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- For the Australian film distribution company, see Antidote Films (Australia).
| Independent Film Company | |
| Headquarters | , |
|---|---|
| Owner | Jeff Levy-Hinte |
| Website | http://www.antidotefilms.com |
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Antidote Films, also known as Antidote International Films, Inc., is an independent filmproduction company founded by producerJeff Levy-Hinte based in the Hudson Square neighborhood of New York City. In 2008, Antidote completed several documentaries, including Soul Power and The Dungeon Masters, both of which premiered at the 2008 Toronto International Film Festival.
Antidote produced Roman Polanski: Wanted and Desired, a documentary directed by Marina Zenovich, which was nominated for the Grand Jury Prize and winner of the Documentary Editing Award at the 2008 Sundance Film Festival, the film will be released domestically by HBO and internationally through The Weinstein Company.[1][2][3][4]
Prior to this, Antidote produced several narrative films until The Last Winter, when the company shifted its focus to documentary.
Other Antidiote productions include the eco-horror thriller The Last Winter; The Hawk Is Dying, adapted from Harry Crews' novel and directed by Julian Goldberger; Mysterious Skin, directed by Greg Araki; and Thirteen, directed by Catherine Hardwicke.
In 2003, Daily Variety announced Antidote's plans for a film adaptation of the JT LeRoy novel 'Sarah', to be directed by Steven Shainberg.[5] According to The New York Times, when Shainberg learned that JT LeRoy was a literary persona and that Laura Albert was the actual author of Sarah, he decided 'to make a 'meta-film,' a triple-layered movie that would blend the novel with the lives of its real and purported authors in a project he took to calling 'Sarah Plus.'[6] The Times also reported that this new project 'required the rights to Laura Albert's story, rights that she in no uncertain terms refused to grant.'[7] In June 2007 Antidote sued Albert for fraud, claiming that a contract signed with JT LeRoy to make a feature film of Sarah was null and void.[8] After a Manhattan jury found Albert liable in monetary damages for the tort of fraud because she had signed her nom de plume to the movie contract, The New York Times noted that Jeffrey Levy-Hinte said, “if Ms. Albert, who never made a fortune from her literary works, could not afford to pay the judgment, he might have to consider laying claim to the rights to her past and future books.”[9] Levy-Hinte's chief lawyer insisted, 'Neither Jeff nor I want to ruin Laura Albert. We just want her to behave with a little more integrity.'[10] After an appeal, the damages awarded were reduced by settlement with Antidote in 2009, and Laura Albert retained the rights to her books and her life story.[11]
Film productions[edit]
- The Kids Are All Right (2010)
- Soul Power (2008)
- The Dungeon Masters (2008)
- Roman Polanski: Wanted and Desired (2008)
- Bomb It (2007)
- The Last Winter (2006)
- Mysterious Skin (2004)
- Chain (2004)
- Thirteen (2003)
- Laurel Canyon (2002)
- American Saint (2001)
- Ghosts of Attica (2001)
- Limon: A Life Beyond Words (2001)
- Wendigo (2001)
- High Art (1998)
References[edit]
- ^'ANTIDOTE'. antidotefilms.com. Retrieved 21 November 2013.
- ^'Antidote Films (I) [us]'. imdb.com. Retrieved 21 November 2013.
- ^'Antidote Films'. debate.org. Archived from the original on 29 July 2014. Retrieved 21 November 2013.
- ^'Antidote Films (I)'. metacritic.com. Retrieved 21 November 2013.
- ^Dunkley, Cathy. 'Antidote taps Louiso, Shainberg'. (September 5, 2003) Daily Variety. Retrieved 2016-9-1. https://www.highbeam.com/doc/1G1-109403371.htmlArchived 2016-10-08 at the Wayback Machine
- ^Feuer, Alan. 'In Writer's Trial, a Conflict Over Roles of Art and Money'. (June 22, 2007) New York Times. Retrieved 2016-9-1. https://query.nytimes.com/gst/fullpage.html?res=9900EFDF113FF931A[permanent dead link]
- ^Feuer, Alan. 'Judge Orders Author to Pay Film Company $350,000 in Legal Fees'. (August 1, 1007) New York Times. Retrieved 2016-9-1. https://www.nytimes.com/2007/08/01/nyregion/01leroy.html?_r=0
- ^Feuer, Alan. 'Writer Testifies About Source of Nom de Plume'. (June 20, 1007) New York Times. Retrieved 2016-9-1. https://www.nytimes.com/2007/06/20/nyregion/20cnd-writer.html?_r=0
- ^Feuer, Alan. 'Jury Finds JT LeRoy Was Fraud'. (June 23, 2007) New York Times. Retrieved 2016-9-1. https://www.nytimes.com/2007/06/23/nyregion/23writer.html?_r=0
- ^Feuer, Alan. 'Judge Orders Author to Pay Film Company $350,000 in Legal Fees'. (August 1, 1007) New York Times. Retrieved 2016-9-1. https://www.nytimes.com/2007/08/01/nyregion/01leroy.html?_r=0
- ^Hogan, Ron. 'Laura Albert Settles Film Company’s ‘Fraud’ Suit'. mediabistro.com. Retrieved 2016-9-1.http://www.mediabistro.com/galleycat/laura-albert-settles-film-companys-fraud-suit_b10026
External links[edit]
- Antidote Films on IMDb
By Rick Geller, MD, MPH, FACMT
Introduction
Ethylene glycol (C2H6O2
Ethylene glycol is an odorless, colorless, sweet-tasting syrupy substance with a molecular weight of 62.07, freezing point of -13°C and a boiling point of 197.6°C. It is most commonly encountered as automotive antifreeze.
Diethylene glycol behaves similarly to ethylene glycol in an overdose. The ethylene glycol molecule is incorporated into the structure of several ethers (e.g., ethylene glycol mono butyl ether and ethylene glycol mono ethyl ether), which may in very large amounts behave similarly to EG.
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Case presentation
A 27 year old male is found in a motel room, after telling an acquaintance that he was going to drink antifreeze. In the motel room is a glass with what looks like antifreeze. The patient says it is, and says that he drank one glass. He is brought to an ED in police custody. They are anxious to take him to jail.
In the ED he is alert and cooperative, oriented to person, place and time. PMH reveals multiple prior suicide attempts. Physical examination is unremarkable. (He has multiple old scars from apparent self-harm efforts.) Initial labs at 20:33 hours are Na 149, Cl 108, CO2 25, K 4.1, BUN 9 and Cr 1.1. Ethyl alcohol is 197 mg/dl. Urine tox screen is negative for drugs of abuse. Urine shows no crystals. Blood ethylene glycol level measurement will not be available for more than 24 hours. The hospital cannot do a measured serum osmolality on site. An EG sample is sent out.
In the absence of a stat EG level or a serum osmolality, the physician caring for the patient elects to follow the serum bicarbonate level as a possible marker of severity of ethylene glycol poisoning. His logic is that, since EG causes over time a profound metabolic acidosis, the absence of an acidosis over time would be presumptive evidence that no significant ingestion had occurred. The following laboratory values were obtained.
| Time | HCO3 |
|---|---|
| 22:33 | 25 |
| 00:20 | 23 |
| 01:10 | 24 |
| 01:55 | 22 |
| 03:42 | 23 |
| 06:48 | 27 |
| 06:48 Alcohol | 74 mg/dl |
By morning, no metabolic acidosis has developed and serum bicarbonate has actually risen. The ethylene glycol level is not back. The patient does not look sick and is released in the custody of police.
Within 24 hours the patient becomes acutely ill while in jail. He arrives back at the hospital profoundly acidotic and hypocalcemic. He suffers a cardiac arrest and cannot be resuscitated. After the patient died, the lab reports that the patient had a highly toxic ethylene glycol level drawn on the first visit.
Questions
- Why did this patient, who was poisoned with ethylene glycol, not become acutely ill until after he left the ED?
- Why was the severity of this intoxication not recognized on the first ED visit?
Epidemiology
A significant number of poisonings with ethylene glycol occur in California each year. In calendar year 2000, the CPCS consulted on 469 exposures to EG. These included 5 patients who later died and 38 who had either moderate or major effects attributed to EG. Minor effects were attributed to 62 exposures. Only 2 serious cases, and no deaths, occurred in persons under age 20.
On a national basis, almost all deaths observed each year are caused by intentional ingestions, with the significant majority of those being suicides.
Pathophysiology
As the parent compound, ethylene glycol produces altered mental status similar to ethyl alcohol. This effect rarely produces serious morbidity or death by itself.
Acute renal failure as well as a severe anion-gap metabolic acidosis results from the metabolism of ethylene glycol into at least 4 distinct metabolites. Alcohol dehydrogenase, the same first step enzyme responsible for the metabolism of methyl and ethyl alcohols, slowly catalyzes conversion of EG to glycoaldehyde. This is, in turn, rapidly converted by aldehyde dehydrogenase into glycolic acid. Glycolate is then metabolized into glyoxylate and finally oxalate.
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In addition to the metabolic acidosis and acute renal failure associated with glycolic acid and oxalic acid, metabolites of ethylene glycol cause cerebral and meningo-encephalitis, pulmonary edema and pneumonitis, as well as myocardial, hepatic and muscle pathology. Because calcium oxalate is a very low solubility product, significant hypocalcemia can result from precipitation of calcium by oxalic acid.
Clinical presentation
Some degree of altered mental status is usually the first sign of ethylene glycol intoxication. (Gastritis some times occurs early, as would symptoms caused by other substances in the case of a mixed ingestion). After a delay of 4 to 12 hours, metabolic acidosis gradually develops. If there simultaneously exists a blood ethyl alcohol level greater than 50-100 mg/dL, no metabolic acidosis will occur until the EtOH level falls. This is because ethanol ties up the rate limiting, first-step enzyme, alcohol dehydrogenase, and prevents metabolism of ethylene glycol into its toxic acid products. This is the basis for use of ethyl alcohol as an antidote.
Elevation of BUN and creatinine is usually not seen until at least 24 hours after ingestion (in the absence of an alcohol level above 50-100 mg/dL.) Other complications from products of toxic metabolism, such as brain damage, respiratory failure, and hepatitis are usually also delayed.
In the absence of a history of ethylene glycol ingestion, the most common presentation of EG intoxication is that of a severe anion gap metabolic acidosis in the context of altered mental status.
Diagnosis
A definitive diagnosis of EG poisoning is made with a serum ethylene glycol level. However, this is rarely immediately available, as almost all hospitals send this test to a reference lab, often to an out-of-state laboratory. We are aware of only 4 hospital laboratories in California that can perform this test on a 'stat' basis. As a result, a level drawn at a given hospital can take up to 8-9 milli-years (several days) to be reported.
Lack of prompt access to EG measurements represents a significant management problem for this poisoning. Because effective treatment must be instituted before blood EG levels can be obtained in most cases, physicians caring for a patient potentially poisoned with ethylene glycol must be skilled at detecting this intoxication indirectly, i.e., in the absence of a blood level. The California Poison Control System offers the assistance of its medical toxicologists for diagnostic help with these and other exposures.
An osmolal gap is frequently utilized in an attempt to detect osmotically active substances, including ethylene glycol. An osmolal gap is the difference between the measured serum osmolality (freezing point depression or vapor pressure may be used for EG), and the estimated serum osmolality calculated using the following formula:
Calculated serum osmolality = 2[Na] + [glucose ÷ 18] + [BUN ÷ 2.8] + [EtOH ÷ 4.6], where Na is in mEq/L and glucose, EtOH and BUN are in mg/dL.
Unfortunately, the presence of an osmolal gap is neither sensitive nor specific for EG. Worse, the negative predictive value is poor, which means that one can have a significant ethylene glycol poisoning with a small or even absent osmolal gap. This is because of two factors. Because ethylene glycol is a large molecule relative to, say, ethanol or methanol, it produces significantly less effect on osmolality per equal weighted dose than do the smaller alcohols. More importantly, if one looks for an osmolal gap after EG has been metabolized, there may no longer be a gap despite the presence of considerable amounts of ethylene glycol metabolites which are the significant poisons.
The presence of an anion gap may suggest significant ethylene glycol poisoning, but false-positive and false-negative results also occur. While one can miss an osmolal gap by looking for one too late in this poisoning, one can miss an anion gap by looking too early. The anion gap will remain normal for several hours until a sufficient amount of EG has been metabolized to toxic acids. Because bicarbonate begins to fall generally after 6 to 12 hours (later if EtOH is present), no anion gap may be present early in even potentially fatal cases. The reason that the bicarbonate failed to fall earlier in the case presented is that the presence of EtOH prevented metabolism of EG into organic acids during the period observed. Other causes of an elevated anion gap acidosis may mimic EG poisoning, such as diabetic ketoacidosis and alcoholic ketoacidosis.
In order to assess a possible EG exposure, CPCS recommends obtaining simultaneous measured and calculated osmolalities (for which electrolytes, BUN and EtOH will be needed), an ethylene glycol level, blood glucose, creatinine, calcium and arterial blood gases. Also occasionally useful is a urinalysis looking for calcium oxalate crystals. Since most antifreeze products contain fluorescein, a Wood's lamp exam of the oral cavity and urine may be helpful, although recent reports suggest a large number of false positive urine tests due to reflection from plastic urine containers or suspended material in the urine. Vengeance essential house vol 4 kickass.
Treatment
Treatment goals include:
- prevention of further metabolism of ethylene glycol via us of antidotes (ethyl alcohol or fomepizole)
- removal of ethylene glycol from the blood using hemodialysis
- correction of metabolic acidosis via administration of sodium bicarbonate and use of dialysis
- correction of hypocalcemia
- co-factor therapy to enhance elimination of toxic metabolites of EG, and
- aggressive supportive care including management of fluids, electrolytes, ventilation, and in severe cases, supportive therapy for acute renal failure.
The most difficult aspect of management of ethylene glycol exposures is that aggressive treatment must often be instituted before a blood level is available. The most common mistake made in management of these patients is in waiting for a blood EG level from the lab while the patient gets progressively worse without appropriate intervention.
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Either ethyl alcohol or fomepizole can be useful antidotes. Both inhibit alcohol dehydrogenase, the first enzyme necessary in the metabolism of ethylene glycol. EG remains in the blood as the parent compound, but causes only mild CNS depression. No further toxic metabolites can be formed during proper antidote administration. Keep in mind, though, that significant amounts of toxic metabolites may already have accumulated by the time antidotal therapy is initiated, and urgent hemodialysis is still necessary in these cases. Specific information on the proper use of alcohol or fomepizole can be obtained from the California Poison Control System.
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Hemodialysis accomplishes three immediate goals. It will correct metabolic acidosis, and reduce both ethylene glycol levels and the toxic EG metabolites. A reasonable endpoint for dialysis is correction of metabolic acidosis and reduction of EG level to less than 50 mg/dL. Generally speaking, four hours of hemodialysis is required to reduce the serum level by 50%. Multiple runs of dialysis are necessary when levels are high. For example, an ethylene glycol level of 300 mg/dL may require 3 four-hour runs to achieve reduction to less than 50 mg/dL. If advanced EG intoxication has occurred, acute renal failure may necessitate continuation of hemodialysis.
Metabolic acidosis should be aggressively corrected with sodium bicarbonate prior to dialysis. Extremely low serum bicarbonate levels and pCO2 may be found in these patients. Starting doses of 1-2 mEq/Kg are frequently necessary. In patients with very low pCO2, intubation and ventilation without either first correcting the low bicarbonate and/or subsequently hyperventilating the patient may result in a precipitous drop in pH.
Co-factor therapy with pyridoxine, 50 mg, IV or IM q 6 hours, and thiamine, 100 mg IM or (slow) IV q 6 hours, may enhance the elimination of toxic metabolites. This is generally of much less importance than the above treatments.
Hypocalcemia may be treated with either intravenous calcium chloride or calcium gluconate. Both are usually available as 10 ml vials of 10% solution. Keep in mind that the chloride salt yields approximately three times as much calcium per vial as the gluconate salt. Both should be injected into large bore veins only.
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Discussion of case questions
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This patient presented to the hospital with a high alcohol level, which served as an effective antidote. Although he was seriously poisoned, he did not develop signs of EG poisoning until many hours later, when his alcohol level had dropped. Similarly, using a falling bicarbonate level as indirect evidence of ethylene glycol poisoning will not work if sufficient 'blocking' levels of alcohol are present. The diagnosis of EG poisoning was not made on the first ED visit because the wrong diagnostic end point was observed. This case demonstrates how the long lab turnaround time for EG can negatively impact management.