Hi Mair I haven't posted in a long time but you mention harm reduction practices and while I was going to start my own thread with this I felt it might have a better chance of getting out there if I just post i1t hear. It potential treatment for dnp overdose.
Apparently hemoperfusion along with certain glucocorticoids helped save the lives a quite a few young kids after a chemical plant mishap.
The very last potential treatment mentioned for a dnp overdose was the muscle relaxant dantrolene but the efficacy has since been questioned.
This is the first time I can remember hearing about a treatment working for multiple people with varying degrees of toxic exposure from terribly severe (two died) to less severe cases -
"In 2009, a serious incident occurred whereby 20 individuals were poisoned. Eleven, who were workers in a chemical factory, were directly exposed to 2,4-DNP (direct contact with skin and respiratory tract) with no protection at first; they only wore standard face shields after encountering the yellow powder. Another nine were their relatives, who indirectly contacted the poison while taking care of them; the contact area was limited to the forearms and hands. Of all the poisoned people, four aged 3–8 years were treated in the Children’s Hospital of Zhejiang Province and 16 patients were treated in our hospital. They were 12 males and 4 females [mean age (36.6±16.5) years, range 12–46 years], and three were less than 16 years old.
The duration from exposure to onset was 2–30 h (mean 17.1 h). Clinical manifestations included flushing of skin, intense thirst, profuse perspiration, hyperpyrexia, restlessness, malaise, dyspnea, tachycardia, tachypnea, and even convulsion, muscle rigor, and coma. The mean oral temperature was 38.3 °C (range 37.8–40.7 °C), and the mean pulse rate was 80 beats/min (range 40–144 beats/min) in 16 patients. Heavy perspiration was the first symptom indicated by all patients, followed by fever, skin redness, and fatigue. Most patients (87.5%, 14/16) had shortness of breath after movement and this symptom was relieved after resting in 62.5% (10/16), while 25.0% (4/16) were not relieved by standard supportive treatment. The contaminated parts of the skin had no feeling of pain or other sensory dysfunction in all patients.
These patients were diagnosed as having acute 2,4-DNP poisoning based on the toxic exposure history, hygienic investigation at the exposure site, clinical manifestations, laboratory examination, and poison identification made by the Zhejiang Disease Control Center and the Zhejiang Public Security Division. It was difficult to accurately estimate the exposure level of each person; we could only make a rough estimate of five mild and eleven severe cases from the exposure time, the type of contact, the degree of skin contamination, and clinical symptoms. However, two severe patients had notable hyperpyrexia with respective body temperatures of 40.7 and 39.8 °C, convulsions, muscle rigidity, and disturbance of consciousness. They were Babinski negative, and death suddenly occurred within 12 h after the onset of symptoms.
2.2. Treatment
Basic treatment was to remove and isolate the polluted clothing, and cut off the contaminated hair and nails. During the rescue, we also tried water, soap, and alcohol to remove the 2,4-DNP dust, without success. Because there is no antidote, all patients received physical cooling with ice bags, symptomatic and supportive treatments including electrocardiogram monitoring, oxygen therapy, and water, electrolyte, and acid-base balance maintaining by administering normal saline and Ringer’s solution. Antioxidants such as intravenous glutathione (GSH), and large doses of vitamins C and E were used during the treatment. Except the two deaths, nine severe cases were given 500 mg/d of methylprednisolone for 3–5 d. Thereafter the dose was decreased gradually and stopped at 8–10 d. As for the five cases with mild symptoms, a dose of 40–80 mg/d was given for 3 d. and was gradually reduced until ceasing at 6–7 d. Hemoperfusion (HP) was applied to the patients within 6 h of admission. Styrene/divinylbenzene copolymer (HA330 macroporous resin, Zhuhai Lizhu Biomedical Materials Co., Guangdong, China) processes a large capacity at a rapid rate, and has good blood compatibility. The five cases with mild symptoms were treated once a day (4–6 h) for three consecutive days, while the nine severe cases were treated once a day (6–8 h) for 6 d. In addition, one case who suffered neutropenia received recombination human granulocyte colony-stimulating factor treatment.
3. RESULTS
In this study, the skin of all 16 patients was dyed yellow, and in some severe cases was even black (Figs.
(Figs.11 and
and2).2). This may be due to the mixing and dissolving of yellow powder of 2,4-DNP with the skin and the subcutaneous adipose layer, after consultation with a dermatologist. A larger stained area of the skin with deeper color accompanied more severe symptoms of fever, sweating, chest tightness, and shortness of breath. The effects of physical cooling and symptomatic treatment were not satisfactory; the symptoms of fever and sweating were not relieved, and only ten cases which had less contact had relief from shortness of breath. The two severe patients died of cardiac arrest within 3 h after admission. The fever, sweating, and shortness of breath were relieved after the first HP. The temperatures of six cases became normal within 12 h after the first HP and fever did not return. The remaining eight patients’ temperatures were also reduced after the first HP, and rose again after about 8 h, although they were always lower than the highest value before HP. After the third HP, the temperature returned to normal.
On Day 3, after the temperatures of all patients were back to normal, no excessive sweating was present and no other evident symptoms were occurring. The contaminated areas of the skin gradually lightened and returned to normal approximately one week later. Hyperlipidemia, especially hypertriglyceridemia, occurred to different degrees in all 14 survivors 7 d after poisoning. The highest level of triglyceridaemia reached 23.5 mmol/L. The level reached a peak at 10–14 d post-exposure, declined afterward, and returned to normal after 3–4 weeks. This phenomenon had no clear correlation with the initial severity of poisoning. No lipid lowering agents were given, only the intake of fats was limited.
Hepatic injury to various degrees appeared in all 14 survivors. The features were presented with an increase of blood glutamic-pyruvic transaminase (GPT) or glutamic-oxalacetic transaminase (GOT) and an elevation of serum bilirubin level. The culmination of hepatic injury ensued within 10 to 20 d post-exposure and became normal about 10 d later. The level of methemoglobinemia was slightly elevated in all the cases at the early stage after poisoning. Furthermore, one case suffered neutropenia, with the lowest level of 1.9×109 cells/L. The myelogram showed a granulocyte series associated with a mild toxic change. This patient recovered after taking recombination human granulocyte colony-stimulating factor treatment for 7 d. The two events had no obvious correlation with the initial severity of poisoning.
All 14 survivors recovered and were discharged after four to six weeks of treatment. No evident poisoning sequelae were found at the three-month follow-up"
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Clinical features and treatment in patients with acute 2,4-dinitrophenol poisoning
Interesting that part of the treatment was intravenous administration of antioxidant glutathione as supplementation was speculated to be beneficial to dnp users in BB forums by bros for quite some time now.
Perhaps you can try and get the word out about this potential treatment?
The entire article is actually quite interesting I suggest all read it.
This is the first time I've e seen this study mentioned on a BB forum.
Something you will probably be interested in as well is that unfortunately the lethal dosage of dnp varies to extreme degrees feom person to person as one person died from ingesting 4mg. Not 400mg, not 4g but four milligrams of the stuff caused hyperthermia in someone.
Because of this fact it can never be recommended since we have no way of testing who may or may not be hyper-sensitive to it.
If that report has since been debunked then I apologize but I dont think it has. (It was a young female as I recall)
However I know people will still use it and if this treatment has any validity then maybe getting it out there can save lives. You seem to have a platform that may extend beyond Meso.
And in the interest of honesty and also human behavior I will also admit to possessing dnp and I will almost certainly try it at some point.
To challenge myself I have tried extreme fasting I once fasted for a little over 4 weeks (34 days) on only electrolyte water and sugarless drink mixes. I went from 260lbs to 211lbs.
Yes I'm a strange one.
Anyways what's up Meso? long time no speak!
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Clinical features and treatment in patients with acute 2,4-dinitrophenol poisoning
