AMong five cases of copper sulphate poisoning, increase in serum amylase and serum lipase manifested in three cases. Anyone likes to comment on these findings.
I have read some papers regarding this topic. The conclusions of the papers' authors are as follows:
1-Ingestion of copper sulphate is a rare form of poisoning. However, given the complications and high mortality rates, it's essential that clinicians are familiar with the management of such patients. The effects of poisoning can have deleterious effects on the upper digestive tract, kidneys, liver and blood (intravascular haemolysis, methaemoglobinaemia). We have observed that one of our patients had typical clinical features of acute pancreatitis (not a recognized complication) with an elevated serum amylase level. It may be worthwhile that physicians treating such patients assess the serum amylase level during the acute illness. We further recommend that restricting the availability of the pulverized powdered form of the compound in the open market might be an effective measure in preventing deliberate self harm by ingestion of copper sulphate.
J Occup Med Toxicol. 2011; 6: 34.
Published online 2011 Dec 19. doi: 10.1186/1745-6673-6-34
PMCID: PMC3269987
Complications and management of acute copper sulphate poisoning; a case discussion
2-Abdominal pain worsened, jaundice increased, and decreased urinary output were noted. Laboratory investigations (Table I) pointed towards diagnosis of pancreatitis.
Upper abdominal pain, vomiting, and jaundice in our patient were due to gastrointestinal toxicity, hepatic damage, and possibly pancreatitis. Cyanosis
developed due to methemogolobinemia. Renal failure was due to acute kidney injury (AKI) resulting from direct and indirect effects mentioned earlier. Diagnosis
of pancreatitis in our patient was questionable as derangement of pancreatic enzymes may be seen in AKI, and imaging was not performed for confirmation.
Table 1 in the paper lists the amylase levels during the hospitalization of the paitents.
Journal of Rawalpindi Medical College (JRMC); 2014;18(2):310-311
310
Case Report
Copper Sulfate Poisoning
Muhammad Khurram, Saba Samreen, Wajeeha Qayyum, Hamama Tul Bushra Khar
http://www.journalrmc.com/volumes/1422985871.pdf
3- Gastrointestinal toxicity
Acute-on-chronic zinc intoxication occurred in seven patients receiving total parenteral nutrition solutions which accidentally contained zinc sulphate 100 mg/L (Faintuch et al, 1978). Six patients developed increased amylase activities (peak activities 557-1850 Klein units; normal range 130-310) (Faintuch et al, 1978).
Another patient who received excess zinc sulphate (7.4 g) in error over 60 hours as part of a parenteral nutrition regime (Brocks et al, 1977) developed diarrhoea, vomiting and increased amylase activity with evidence of cardiovascular, hepatic and renal toxicity (see below) and died on the 47th day with bronchopneumonia. The peak serum zinc concentration was 41.8 mg/L.
I notice high amylase levels in homocysteinurea patients clinically presenting with N/V, abdominal pain characteristic of impending pancreatitis. Incidentally, they also have a relatively high copper levels with altered copper zinc ratios.
According to this study [https://www.gastrojournal.org/article/S0016-5085(82)80289-8/pdf] high copper concentration promotes release of amylase from pancreatic cells.
This makes me think if beside ‘sulphate toxicity’ in copper sulphate ingestion cases, could it be that copper is playing a role too. In my opinion, copper:Zinc ratio in general should be checked and a high ratio can be considered as a biomarker for pancreatitis risk in patients population who are more vulnerable to develop it. What are your thoughts on it?