Irukandji syndrome is a condition that results from envenomation by certain box jellyfish. In rare instances the sting may result in cardiac arrest and death. The most common jellyfish involved is the Carukia barnesi, a species of Irukandji jellyfish. Those stung may experience severe or even excruciating pain. The syndrome was given its name in 1952 by Hugo Flecker, after the Aboriginal Irukandji people who live in Palm Cove, north of Cairns, Queensland, Australia, where stings are common. Signs and symptoms
Most stings occur during the summer wet season in October–May in North Queensland, with different seasonal patterns elsewhere. Because the jellyfish are very small, the venom is only injected through the tips of the nematocysts (the cnidocysts) rather than the entire lengths; as a result the sting may barely be noticed at first. It has been described as feeling like little more than a mosquito bite. The symptoms, however, gradually become apparent and then more and more intense in the subsequent 5 to 120 minutes (30 minutes on average). Irukandji syndrome includes an array of systemic symptoms, including severe headache, backache, muscle pains, chest and abdominal pain, nausea and vomiting, sweating, anxiety, hypertension, tachycardia, and pulmonary edema. Symptoms generally improve in four to 30 hours, but may take up to two weeks to resolve completely. Toxicity
When properly treated, a single sting is almost never fatal; however, two people in Australia are believed to have died from Irukandji stings, which has greatly increased public awareness of Irukandji syndrome.
In the other enzymatic reaction, methylcobalamin supports the methionine synthase reaction, which is essential for normal metabolism of folate. The folate-cobalamin interaction is pivotal for normal synthesis of purines and pyrimidines and the transfer of the methyl group to cobalamin is essential for the adequate supply of tetrahydrofolate, the substrate for metabolic steps that require folate. In a state of vitamin B12 deficiency, the cell responds by redirecting folate metabolic pathways to supply increasing amounts of methyltetrahydrofolate. The resulting elevated concentrations of homocysteine and MMA are often found in patients with low serum vitamin B12 and can usually be lowered with successful vitamin B12 replacement therapy. However, elevated MMA and homocysteine concentrations may persist in patients with cobalamin concentrations between 200 and 350 pg/mL. Supplementation with vitamin B12 during conditions of deficiency restores the intracellular level of cobalamin and maintains a sufficient level of the two active coenzymes: methylcobalamin and deoxyadenosylcobalamin. See also
Methylcobalamin
Cyanocobalamin
Adenosylcobalamin
 Vitamin B12
Cobalamin biosynthesis
Nitric oxide

References
External links
Hydroxocobalamin in the ChEBI database
"Hydroxocobalamin". Drug Information Portal. U.S. National Library of Medicine.