Ethylene glycol poisoning

Leth, Peter Mygind; Gregersen, Markil

doi:10.1016/j.forsciint.2004.11.012

Cited by 98 publications

(79 citation statements)

References 24 publications

(18 reference statements)

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“…Evidences in previous studies have shown that, in response to 14 days period of (0.75 % v/v) ethylene glycol and (1.0 %) of ammonium chloride administration, young albino rats form urinary stones composed mainly of CaOx. Generally, in mammals and by enzymatic medium, ethylene glycol is decomposed in vivo into four organic acids; glycolaldehyde, glycolic acid, glycooxalique acid and oxalic acid beginning to hyperoxaluria which is the essential factor of urolithiasis formation, composed mainly of oxalate (Leth and Gregersen 2005). The enzyme disturbances are the cause factors for the idiopathic hyperoxaluria; while, the defective intestinal absorption of oxalate plays an vital role in enteric hyperoxaluria and leads to an increase in urinary oxalate concentration (Williams and Wandzilak 1989).…”

Section: Discussionmentioning

confidence: 99%

Nephroprotective and Diuretic Effect of Nigella Sativa L Seeds Oil on Lithiasic Wistar Rats

Benhelima¹,

Kaid-Omar²,

Hemida³

et al. 2016

AJTCAM

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Background and objective: The purpose of the current investigation was to study the influences, preventive and diuretic, of Nigella sativa L. seeds oil (NSSO) on calcium oxalate (CaOx) urolithiasis induced in Wistar male rats. Methodology: Seeds of Nigella sativa L. (N.S) were analysed for the evaluation of the concentration of oxalate and calcium. Nigella sativa L. seeds oil is obtained by hydrodistillation and HPTLC densitometric method was adopted to determine the amount of thymoquinone (TQ) present. Thirty male Wistar rats were divided into 5 groups (N=6). Group I, negative control, drank tap water. The other groups were II Positive control, III, IV and V received a treatment model inducing calcium oxalate urolithiasis for 28 days, using an aqueous solution involve 0.75% (EG) ethylene glycol and 1.0 % (AC) chloride ammonium. Rats in group III received in addition, 750 mg/kg Cystone from the beginning to the end of calculi induction experimentation. However, rats in Groups IV and V received (NSSO) at 5 ml/kg b.w by gavage on days 1 st to 28 th and 15 th to 28 th days, respectively. On days 0, 7, 14, 21 and 28, body weights were measured and the 24-hour urine samples were accumulated and analysed for biochemical elements. On the 28 th day, blood samples were collected for the estimation of serum parameters including creatinine, BUN and uric acid. All animals were sacrificed at the end of the experiment and the kidneys were detached for histopathological examination. Results: Administration of (NSSO) at 5 ml/kg body weight/dose/day for 28 days exerts a protective effect by reducing significantly (p <0.01) urinary and serum rates of calcium, phosphate and oxalate. This preventive diet could increase the volume of urine excreted. Conclusion:The nephroprotectrice and diuretic activity demonstrated by Nigella sativa L. gives a scientific basis that approves their traditional use like a remedy against urolithiasis.

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Section: Discussionmentioning

confidence: 99%

Nephroprotective and Diuretic Effect of Nigella Sativa L Seeds Oil on Lithiasic Wistar Rats

Benhelima¹,

Kaid-Omar²,

Hemida³

et al. 2016

AJTCAM

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“…Acute renal failure (ARF), myocardial dysfunction, neurologic function, and possibly pulmonary dysfunction result from deposition of oxalate with calcium in the kidney, heart, brain, and lung (8,13,37). Deposition of calcium oxalate in tissues also produces hypocalcemia, which depresses cardiac function and BP (13,37,80).…”

Section: Pathophysiologymentioning

confidence: 99%

“…Autopsy studies have revealed cerebral edema with calcium oxalate crystals in brain tissue at this point. Many of the deaths with ethylene intoxication have been reported to occur at this stage or shortly thereafter (37,80).…”

Section: Clinical Findingsmentioning

confidence: 99%

Toxic Alcohol Ingestions

Kraut¹,

Kurtz²

2008

Clinical Journal of the American Society of Nephrology

354

326

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Alcohol-related intoxications, including methanol, ethylene glycol, diethylene glycol, and propylene glycol, and alcoholic ketoacidosis can present with a high anion gap metabolic acidosis and increased serum osmolal gap, whereas isopropanol intoxication presents with hyperosmolality alone. The effects of these substances, except for isopropanol and possibly alcoholic ketoacidosis, are due to their metabolites, which can cause metabolic acidosis and cellular dysfunction. Accumulation of the alcohols in the blood can cause an increment in the osmolality, and accumulation of their metabolites can cause an increase in the anion gap and a decrease in serum bicarbonate concentration. The presence of both laboratory abnormalities concurrently is an important diagnostic clue, although either can be absent, depending on the time after exposure when blood is sampled. In addition to metabolic acidosis, acute renal failure and neurologic disease can occur in some of the intoxications. Dialysis to remove the unmetabolized alcohol and possibly the organic acid anion can be helpful in treatment of several of the alcohol-related intoxications. Administration of fomepizole or ethanol to inhibit alcohol dehydrogenase, a critical enzyme in metabolism of the alcohols, is beneficial in treatment of ethylene glycol and methanol intoxication and possibly diethylene glycol and propylene glycol intoxication. Given the potentially high morbidity and mortality of these intoxications, it is important for the clinician to have a high degree of suspicion for these disorders in cases of high anion gap metabolic acidosis, acute renal failure, or unexplained neurologic disease so that treatment can be initiated early. Table 1. Methanol, ethylene glycol, diethylene glycol, and propylene glycol intoxication and alcoholic ketoacidosis can produce hyperosmolality and metabolic acidosis (3-9). Isopropanol intoxication is usually associated with hyperosmolality alone (4,5). Importantly, several of these disorders can be fatal or produce irreversible tissue damage if they are not quickly recognized and treated appropriately (4 -15). Effect of Alcohols on Serum Osmolality and the Osmolal GapThe normal serum osmolality of 285 to 290 mOsm/L is due to sodium and its counterbalancing ions, bicarbonate and chloride, and glucose and urea. It can be calculated using the following equation:Serum osmolality (mOsm/L) ϭ 2 ϫ Na ϩ ϩ blood urea nitrogen (mg/dl)/2.8 ϩ glucose (mg/dl)/18. The serum osmolality measured by freezing point depression is usually within 10 mOsm/L of the calculated serum osmolality (16). Accumulation of low molecular weight substances in the serum (such as each of the alcohols) will raise the measured serum osmolality above that of the calculated serum osmolality, producing an osmolal gap (4,5,16 -18). The effect of each of the alcohols on serum osmolality is shown in Table 2. Methanol gives rise to the greatest increment in serum osmolality, followed by ethanol, isopropanol, ethylene glycol, propylene glycol, and diethylene glycol in that...

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“…The metabolites are cell toxins that cause central nervous system depression and cardiopulmonary and renal failure. Glycolic acid causes severe acidosis and oxalate is precipitated as calcium oxalate in the kidneys and other tissues (Leth and Gregersen, 2005).…”

Section: Introductionmentioning

confidence: 99%

Antilithiatic Influence of Spirulina on Ethylene Glycol-Induced Nephrolithiasis in Male Rats

Al-Attar¹

2010

American Journal of Biochemistry and Biotechnology

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Problem statement: Nephrolithiasis or renal stone disease remains a significant health problem in the adult population. Nephrolithiasis is a recurrent disorder prominent in males. It is significant medical and surgical problem because of incidence, recurrence and severe consequences. The present day medical management of nephrolithiasis is either costly or not without side effects. Invasive procedures for the treatment of nephrolithiasis may cause serious complications and they also impose a great load of costs to the healthcare system. Hence the search for antilithiatic drugs from natural sources has assumed greater importance. Approach: The aim of the present study was to evaluate the antilithiatic activity of spirulina supplementation on ethylene glycol induced nephrolithiasis in male rats. Healthy male Wistar rats were used in the present study and were divided randomly into 4 groups. Rats of 1st group were served as normal control. Rats of 2nd group were received 0.75% ethylene glycol in drinking water for three weeks and drinking tap water for the next three weeks. Rats of 3rd group were received 0.75% ethylene glycol in drinking water for three weeks and fed with spirulina solution (20 mg kg −1 body weight) for the next three weeks. Animals of 4th group were treated as 1st group for the first three weeks and fed with spirulina solution ate the same dose given to 3rd group for the last three weeks. After six weeks, serum levels of sodium, chloride, potassium, calcium, phosphorus, Blood Urea Nitrogen (BUN), uric acid, creatinine, Alanine aminotransferase (ALT), Aspartate aminotransferase (AST) were measured. Results: Statistically increases in the levels of sodium, chloride, BUN and ALT and a decrease in the level of calcium were noted in rats treated with ethylene glycol. Supplementation of spirulina for the last three weeks mostly recovered the rats from nephrolithiasis and completely from hepatotoxicity induced by ethylene glycol. Conclusion:This study suggested that spirulina is a safety and promising agent as a functional food for the management of nephrolithiasis induced by ethylene glycol and may be also by other chemical factors.

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Ethylene glycol poisoning

Cited by 98 publications

References 24 publications

Nephroprotective and Diuretic Effect of Nigella Sativa L Seeds Oil on Lithiasic Wistar Rats

Nephroprotective and Diuretic Effect of Nigella Sativa L Seeds Oil on Lithiasic Wistar Rats

Toxic Alcohol Ingestions

Antilithiatic Influence of Spirulina on Ethylene Glycol-Induced Nephrolithiasis in Male Rats

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