of the time factor. Drug metabolism was impaired in patients with alpha-methyldopa-induced liver damage, as indicated by low cytochrome P-450 level in liver biopsies and prolonged antipyrine elimination rate from plasma. Disappearance of the symptoms and normalisation of the liver tests after drug withdrawal occurred faster in patients with an acute type of hepatotoxicity than in subjects with delayed onset of the symptoms. The occurrence of hepatotoxicity in four members of a family suggests a genetic disposition to alpha-methyldopa-induced hepatic injury. The occurrence of two phases of liver damage suggests that a possible mechanism for acute hepatotoxicity might be an allergic reaction to metabolic intermediates produced during breakdown of alphamethyldopa in the liver. For cases of delayed onset the cause might be increasing damage to microsomal liver protein due to covalent binding during longterm exposure to the drug.
Syndrome of inappropriate antidiuretic hormone associated with escitalopram therapy
CNS spectrums
Escitalopram is the selective serotonin reuptake inhibitor (SSRI) most recently approved for use in the United States. It is structurally related to citalopram, but is felt to have a more tolerable side-effect profile than its parent compound. Side effects are not generally serious and include headache, diarrhea, and nausea. While hyponatremia and the syndrome of inappropriate antidiuretic hormone (SIADH) have been associated with treatment with other SSRIs, there has only been one case of escitalopram-induced SIADH reported in the literature to date. We now report another case of a patient who developed SIADH after being treated with escitalopram for 4 weeks. The patient's hyponatremia improved following the discontinuation of escitalopram. Clinicians should be aware of this uncommon but significant side effect of SSRIs and monitor high-risk patients for the development of SIADH.
Syndrome of inappropriate antidiuretic hormone secretion (SIADH) has various causes including central nervous system disorders, pulmonary and endocrine diseases, paraneoplastic syndromes, and use of certain drugs. SIADH induced by chemotherapy with irinotecan-cisplatin is not a common complication. Here, we review a case of SIADH after treatment with irinotecan-cisplatin. A 45-year-old woman received adjuvant chemotherapy (paclitaxel-carboplatin) for ovarian clear cell carcinoma, but the cancer recurred within 9 months of chemotherapy. Subsequently, a second line of combination chemotherapy containing irinotecan-cisplatin was initiated. However, 5 days after chemotherapy administration, her general condition began to deteriorate; her hematological tests revealed hyponatremia. Therefore, it is imperative to consider the possibility of SIADH in patients being treated with irinotecan-cisplatinbased chemotherapy. Proper monitoring of serum sodium levels and assessment of clinical symptoms should be performed in such patients for early diagnosis and prompt management.
Complete Atrioventricular Block Induced by Methyldopa
Pacing and Clinical Electrophysiology, 1988
ROSEN, B., ET AL.: Complete atrioventricular block induced by methyldopa. We present two patients who developed compJete heart block due to treatment with methyldopa. After discontinuing methyidopa, conduction disturbances completeJy disappeared and recurred upon rechallenge with the medication. It is assumed that methyldopa can impair the myocardiaJ conduction system by its central sympathoJytic effect. Conduction anomalies should be excluded prior to treatment with methyldopa, and during treatment with the medication, the patients should be routinely screened for the presence of conduction anomalies.
The Impact of the Drug Methyldopa in Both Medical and Industrial Applications
Al-Nahrain Journal of Science
Methyldopa is a medication usually used to regulate and treat hypertension. It is one of the most commonly used therapies for high blood pressure during pregnancy. Methyldopa acts on blood vessels by providing additional relaxation, therefor blood can flow more easily through the body. Also, Methyldopa is a common medication used during pregnancy and is unlikely to cause any risk to the baby.