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Tren/Injection cough explained (Backed by a clinical studies)
Over the years I have seen numerous threads containing questions and concerns in regards to "Tren cough" or "Post injection cough"..
As it seems to be a phenomenon in the Body Building community,and people could not come up with a definitive answer/reasonable explanation other than "Some of your compound must have entered the blood stream by means of nicking a vein ", other times I see people posting ideas and theories,failing to provide any conclusive evidence..
Well today I'm going to explain exactly what's taking place inside your body/respiratory system post injection..This may be old news for some,and knew news for others!
As it seems to be a phenomenon in the Body Building community,and people could not come up with a definitive answer/reasonable explanation other than "Some of your compound must have entered the blood stream by means of nicking a vein ", other times I see people posting ideas and theories,failing to provide any conclusive evidence..
Well today I'm going to explain exactly what's taking place inside your body/respiratory system post injection..This may be old news for some,and knew news for others!
I myself have experienced this "coughing/struggling to breath"on numerous occasions,and not just from Trenbolone,and believe it or not I've experienced this with Testosterone in the presence of a deep IM (intramuscular Injections) shot..I'll never forget the first time this happened, I swore I seen the light as my life flashed before my eyes,sheer panic is an understatement..(If that's what WaterBoarding is like,I'm ashamed to admit,I would most likely admit everything I knew)
Why does this take place? What is the causes and effects? Can this be avoided?
There's a few variables that can be taking place here in regards to the symptoms that one feels almost immediately post IM, ranging from trouble breathing,mild to violent coughing fits,eyes watering,mild to extreme flush feeling,feeling dizzy or faint,pressure in the chest,ext ext. This can last anywhere from 1-3 mins, and at times 5-10 mins (some cases have been reported lasting for days with random coughing fits)..
I often hear people advocate that it's the acetate ester,or most with Tren period..It's not entire true,but there is some truth behind that,I'll explain more later..
However,This can happen with any compound regardless of the ester..
I often hear people advocate that it's the acetate ester,or most with Tren period..It's not entire true,but there is some truth behind that,I'll explain more later..
However,This can happen with any compound regardless of the ester..
What is the cause and effects?
Like I stated prior,there's a few reasons you could experience this..I'll start with the leading one!
It's known as
"POME" Pulmonary oil microembolism..What is that? It's simply a case of acute respiratory distress and hypoxemia,following the accidental intravenous injection of an oil steroid solution (I'll enclose a study on this)..The oil solution is carried through the blood stream making is way to the lungs, in which the reaction of coughing is simply your bodies way of clearing it out!It's known as
Speaking of solution, Benzyl Benzoate (BB is found present in MOST UGL products) Is an other agent that's known for causing respiratory distress, which in this is temporary acute onset of "Anaphylaxis" (I'll enclose a study on this as well)..
Can this be avoid?
Not really because this can happen just from passing through a vein,but it's great practice to aspirate in areas that are prone to posses more veins and arteries!
Why does this seem to happen most when it pertains to Trenbolone?
Trenbolone increases the rise of prostaglandin production which can have great influence over bronchial constriction..
What are prostaglandins? There group of hormone-like lipid compounds/cells that are derived enzymatically from fatty acids that are precursors of Cyclooxygenase & Lipoxygenase..
Lipoxygenase has some dictation through pathways which is expressed through branches of bronchi, in the entire respiratory system..When the Cox-2 (lipo) levels increase it tends to have restriction or expulsion in the respiratory region..Thus,this is what dicates the "Tren cough"..
This tends to happen more with the Ace ester as it cause a faster metabolization and a faster rise with the prostaglandin levels!
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I included Some studies below that may help explain in great detail for those that wish to geek out on this topic!
Enjoy,
Vision
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Pulmonary Oil Microembolism (POME) and Anaphylaxis in Controlled Clinical Studies
Medical Editor: John P. Cunha, DO, FACOEP
Adverse events attributable to pulmonary oil microembolism and anaphylaxiswere reported in a small number of patients in controlled clinical trials. In the 84-week clinical trial of Aveed, 1 patient experienced a mild coughing fit lasting 10 minutes after his third injection, which was retrospectively attributed to POME. In another clinical trial of intramuscular testosterone undecanoate (1000 mg), a hypogonadal male patient experienced the urge to cough and respiratory distress at 1 minute after his tenth injection, which was also retrospectively attributed to POME.
During a review that involved adjudication of all cases meeting specific criteria, 9 POME events in 8 patients and 2 events of anaphylaxis among 3,556 patients treated with intramuscular testosterone undecanoate in 18 clinical trials were judged to have occurred.
Postmarketing Experience
The following adverse reactions have been identified during post-approval use of Aveed. Because the reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure.
Pulmonary Oil Microembolism (POME) and Anaphylaxis
Serious pulmonary oil microembolism (POME) reactions, involving cough, urge to cough, dyspnea, hyperhidrosis, throat tightening, chest pain, dizziness, and syncope, have been reported to occur during or immediately after the injection of intramuscular testosterone undecanoate 1000 mg (4 mL) in post-approval use outside the United States. The majority of these events lasted a few minutes and resolved with supportive measures; however, some lasted up to several hours and some required emergency care and/or hospitalization.
In addition to serious POME reactions, episodes of anaphylaxis, including life-threatening reactions, have also been reported to occur following the injection of intramuscular testosterone undecanoate in post-approval use outside of the United States.
Both serious POME reactions and anaphylaxis have been reported to occur after any injection of testosterone undecanoate during the course of therapy, including after the first dose.
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An other studyCase Reports in MedicineVolume 2012 (2012), Article ID 384054, 3 pages
http://dx.doi.org/10.1155/2012/384054
Anaphylaxis Triggered by Benzyl Benzoate
Abstract
We report the first case of an anaphylactic reaction to Reandron 1000 (depot testosterone undecanoate with a castor oil and benzyl benzoate vehicle). While considered to have a favourable safety profile, serious complications such as oil embolism and anaphylaxis can occur. In our patient, skin testing identified benzyl benzoate to be the trigger, with no reaction to castor oil or testosterone undecanoate components. As benzyl benzoate exists in multiple pharmaceuticals, foods, and cosmetics, individual components of pharmaceuticals should be tested when investigating drug allergies. Doctors should be alert to the potential for serious reactions to any of the components of Reandron 1000.1. Introduction
In men requiring testosterone therapy, depot testosterone undecanoate (TU) is a useful option. Compared to conventional testosterone esters, depot TU maintains adequate testosterone levels with less frequent injections and has better pharmacokinetics. Specifically, depot TU comparatively achieves higher trough serum testosterone concentrations without the wide variation between peak and trough levels between doses [1]. TU was initially developed in the 1970s as an oral testosterone replacement preparation, with a transdermal patch available in the 1990s [1]. In China, a depot TU preparation with a Chinese teaseed oil vehicle was manufactured for intramuscular use and found to have a long half-life of 21 days, longer than conventionally used testosterone esters [2, 3]. Depot TU is currently marketed with a castor oil and benzyl benzoate vehicle [4], as the castor oil affords an even longer half-life (33.9 days) than the original Chinese depot preparation [2,5].The long-term overall safety profile of depot TU has been generally favourable [6, 7]. Anaphylaxis to depot TU has not been specifically reported although hypersensitivity is listed as an uncommon adverse effect in the manufacturer’s product information [4]. Hypersensitivity reactions have not been described in cohorts who have used this preparation from 4 to 8 years.Here, we report the first documented case of anaphylaxis to Reandron 1000, a depot preparation of TU. This case is notable for the fact that the responsible agent was not the main active ingredient.2. Case Presentation
A 16-year-old boy with primary hypogonadism due to bilaterally absent testes, but otherwise without remarkable medical history, was converted from monthly intramuscular injections of testosterone esters (Sustanon, Schering-Plough) to depot testosterone undecanoate (Reandron 1000, Bayer) due to debilitating fluctuations in mood and energy levels. There was significant improvement in symptoms on the depot preparation.Within four minutes after his third dose was administered, he developed sweatiness, facial swelling, itching, urticaria, and sensation of throat obstruction with chest tightness. He was normotensive without tachycardia. He was treated with intravenous promethazine and hydrocortisone 250 mg and observed in an emergency department. Adrenaline (epinephrine) was not administered. The differential diagnosis of oil embolism was not pursued in view of the classical clinical features of anaphylaxis.A skin prick test found definite reaction to Reandron 1000 with a 10 × 8 mm wheal, but no reaction to testosterone esters gel or saline solution control. Testing of the components of Reandron 1000 found that non-skin-irritating concentrations of benzyl benzoate resulted in a 10 × 10 mm wheal and smaller peripheral lesions. Neither castor oil nor TU induced a response. His father was tested as a control and did not react to any of the components.Since discontinuation of Reandron 1000, the patient has used topical testosterone ester gel and crystalline testosterone pellets were implanted subcutaneously. There have been no further episodes of anaphylaxis.3. Discussion
We report a case of anaphylaxis to a depot preparation of TU comprising three components. Testing of each component identified benzyl benzoate as the likely trigger and demonstrates the importance of testing every component when investigating and managing medication-related anaphylaxis. Neither Reandron 1000 nor benzyl benzoate has been previously reported as a trigger for anaphylaxis.Excipients are the components of pharmaceuticals apart from the active substance. They fulfil a variety of different roles including colouring, flavouring, and alteration of the stability, solubility, durability, or permeability of the active ingredient. These agents are capable of inducing severe adverse drug reactions, particularly in the paediatric population [8]. Immunologically mediated hypersensitivity reactions can manifest as immediate (within 1 hour) onset of urticaria, angioedema, or anaphylaxis. Alternatively, there can be a delayed (>1 hour) onset of mostly cutaneous symptoms which, as in Stevens-Johnson syndrome, can still be severe [9]. In Reandron 1000, the excipient agents are benzyl benzoate and castor oil, while the active ingredient is TU.Benzyl benzoate (chemical formula C[SUB]14[/SUB]H[SUB]12[/SUB]O[SUB]2[/SUB]) is a colourless oily liquid which is rapidly metabolised by the body to benzoic acid and benzyl alcohol [10]. The agent is widely used as an additive in many different pharmaceutical and nonpharmaceutical products for human consumption. For instance, it is used as a preservative, a solvent in perfumes, a flavouring agent in foods and medications, and in insecticides and insect repellents [10, 11]. In oil-based vehicles for depot steroids, it lowers viscosity to improve ease of administration [12] and prevents crystallisation of steroids during storage [10, 13]. In testosterone preparations, it is also found in testosterone cypionate (Depo-Testosterone, Pharmacia) but not testosterone esters (Sustanon) or testosterone gel.In its role as a topical insecticide for scabies, benzyl benzoate is applied in a diluted solution with a concentration between 10% and 25%. It is known to cause skin irritation and contact dermatitis in this context, but hypersensitivity reactions have not been recorded in existing studies. No information is available as to whether or not benzyl benzoate possesses the intrinsic ability to induce mast cell degranulation. Databases for adverse reactions have also identified convulsions occurring with ingested benzyl benzoate [10, 14].Although not previously reported, hypersensitivity reactions to benzyl benzoate are unlikely to be isolated to our patient. Its presence in numerous consumer products raises the possibility of underreporting due to lack of awareness and failure to identify it as the trigger. Existing guidelines by the British Society for Allergy and Clinical Immunology [15] recommend skin prick testing if a compatible history of IgE-mediated drug hypersensitivity exists. In our patient, signs and symptoms of anaphylaxis to testosterone therapy and the clinical need for ongoing testosterone therapy warranted such investigation. Although intuitive and in common practice, there are no specific recommendations regarding testing of individual components of pharmaceutical preparations in either British or Australian [16] guidelines. In our patient, discovery of a reaction to a single component of the depot vehicle will better guide selection of testosterone replacement therapies. It will also allow him to remain vigilant to benzyl-benzoate-containing products.Castor oil has been used as a vehicle for steroid hormones for decades, prolonging their effect compared to equivalent aqueous suspensions by increasing storage in fatty depots in the body [12]. While there have been no reports of anaphylaxis to castor oil, sudden onset of respiratory symptoms can signify oil-related pulmonary microembolism after entry via the lymphatic or venous system. This complication is rare [17].In this case, our patient received supportive care for anaphylaxis with antihistamines and glucocorticoids. The immediate management of anaphylaxis is not guided by randomised placebo-controlled trials which are unethical due to the potential for rapid progression to fatality arising from delay of treatment. The use of adrenaline (epinephrine) is widespread and recommended in multiple guidelines as first-line therapy based upon results of uncontrolled studies [18]. However, recommendations for use of adjunctive agents such as antihistamines and glucocorticoids are more heterogeneous. The use of H1-antagonists as a first-line agent is not recommended, as they are of slow onset, fail to relieve bronchospasm or gastrointestinal symptoms, and have anticholinergic effects which can induce drowsiness and confuse the clinical picture in a critically ill patient [19]. Similarly, glucocorticoids do not acutely relieve symptoms but prevent prolonged or biphasic symptoms of anaphylaxis [18]. These agents are best used in conjunction with, rather than in place of adrenaline.4. Conclusion
Anaphylactic reactions can occur to the benzyl benzoate component of depot preparations of testosterone undecanoate. It is potentially unrecognised or can be misdiagnosed as oil embolism and underreported. Testing for reactions to the individual components of pharmaceutical agents may prevent inappropriate exclusion of all available preparations of a particular agent if it is the vehicle rather than the active ingredient that is causative. Similarly, it will alert the patient to risk of hypersensitivity to unrelated products which may utilise the same agent. Doctors should remain aware of the potential for serious reactions to testosterone replacement therapies and should consider appropriate further investigation.Conflict of Interests
There is no conflict of interests that could be perceived as prejudicing the impartiality of the research reported. This research did not receive any specific grant from any funding agency in the public, commercial, or not-for-profit
sector.
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And last but not least!
Can Respir J. 2011 Jul-Aug; 18(4): e59–e61.
Michael Russell, MD PhD,1Aric Storck, MD,2 and Martha Ainslie, MD3
Acute respiratory distress following intravenous injection of an oil-steroid solution
[FONT="]Abstract
A case of acute respiratory distress and hypoxemia following accidental intravenous injection of an oil-steroid solution in a body builder is presented. Chest roentography at the time of presentation showed diffuse bilateral opacities, and computed tomography revealed predominantly peripheral ground-glass opacifications. The patient’s symptoms gradually improved over 48 h and imaging of the chest was unremarkable one week later. The pathophysiology, diagnosis and treatment of this rare but potentially life-threatening complication of intravenous oil injection are discussed.
Keywords: Pulmonary oil embolism, Steroid-oil injection
[FONT="]CASE PRESENTATION
A previously healthy 21-year-old man presented to the emergency department with acute onset dyspnea approximately 24 h following self-administered injection of an oil-steroid solution into his right buttock. The patient admitted to a single injection of a mixture of anabolic steroids suspended in oil, including commercially available preparations of testosterone enanthate and boldenone undecylenate. At the time of injection, he aspirated blood before administering the anabolic steroid, then repositioned but did not withdraw the needle. Within 1 min of injection, he developed transient shortness of breath that resolved initially but subsequently recurred and progressed to the point he presented to the emergency department 24 h later.
Medical history was significant for a previous emergency room assessment for acute respiratory distress, at which time pulmonary embolus was ruled out with a computed tomography (CT)-pulmonary embolism protocol. The patient was a nonsmoker, and denied recreational or intravenous drug use, significant alcohol use or any recent unusual inhalation exposures. He was self-employed as a tattoo and graphic design artist. The patient indicated that he had been sexually active with multiple partners over the previous year and had tested negative for both HIV and hepatitis C virus within the year before presentation.
The patient was hypoxic at rest, with oxygen saturations of 88% to 92% on peripheral pulse oximetry, and experienced significant desaturation to 82% to 85% with minimal activity. Heart rate, blood pressure and temperature were within normal limits. A physical examination revealed a fit man of average height and weight with a muscular build. The patient’s work of breathing was normal when stationary, but he rapidly became tachypneic on exertion. Lung auscultation revealed decreased breath sounds in the lower lung fields, with coarse crepitations and faint expiratory wheezing bilaterally, as well as a mildly prolonged expiratory phase. The remainder of the physical examination was unremarkable, notably including an absence of petechial rash and a grossly normal neurological examination.
Complete blood count plus differential, serum electrolytes and coagulation studies were within normal limits. D-dimer was elevated at 1.43 mg/L (upper limit of normal for reference range 0.51 mg/L). An electrocardiogram and urinalysis were unremarkable. Arterial blood drawn in the emergency department for gas analysis on room air demonstrated mild alkalosis (pH 7.45, calculated HCO3 25 mmol/L) and significant hypoxemia (arterial PO2 54 mmHg) with no evidence of hypercapnia (arterial PCO2 36 mmHg).
A chest x-ray taken at the time of initial assessment showed diffuse bilateral opacities (Figure 1A) and CT-pulmonary embolism of the thorax revealed multifocal regions of ground-glass opacification in a predominantly peripheral distribution throughout the lungs, but no evidence of pulmonary embolus (Figure 1B). The patient was admitted with a working diagnosis of pulmonary oil embolism and started on supplemental oxygen therapy at 2 L/min via nasal cannula.
Figure 1)A Chest radiograph showing diffuse opacification and increased vascular markings bilaterally. B Axial slice from computed tomography scan of the thorax demonstrating discrete ground-glass opacities bilaterally in a peripheral predominant distribution. ...
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[FONT="]DISCUSSION
The present report is the first to describe a case of pulmonary oil embolism following accidental intravascular injection of an oil-steroid solution. Acute lung injury and respiratory distress following intravascular introduction of oil is uncommon and has only been described in a small number of case reports (1–6). The pathophysiology underlying this phenomenon is postulated to be similar to that observed with the more extensively studied fat embolism syndrome (FES). Although the precise mechanism by which intravascularization of lipid emboli leads to the clinical features of FES has yet to be completely described, two theories have been proposed to explain the pulmonary dysfunction that occurs.
The mechanical theory postulates that fat emboli become physiologically lodged in the pulmonary capillaries, resulting in a ventilation-perfusion mismatch. Alternatively, the biochemical theory suggests that hormonal changes induce the systemic release of free fatty acids that are toxic to pneumocytes and the capillary endothelium of the lung, causing interstitial hemorrhage, edema and chemical pneumonitis (7). A symptom-free period precedes the development of clinical features, suggesting that the formation of toxic biochemicals is necessary for the clinical syndrome to develop. The mechanical and biochemical theories are not mutually exclusive and the clinical picture associated with pulmonary oil embolism likely results from several physiological processes.
FES is characterized by an initial asymptomatic latent period following introduction of lipid emboli into the systemic circulation, with subsequent development of ventilation-perfusion mismatch and toxic insult to pneumocytes and capillary endothelial cells resulting in dyspnea, tachypnea and hypoxia within 12 h to 72h after lipid embolization (7). The clinical presentation of FES is highly variable, ranging from asymptomatic to mild respiratory distress, hypoxia and non-productive cough, to the life-threatening triad of FES consisting of respiratory difficulty, petechial hemorrhages and neurological changes. The classic triad of FES is relatively uncommon, occurring in only 3% to 4% of cases despite the relatively high incidence of fat emboli following long bone fractures (greater than 90%) (8–10). The relatively low incidence of symptomatic events following intravascular introduction of lipid emboli suggests that the majority of cases of lipid embolization are not clinically relevant and go undetected.
Diagnosis of respiratory distress due to intravascular oil embolization can be challenging given the nonspecific nature of the symptoms and the latent period that often precedes symptom onset. Bronchoalveolar lavage to detect fat droplets in alveolar macrophages has been examined as a means to diagnose pulmonary fat emboli (11); however, the invasive nature of this procedure limits its utility as a diagnostic tool. Furthermore, no uniformly specific diagnostic imaging findings have been described to date. However, several case reports have identified patterns that may be suggestive of pulmonary lipid embolism in the appropriate clinical setting.
Kiyokawa et al (3) reported finding a combination of interstitial and alveolar patterns in a peripheral-predominant distribution on chest roentography in a case of acute lung injury following intentional injection of vegetable oil. The authors noted, however, that in most cases, chest x-ray findings are normal. Arakawa et al (12) reviewed chest roentograms and CT scans of six patients with pulmonary FES, and found focal areas of consolidation and/or ground-glass opacities with a predominantly upper lobe distribution as well as diffuse ground-glass opacification in the majority of cases. Moreover, Malagari et al (8) described bilateral ground-glass opacities with a predominantly peripheral distribution on high-resolution CT imaging of the thorax in mild pulmonary FES. Although not diagnostic of fat embolism, these imaging patterns – similar to those observed in the present case – may be suggestive in the setting of a compatible history and physical findings. Although specific features on high-resolution CT imaging of the chest were reported in this case series, the diagnostic value of this imaging pattern in the setting of a highly variable clinical picture remains to be determined.
Treatment options in cases of suspected or confirmed pulmonary oil embolism have been largely limited to supportive care in previous reports of intravenous lipid injection (1–6). Chin et al (13) reported the successful treatment and subsequent resolution of one case of idiopathic lipoid pneumonia with oral prednisolone. However, we were unable to locate any other reports or controlled studies to validate the use of steroids as a therapeutic option in the treatment of pulmonary lipid emboli. Therefore, the best treatment at this time remains early diagnosis and introduction of supportive care measures.
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[FONT="]CONCLUSION
In contrast to classic cases of FES, which are typically preceded by a symptom-free latent period, the patient described in the present report experienced an acute dyspneic reaction following introduction of oil into the blood stream. Similar reactions preceding the development of overt pulmonary lipiodol embolism have been described within 1 h of transcatheter arterial chemoembolization for hepatocellular carcinoma (14), suggesting that introduction of lipid droplets into the circulation can lead to rapid onset of respiratory distress. The injection of oil-steroid solution was unwitnessed in the present case and it was, therefore, difficult to discern whether the initial shortness of breath was truly respiratory difficulty due to arterial injection of oil or more a subjective experience related to the injection event itself.
The patient’s condition improved dramatically over the 36 h following initial presentation, and he was subsequently discharged home with a resting oxygen saturation of 93%, with desaturation to 90% on exertion. Chest x-rays at the time of discharge and one week later (Figure 1C) were both unremarkable, with no evidence of the bilateral changes seen on the initial roentograms.
The present case illustrates the need for timely diagnosis of pulmonary oil embolism and institution of supportive care measures to limit the morbidity and mortality associated with this rare, but potentially life-threatening condition. A high index of suspicion is necessary to make an accurate diagnosis given the variability of clinical presentation and the relative paucity of specific findings on diagnostic imaging and laboratory testing results. However, in the setting of acute respiratory distress and a mechanism of injury suspicious for vascular introduction of lipid emboli, chest roentography and CT can be useful in prompting physicians to consider the possibility of pulmonary oil embolus as a diagnosis.[/FONT][/FONT]
