Hepato-renal toxicity-associated with methyl parathion exposure

Acute organophosphate (OP) poisoning is a significant cause of morbidity and mortality in the world.1 OPs lead to many well-defined complications such as cholinergic crisis, intermediate syndrome, besides these complications, they also cause very rare complication such as acute respiratory distress syndrome, acute kidney injury (AKI).2^,3 This is a rare case report of a patient who developed hepato-renal toxicity after methyl parathion (MP) exposure.

A 30 years old man carried out pesticide (Metacid, methyl parathion) spraying in his apple orchard on two consecutive days for about 4 h each day. During this activity he did not take the precaution to wear a face mask. On the third day the patient became unwell, experiencing a generalized crampy abdominal pain, this later became localized to both loins. There was a history of 5–6 episodes of vomiting. Patient had excessive salivary secretion and choking sensation in the throat. There was no history of diarrhea, excessive lacrimation, sweating, fasciculations, seizure or encephalopathy. Patient was hospitalized at local hospital where he was treated with injection atropine, intravenous fluids and other symptomatic therapy. Ultrasound abdomen was normal. The blood investigations done twice revealed deranged kidney functions (serum creatinine values of 2.9 and 3 mg/dL) and the patient was referred for nephrology consultation. He was hemodynamically stable and no abnormality was found on systemic examination. His investigations were suggestive of hepatitis along with AKI (Table 1). A depressed plasma cholinesterase levels suggested that exposure to methyl parathion was responsible for this hepato-renal dysfunction. The patient was advised supportive therapy and the hepato-renal dysfunctional resolved on follow-up.

Table 1. Time course of evolution of hepato-renal dysfunction.

Day	6	8	16	19	30	60
Hemoglobin (g/dL)	11.6	12.6	15.3		15.4	15
Urea (mg/dL)	59	56	32.4	26	24	22
Creatinine (mg/dL)	2.9	3	1.4	1.2	1.1	0.9
Aspartate aminotransferase  (IU/L)			59	87	67	27
Alanine amintransferase  (IU/L)			224	261	166	30
Alkaline phosphastase  (IU/L)			126	138	102	80
Bilirubin (mg/dL)			0.63	0.83	0.6	0.6
Albumin (g/dL)			4.5	4.9	3.5	4.2

Notes: The other blood investigations were: Total white blood cell (WBC) count 7800/mm³ with a normal differential, platelets 160 × 10³/mm³, sodium 143 meq/L, potassium 4.4 meq/L, chloride 103 meq/L, calcium 8.7 mg/dL, phosphorous 2.9 mg/dL, uric acid 7.2 mg/dL, protein 7.6 gm/dL, albumin 4.5 gm/dL, blood sugar 75 mg/dL, cholesterol 140 mg/dL, serum creatine phosphokinase 124 U/L (Normal range <190 U/L), lactate dehydrogenase 267 IU/L (normal 200–400 IU/L). Prothrombin time was 15.4 s and plasma (pseudo) cholinesterase 2.3 U/mL (normal range 5–12.5). Serology for hepatitis B and C were negative. Urinalysis showed a specific gravity 1.020, pH acidic, albumin trace, red blood cells occasional, WBCs 3–4 phf, urine sodium 25 mmol/L, urine culture was sterile and 24 h urine protein 120 mg.

The people who are at the greatest risk of being exposed to MP are farm workers, chemical sprayers and people who work in factories handling MP. The main route of human exposure is inhalation, but dermal contact and inadvertent ingestion can also be substantial. After exposure to MP a higher concentration of the chemical is found in the liver and the kidney as compared to that in the adipose tissue. Inhaled MP intoxication has been reported to cause pulmonary edema, cardiovascular lesions, AKI and liver lesions.4 Besides their inhibitory effects on acetylcholinesterase enzymes, OP compounds may induce oxidative stress leading to generation of free radicals and alterations in antioxidants status or reactive oxygen species (ROS) scavenging enzymes because cytochrome P450 enzymes and glutathione are involved in their metabolism. The lipophilic nature of OP facilitates their interaction with the cell membrane and leads to perturbation of the phospholipids bilayer structure.5

The case reported here developed toxic hepatitis along with AKI without evidence of rhabdomyolysis. OP compounds can cause liver damage due to hepatic necrosis and AKI from the proximal renal tubular damage with a benign and reversible clinical course. Hepatotoxicity results from the deleterious effects of OP on the cytochrome P450 system and mitochondria. Nephrotoxic effects of OPs are thought to be due generation of ROS leading to renal oxidative stress and toxicity.5 However, in some patients AKI may be due to rhabdomyolysis which is relatively frequent in severe OP poisoning.2^,3

Declaration of interest

The author declared no competing interests.