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Cardiovascular Drugs during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
No epidemiological studies of bumetanide (Bumex) during pregnancy have been published. No increase in malformations was found in offspring of animals receiving several times the usual adult human dose of bumetanide (McClain and Dammers, 1981). Five infants were exposed to bumetanide in the first trimester in the Swedish Birth Defects Registry (Kallen, 2019).
Sodium Intake and Hypertension
Published in Austin E. Doyle, Frederick A. O. Mendelsohn, Trefor O. Morgan, Pharmacological and Therapeutic Aspects of Hypertension, 2020
T. O. Morgan, F. A. O. Mendelsohn, A. E. Doyle
The future development would appear to be to develop diuretics which have specific other actions that prevent the development of side effects. Tienylic acid and indanone are examples of such drugs. Indapamide may be a drug possessing antihypertensive action in excess of its diuretic properties. Bumetanide may not cause loss of magnesium, and in certain circumstances this may be advantageous.
Therapeutic Use of Carbonic Anhydrase Inhibitors and Their Multiple Drug Interactions
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Andrea Angeli, Claudiu T. Supuran
Bumetanide and indapamide showed antagonistic effects when using with probenecid producing natriuresis and hyperreninemia. These effects are not due to a direct action on sodium excretion but are probably secondary to its inhibitory effect on renal tubular secretion of diuretic drugs (Opie, 2012; Holland and Williamson, 1979). This interaction, however, can be used to increase brain levels of bumetanide and decrease its elimination, which could have therapeutic potential in the treatment of brain disorders (Töllner et al., 2015). On the other hand, absorption of Hydrochlorothiazide is impaired in the presence of anionic exchange resins such as Cholestyramine. Single doses of it bind the Hydrochlorothiazide and reduce its absorption from the gastrointestinal tract (Hunninghake and Hibbard, 1986; Hunninghake et al., 1982).
Usefulness of acetazolamide in the management of diuretic resistance
Published in Baylor University Medical Center Proceedings, 2021
Dalvir Gill, Naga Vaishnavi Gadela, Ayesha Azmeen, Abhishek Jaiswal
A 66-year-old obese (body mass index 34 kg/m2) woman with hypertension, diabetes mellitus type 2, and HF with preserved ejection fraction on bumetanide 2 mg daily at home presented for decompensated HF with fluid overload. In the outside hospital, her blood pressure was 145/75 mm Hg and her respiratory rate was 24 breaths/minute with an oxygen saturation of 96% on 2 L of nasal cannula. Examination revealed respiratory distress with accessory muscle use, inspiratory crackles, bilateral pitting lower-extremity edema, and elevated jugular venous pulse. Admission serum creatinine was 1.2 mg/dL; sodium, 138 mmol/L; potassium, 3.2 mmol/L; bicarbonate, 28 mg/dL; pro-brain natriuretic peptide, 3492 pg/mL; and troponin, <0.03 ng/mL. Chest radiograph showed pulmonary congestion, and an electrocardiogram showed sinus rhythm, with old Q waves in V1 to V4. On day 1, the patient received 40 mg of intravenous furosemide and a furosemide infusion at 10 mg/h to which she remained oliguric. On day 2, an intravenous bolus of 40 mg furosemide was given, and the infusion was increased to 20 mg/h with no response. On day 3, she was transitioned to bumetanide infusion at 1 mg/h without any improvement in urine output. On day 4, bumetanide infusion was increased to 1.5 mg/h in addition to 5 mg metolazone. Continued suboptimal urine output led to an increasing bumetanide infusion to 2 mg/h and another dose of 10 mg metolazone twice on day 5 with a somewhat improved urine output of 950 mL in 24 hours. During this period, her creatinine increased to 3.9 mg/dL.
Investigational drugs in early-stage clinical trials for autism spectrum disorder
Published in Expert Opinion on Investigational Drugs, 2019
Michael P. Hong, Craig A. Erickson
Bumetanide is a well-known diuretic that inhibits the Na-K-Cl cotransporter 1 (NKCC1), a channel that also regulates the import of chloride in neuronal cells. Through this action, bumetanide is also believed to reduce intracellular chloride and enhance GABAergic inhibitory signaling [60,61]. Bumetanide has been shown to have neural effects in individuals with ASD, specifically with regards to social and emotional processing [62,63]. A double-blind, randomized study of daily bumetanide for 3 months in children with autism or Asperger syndrome revealed improvements in multiple measures of autism-related symptomology [64]. Further, bumetanide was shown to enhance the effects of Applied Behavior Analysis (ABA) therapy in individuals with ASD [65]. A multicenter, phase 2B randomized control trial of 3-months of oral liquid bumetanide in 2–18-year-olds with ASD confirmed findings of positive effects on social functioning and autism-related behavior [66]. Bumetanide is associated with many adverse effects, including hypokalemia, increased urination, loss of appetite, dehydration, and asthenia, but dosing 1 mg twice daily was found to reduce side effects while maintaining efficacy [66]. The exact mechanisms underlying bumetanide’s effects must be further researched, but early phase clinical trials show promise as a therapeutic target in treatment of ASD.
Select hyperacute complications of ischemic stroke: cerebral edema, hemorrhagic transformation, and orolingual angioedema secondary to intravenous Alteplase
Published in Expert Review of Neurotherapeutics, 2018
There are several promising medical treatments on the horizon for the management of cerebral edema from ischemic infarction. As stated previously in the discussion of ionic edema it has been shown in animal models that blockade of SUR1-TRPM4 channel reduces cerebral edema [8]. The Glyburide Advantage in Malignant Edema and Stroke (GAMES-RP) trial was a phase 2 double blind randomized controlled trial of the use of intravenous glyburide in patients at risk of developing MCE from anterior circulation strokes [68]. Unfortunately this industry-sponsored study was stopped prematurely due to lack of funding after enrolling only 86 patients. It failed to show a difference between the two groups for the primary outcome of mRS 0–4 at 90 days without decompressive craniectomy. However IV glyburide did reduce midline shift of the brain at 72–96 h from 8.5 mm (5.0–14.2) in the placebo group down to 4.6 mm (2.0–6.6, p = 0.0006) in the treatment group [68]. The Na(+)-K(+)-2Cl(-) co-transporter (NKCC1) is expressed on the luminal surface of endothelial cells and plays an important role in the movement of Na and Cl into endothelial cells [69]. Cerebral ischemia has been shown to lead to up regulation of this ion channel [70]. Furthermore, bumetanide has been shown to inhibit this ion channel and in an animal model attenuated cytotoxic edema and neuronal death [71]. Human trials are likely in the near future in regards to using low dose bumetanide in patients at risk of developing MCE. It is reasonable to consider a combined approach of using both bumetanide along with glyburide in future clinical trials since they potentially could work synergistically given that they target different mechanisms of cerebral edema formation.