Context of Methylene Cyclopropyl Glycine:
Methylene Cyclopropyl Glycine cause for worry in the children’s due to excessive consumption of Litchi.
Acute encephalitis syndrome (AES) in Bihar’s Muzaffarpur, Vaishali, Sheohar and East Champaran districts has so far claimed the lives of over 100 children and more than 400 remains serious admitted to various hospitals. Most of the deaths have been attributed to low blood sugar levels (hypoglycemia).
Acute Encephalitis Syndrome:
Meningitis caused by viruses or bacteria, encephalitis (mostly Japanese encephalitis) caused by a virus, encephalopathy, cerebral malaria, and scrub typhus caused by bacteria are collectively called acute encephalitis syndrome.
In the present case, the encephalopathy is associated with hypoglycemia and hence called hypoglycaemic encephalopathy.
Difference between hypoglycaemic encephalopathy and encaphilitis:
- Fever onsets after brain dysfunction begin and not necessary.
- The blood sugar level is low
- Children go to bed without any illness but manifest symptoms such as vomiting, convulsion, and semi-consciousness early the next morning.
- No increase in white blood cells is seen in cerebrospinal fluid as there is no inflammation in the brain.
- The blood sugar level is normal.
- Fever on the first day is one of the symptoms of encephalitis before brain dysfunction begins.
- There are more white blood cells per unit volume of cerebrospinal fluid, which is a reflection of inflammation in the brain.
Which is the associated cause?
In 2012-2013, a two-member team headed by virologist Dr. T. Jacob John suspected, and confirmed the next year, a toxin found in litchi fruit that was responsible for causing hypoglycaemic encephalopathy.
In 2017, an India-U.S. team confirmed the role of the toxin called methylene cyclopropyl glycine (MCPG).
Litchi does not cause any harm in well-nourished children, but only in undernourished children who had eaten litchi fruit the previous day and gone to bed on an empty stomach.
How it leads to death?
The toxin acts in two ways to harm the brain and even cause death. Because of the toxin, the body’s natural mechanism to correct low blood glucose level is prevented thus leading to a drop in fuel supply to the brain.
This leads to drowsiness, disorientation and even unconsciousness. When the toxin stops the fatty acid conversion into glucose midway, amino acids are released which are toxic to brain cells. The amino acids cause brain cells to swell resulting in brain edema. As a result, children may suffer from convulsions, deepening coma and even death.
Early morning, it is normal for blood sugar to dip after several hours of no food intake. Undernourished children who had gone to sleep without a meal at night develop hypoglycemia.
The brain needs normal levels of glucose in the blood. The liver is unable to supply the need. So the alternate pathway of glucose synthesis, called fatty acid oxidation, is turned on. That pathway is blocked by MCPG.
Why dangerous for Undernourished Children?
In well-nourished children, reserve glucose is stored as glycogen (glucose polysaccharide) in the liver. Whenever the glucose level goes down, glycogen is broken down into glucose and circulated in the blood for use. But undernourished children lack sufficient glycogen reserve that can be converted into glucose. Therefore, the natural mechanism in undernourished children is unable to correct the glucose level in the blood, leading to hypoglycemia.
Normally, when glycogen reserve in the liver is exhausted or is not sufficient, the body converts the fatty acid (non-carbohydrate energy source) into glucose. But in the presence of the litchi toxin, the conversion of fatty acid into glucose is stopped midway. As a result, no glucose is generated and the low blood glucose level is not corrected by the body.
- Undernourished children need not eat plenty of litchi fruit, ensuring they eat some food and not go to bed on an empty stomach.
A full and complete recovery can be achieved if children with hypoglycaemic encephalopathy are infused with 10% dextrose within four hours after the onset of symptoms.
If dextrose infusion is not started within four hours after the onset of symptoms, the brain cells may not recover but will die causing serious problems.
Infusing 10% dextrose not only restores blood sugar to a safe level but also stops the production of amino acid that is toxic to brain cells by shutting down the body’s attempt to convert the fatty acid into glucose.
Together with dextrose infusion, infusing 3% saline solution helps in reducing edema of the brain cells.
The concentration of ions in the fluid outside the brain cells becomes more than what is inside the cell; this causes the fluid from the cells to come out thus reducing edema and damage to brain cells.
Source: The Hindu