scholarly journals Tetraparesis with Major Hypokalaemia and Rhabdomyolysis Induced by Chronic Liquorice Ingestion

Author(s):  
Hassene Attout ◽  
Andry Randriajohany ◽  
Françoise Josse ◽  
Vincent Appavoupoule ◽  
Yoga Thirapathi

Chronic ingestion of liquorice induces a syndrome with findings similar to those for primary hyperaldosteronism. This is characterized by hypokalaemia, hypertension, metabolic alkalosis and suppression of the renin-aldosterone system. We describe a 30-year-old woman who, with a plasma potassium level of 1.5 mmol/l, presented with tetraparesis and severe rhabdomyolysis (CK up to 35,460 U/l). She admitted to a daily consumption of nearly 300 g of liquorice sweets during the previous 6 months. This case emphasizes the importance of a detailed anamnesis, which is essential for diagnosis, avoids unnecessary and expensive investigations and reduces the duration of hospitalization.

1951 ◽  
Vol 221 (6) ◽  
pp. 678-687 ◽  
Author(s):  
S. J. Farber ◽  
E. D. Pellegrino ◽  
N. J. Conan ◽  
D. P. Earle

2013 ◽  
Vol 288 (14) ◽  
pp. 10124-10131 ◽  
Author(s):  
Luciana Morla ◽  
Gaëlle Brideau ◽  
Marc Fila ◽  
Gilles Crambert ◽  
Lydie Cheval ◽  
...  

1952 ◽  
Vol 31 (5) ◽  
pp. 440-444 ◽  
Author(s):  
Abraham Dury ◽  
Jacob W. Holler ◽  
Caleb Smith ◽  
Thomas N. Johnston

Endocrinology ◽  
1951 ◽  
Vol 49 (5) ◽  
pp. 663-670 ◽  
Author(s):  
ABRAHAM DURY ◽  
L. F. VITELLO ◽  
T. N. JOHNSTON

2018 ◽  
Vol 24 (1) ◽  
pp. 5-10
Author(s):  
Ye.A. Dudka ◽  
I.I. Zamorskii ◽  
A.Ye. Petriuk ◽  
T.S. Shchudrova

Aminoglycosides are effective antibiotics, but their accumulation in kidney cortex causes nephrotoxic effects in 20-30% of patients, which significantly limits their use. For this reason, search for the new therapies aimed at prevention of gentamicin-induced acute kidney injury (AKI) is highly relevant. Thus, the objective of our research was to study the functional and histopathological changes in kidneys of rats with gentamicin-induced AKI, and estimate the renoprotective potential of pineal hormone melatonin, which possesses antioxidant, anti-inflammatory and immunomodulatory effects. The study was conducted on 24 non-linear male rats. Gentamicin-induced AKI was modeled by daily administration of 4% gentamicin sulphate (80 mg/kg) for 6 days. Melatonin (Sigma Aldrich, USA) was injected daily at a dose of 5 mg/kg. Functional state of kidneys was assessed by diuresis, creatinine clearance, urine protein excretion, fractional excretion of sodium, and plasma potassium level. Documentation of the pathological processes was performed by the computer morphometry of objects in histological preparations. Statistical analysis of the data was performed using SPSS 17.0 software. Administration of gentamicin resulted in a significant impairment of renal function of experimental animals. A decrease in creatinine clearance by 3.1 times along with a reduction of diuresis by 1.9 times, and an increase in plasma creatinine concentration by 2.6 times was observed. There also was an increase in urine protein level by 5.2 times, an elevation of fractional sodium excretion and a reduction of plasma potassium level. Use of melatonin caused a significant improvement of renal function comparing to model pathology group. Functional disturbances were accompanied with the significant histopathological changes in kidney tissue: necrosis of the 27±5.2% epithelial cells of proximal tubules with the signs of hydropic vacuolization (7±2.1%) or reversible hydropic swelling (76±1.5%) in the rest of cells; swelling or deformation of some glomeruli. In the medulla tubular lumen were dilated and partially filled with hyaline casts, tubular cells had signs of dystrophy. Use of melatonin contributed to the restraint of the histopathological changes, confirmed by the decrease of the prevalence and severity of tubular necrosis (1.2%), dystrophy (64±2.3%), and injury of glomeruli. Obtained results verify the significant nephroprotective effect of pineal hormone melatonin, providing a background for the further in-depth study of its renal effects as well as its prospects as a nephroprotector.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Vojtech Melenovsky ◽  
Adrian Reichenbach ◽  
Luca Monzo ◽  
Hikmet Al-Hiti ◽  
Ivana Jurcova ◽  
...  

Introduction: In advanced HFpEF, acute phosphodiesterase 5 (PDE5) inhibition leads to favorable change in pulmonary vascular resistance (PVR) and to an increased cardiac output (CO) of variable degree. The determinants of the response are poorely understood. Methods: 47 HFrEF patients (85% males, 57±11 years, NYHA 2.9±0.5, 55% non-ischemic, PAmean 42±8 mmHg, 43% RV dysfunction) underwent clinical exam, echocardiography, biochemical tests and right heart catheterization (RHC) before and after I.V. administration of sildenafil (20 mg). Baseline predictors of absolute and relative (%diff) change of PVR and CO were studied. Results: PDE5i led to highly significant (p<0.001) reduction of pulmonary artery (PA) mean pressure (-11±9 mmHg), PVR (-2.2±1.6 WU;-42±24%), PA wedge pressure (-5.2±7.3 mmHg), CVP (-3.2±2.3 mmHg) and to increase in cardiac output (+0.6±0.7 l/min; +18±23%). PVR decreased more than systemic resistance (PVR/SVR -27±30%diff). Predictors of high CO response (COdiff%) were: low BMI, no diabetes, low baseline CO and severity of mitral or tricuspid regurgitation (r=0.53 or =0.43, both p<0.003). The strongest predictor of high PVR%diff was plasma potassium level. HF etiology, renal function, gender, RAAS inhibitor dose, renin or aldosterone levels were unelated to pulmonary vasoreactivity. Patients who dropped PVR<3 WU after PDE5i had higher plasma K+ (4.1±0.5 vs 4.5±0.3 mmol/L, p=0.01) than those who did not, similar relation was found for K+ and PDE5i-induced change of transpulmonary gradient. Conclusions: The largest increase in CO after PDE5i is observed in HFrEF patients with severe mitral (or tricuspid) regurgitation, probably due to chamber unloading and reduction of regurgitant SV. Pulmonary vasodilator response to PDE5i may be influenced by plasma potassium level. High-normal plasma potassium levels may preserve normal pulmonary vasoreactivity in HFrEF, perhaps by influencing K-channels in pulmonary vascular smooth muscle cells.


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