Some preliminary laboratory experiments using the venom extracted from Malo maxima (the Broome Irukandji) on rat cardiovascular tissue in vitro has suggested that magnesium does in fact block many of the actions of this venom. Epidemiology
Reports of Irukandji syndrome have come from Australia, the United States (Hawaii and Florida), the French Antilles, Bonaire, the Caribbean, Timor Leste and Papua New Guinea. Cubozoan species other than Carukia barnesi are presumed to be responsible for envenomations outside Australia. History
In 1964 Jack Barnes confirmed the cause of the syndrome was a sting from a small box jellyfish: the Irukandji jellyfish, which can fire venom-filled stingers out of its body and into passing victims. To prove that the jellyfish was the cause of the syndrome, he captured one and deliberately stung himself, his 9-year-old son and a local lifeguard, then observed the resulting symptoms. Other cubozoans possibly can cause Irukandji syndrome; those positively identified include Carukia barnesi, Alatina mordens, Alatina alata, Malo maxima, Malo kingi, Carybdea xaymacana, Keesingia gigas, an as-yet unnamed "fire jelly", and another unnamed species. Culture and society
A 2005 Discovery Channel program, Killer Jellyfish, portrayed the severity of the pain from an Irukandji jellyfish sting when two Australian researchers (Jamie Seymour and Teresa Carrette) were stung. Another program aired on the Discovery Channel, Stings, Fangs and Spines, featured a 20-minute spot on Irukandji syndrome.
Blood and urine samples are collected for evaluation of kidney and liver function and determination of the presence of a monoclonal protein. Imaging studies such as echocardiography and an ultrasound of the abdomen will be performed. A CT scan, magnetic resonance imaging (MRI) or positron emission tomography (PET) may also be indicated. In patients with LCDD, a biopsy of the affected organ will show deposited light chains. A bone marrow biopsy will be done in order to rule out multiple myeloma. Treatment
Decreasing production of the organ-damaging light chains is the treatment goal. Options include chemotherapy using bortezomib, autologous stem cell transplantation, immunomodulatory drugs, and kidney transplant.There is no standard treatment for LCDD. High-dose melphalan in conjunction with autologous stem cell transplantation has been used in some patients. A regimen of bortezomib and dexamethasone has also been examined. Prognosis
The median time to progression to end stage renal disease is 2.7 years. After 5 years, about 37% of patients with LCDD are alive and do not have end stage renal disease. References
External links
National Institutes of Health Genetic and Rare Diseases Information Center
Emedicine