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Life threatening abdominal complications following cocaine abuse

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... Acute cocaine toxicity and longterm use can lead to life-threatening complications such as acute coronary syndrome, stroke, renal failure, and death [2]. Rarely, cocaine use can lead to gastrointestinal complications, including bowel ischemia, bowel perforation, and gastrointestinal hemorrhage [3]. ...
... Cocaine-induced bowel ischemia, perforation, and gastrointestinal hemorrhage have been described in scarce reports in the literature [3,[5][6][7][8]. Gastrointestinal complications resulting from cocaine abuse are rare, and the simultaneous occurrence of three such complications occurs even more infrequently. ...
... The pathophysiology of cocaine-induced ischemia is explained via the inhibition of norepinephrine reuptake at presynaptic terminals, leading to its collection at postsynaptic terminals [3]. This accumulation of catecholamines causes extensive vasoconstriction and ischemia and can lead to potentially lethal complications such as gastrointestinal perforation and ulceration, acute coronary syndromes, stroke, and thrombosis [3]. ...
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Cocaine use is rising in persons ≥50 years old and in black and socioeconomically disadvantaged communities. Cocaine-induced bowel ischemia and gastrointestinal injury are deadly findings that have been previously described in the literature. In this report, we present a case of small bowel ischemia, perforation, and upper gastrointestinal hemorrhage co-occurring in a 62-year-old incarcerated male with a 15-year history of cocaine use. The patient presented from jail, peritonitic in septic shock, and was promptly taken for emergent surgical exploration. He was found to have massive fecal peritonitis secondary to full-thickness ischemia and perforation of the jejunum and ileum. Immediately postoperatively, the patient developed a large volume of hemorrhage from multiple gastric and duodenal ulcers refractory to endoscopic intervention, ultimately requiring emergent embolization of the gastroduodenal artery. His course was further complicated by severe septic shock with a blunted response to catecholamine vasopressors. Early recognition and aggressive treatment of the gastrointestinal complications and the unique critical care challenges associated with cocaine use facilitated this patient's eventual full recovery.
... It has been documented to cause pulmonary complications such as pulmonary hypertension, pulmonary edema, pneumothorax, pneumomediastinum, pulmonary fibrosis, interstitial pneumonitis, and barotrauma. Other complications include retroperitoneal fibrosis, placental abruption, spontaneous abortion, and drug-induced psychosis [1][2][3][4]. The effects of cocaine on the gastrointestinal tract have been studied to a lesser extent, but studies have been limited to case reports and are rare. ...
... The effects of cocaine on the gastrointestinal tract have been studied to a lesser extent, but studies have been limited to case reports and are rare. There are documented cases of cocaine-induced gastric and duodenal ulcer perforation, pancreatitis, intestinal ischemia, mesenteric ischemia, ischemic colitis, as well as small and large bowel perforation [1][2][3][4][5][6][7]. To the best of our knowledge, there are no documented cases of cocaine-induced biliary tree lymphadenopathy causing obstructive jaundice; however, we strongly believe that a chemical the cocaine was adulterated with caused periportal lymphadenopathy, resulting in extrinsic compression of the patient's common bile duct. ...
... Cocaine can cause many different pathophysiological processes, including myocardial infarction, arrhythmias, pulmonary edema, pulmonary fibrosis, renal fibrosis, vasoconstriction, and intestinal ischemia [1][2][3][4]. Prior to being transported to the United States, cocaine is usually adulterated with various agents to increase profitability. These chemicals can include pharmacologically active and inactive chemicals such as sugars, starches, caffeine, phenacetin, lidocaine, benzocaine, acetaminophen, diltiazem, talcum powder, silica, calcium, quinine, cornstarch [3]. ...
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A sixty-two-year-old male with a history of extensive crack cocaine use and cholecystectomy presented to the emergency department with abdominal pain, nausea, vomiting, and urobilia. The physical exam revealed moderate epigastric tenderness without scleral icterus or jaundice. The patient's total bilirubin was elevated at 5.2, and his direct bilirubin was 3.7. A computed tomography angiogram (CTA) of the abdomen and pelvis subsequently showed a 3.1 x 2.8 cm mass compressing porta hepatis. A magnetic resonance cholangiopancreatography (MRCP) showed a 4.9 x 3.0 cm mass at the porta hepatis with corresponding biliary duct obstruction at that level. An endoscopic retrograde cholangiopancreatography (ERCP) was performed with stent placement and brush biopsy, which showed predominantly benign ductal epithelium with rare, atypical cells and stenosis of the proximal common bile duct suggestive of cholangiocarcinoma. Cytology was performed on the ductal fluid and was also negative. The carbohydrate antigen (CA) 19-9 level at that time was 94.3. We discussed the possibility of performing surgery as an inpatient, but the patient had various psychosocial issues, which prompted a psychiatric evaluation. He subsequently had an internal-external biliary drain placed. The patient was discharged with plans to obtain an endoscopic ultrasound as an outpatient. He was admitted and discharged several times over the span of six months for various issues. He received an endoscopic ultrasound (EUS) at a surrounding hospital. The results were inconclusive, and a repeat EUS was recommended. On the last admission to the hospital for abdominal pain, a CT scan showed no biliary tree obstruction, which was further confirmed with an MRCP. The internal-external biliary drain was removed without recurrence of hyperbilirubinemia. We suspect that the patient's initial symptoms and radiographic findings of a biliary tree mass may have been induced by extrinsic compression secondary to lymphadenopathy caused by an adulterant used in the cutting process of abused cocaine. This is a rare occurrence that has not been described in the literature. There are associations of cocaine use to pulmonary hilar lymphadenopathy, but not biliary lymphadenopathy. We strongly suspect that this patient's obstructive jaundice and extrinsic biliary tree obstruction were caused by underlying cocaine use.
... Although the complications of cocaine abuse are generally more likely to be cardiovascular or respiratory in nature than gastrointestinal [2], cocaine use can affect the entire gastrointestinal tract. Complications of the upper gastrointestinal tract (prepyloric or duodenal perforation) are more common than complications of the lower gastrointestinal tract (bowel ischemia, gangrene, or perforation) [2]. ...
... Although the complications of cocaine abuse are generally more likely to be cardiovascular or respiratory in nature than gastrointestinal [2], cocaine use can affect the entire gastrointestinal tract. Complications of the upper gastrointestinal tract (prepyloric or duodenal perforation) are more common than complications of the lower gastrointestinal tract (bowel ischemia, gangrene, or perforation) [2]. Although intestinal ischemia in cocaine users has been described in the literature, the distal ileum is the most commonly affected small bowel segment [3]. ...
... Although intestinal ischemia in cocaine users has been described in the literature, the distal ileum is the most commonly affected small bowel segment [3]. Bowel injury occurs via a pathophysiologic mechanism in which cocaine blocks the reuptake of norepinephrine, leading to arterial vasospasm or vasoconstriction and subsequent intestinal ischemia with mucosal and transmural necrosis [2]. Cocaine also has a direct toxicity on gut mucosa which further contributes to intestinal ischemia [1]. ...
Article
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This case highlights one of the infrequent complications of a commonly abused substance. A particular high index of suspicion of ischemic bowel is associated with cocaine abuse and should be included in the differential diagnosis of any young adult or middle-aged patient with abdominal pain and/or bloody diarrhea, particularly in the absence of other predisposing factors. To our knowledge, we report a rare case of ischemic small bowel associated with gangrene and pneumatosis intestinalis due to cocaine abuse.
... Cocaine enteropathy is a phenomenon that has been described in the medical literature along with other causes of reversible ischemic bowel disease [1][2][3]. However, there have been no reports of the imaging findings of cocaine-induced enteritis. ...
... Cocaine inhibits the reuptake of norepinephrine at presynaptic terminals, which subsequently leads to catecholamine accumulation at postsynaptic membranes [1]. Some of the effects of the catecholamine surge are tachycardia, vasoconstriction and hypertension. ...
... Vasoconstriction can lead to ischemia, which in turn involves multiple organ systems. Another mechanism of ischemia includes cocaine's vasoconstrictive effect on the arterial endothelium via changes in calcium channels [1]. ...
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While the clinical findings of cocaine-induced enteropathy from mesenteric ischemia are fairly well understood, there is a paucity of imaging description and detail in the literature that describes these findings. Imaging characteristics of cocaine-induced mesenteric ischemia on CT examination include bowel edema, mucosal enhancement, venous engorgement, mesenteric free fluid, and dilatation of the small bowel lumen. A thorough history, physical examination, and laboratory testing are critical for the diagnosis and prompt surgical intervention may be necessary. We present a case of cocaine-induced mesenteric ischemia in a 49 year old male which resolved within 24 hours of supportive therapy.
... Complications of the upper gastrointestinal tract (prepyloric or duodenal perforation 3,4 ) are more common than complications of the lower gastrointestinal tract (bowel ischemia, gangrene, or perforation 2 ), but ischemic colitis in cocaine users has been described. 2,[5][6][7][8] The distal ileum is the most commonly affected small bowel segment. 9 Bowel injury occurs via a pathophysiologic mechanism in which cocaine blocks the reuptake of norepinephrine, leading to arterial vasospasm or vasoconstriction and subsequent intestinal ischemia with mucosal and transmural necrosis. ...
... 9 Bowel injury occurs via a pathophysiologic mechanism in which cocaine blocks the reuptake of norepinephrine, leading to arterial vasospasm or vasoconstriction and subsequent intestinal ischemia with mucosal and transmural necrosis. 2,5,10 Ischemic injury occurs most often in the areas of the colon that are more vulnerable to a low-flow state, such as the watershed areas (the splenic flexure and rectosigmoid junction), which have limited collateral networks. Although any area of the colon can be affected, approximately 75% of cases involve the left colon, and approximately 25% of these involve the splenic flexure. ...
... 9 The interval between drug ingestion and the onset of symptoms varies from 1 hour to 2 days. 2,6 After intake of the drug, abusers commonly develop abdominal pain and tenderness, and bloody diarrhea may occur. 2 Most cases reported in the literature have involved ischemia of the small, rather than the large, bowel. 9 In this rare case of ischemic colitis in a 44-year-old man, the cause was recreational cocaine use. ...
... La etiología del síndrome se demuestra mediante exámenes toxicológicos. (2) Se ha descrito que el abuso de cocaína también causa complicaciones gastrointestinales, por isquemia (secundaria a espasmo vascular arterial -vasoconstricción) o trombosis vascular mesentérica y liberación de mediadores vasoactivos (3) . Del mismo modo, la isquemia puede afectar el páncreas ocasionando pancreatitis aguda (4) . ...
... Las consecuencias más graves del abuso de cocaína -independientemente de la dosis o vía de administración -, son complicaciones cardíacas (arritmias ventriculares, taquicardia, hipertensión sistémica, infarto agudo de miocardio, hipertrofia ventricular izquierda y/o síndrome coronario agudo) y cerebrovasculares (7) . Las complicaciones gástricas o pancreáticas no son frecuentes (3,4) . La forma anatomopatológica necrótica y hemorrágica de pancreatitis aguda es la más severa (8) . ...
Article
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Sudden death of an individual, in agitated delirium secondary to alcohol and cocaine acute intoxication, due to police restriction is presented. The autopsy findings included gastrointestinal and acute hemorrhagic pancreatitis, findings that raise questions about the cause of death and the combined effect of the toxic substances.
... Cocaine intoxication has been associated with a number of splenic [4][5][6][7] and gastrointestinal complications [8][9][10][11]. The patient in the present case had an atraumatic rupture of the spleen, a rare but reported complication following acute cocaine intoxication [2]. To the best of our knowledge, SBO associated with intravenous cocaine use has not been previously reported. ...
... Vasospasm and in situ thrombosis are suspected mechanisms. Whereas cocaine most often causes ischemia or perforation of the distal small bowel or colon, crack cocaine is associated with proximal small bowel perforations [8][9][10][11]. One retrospective series reported 50 patients with gastroduodenal perforations following acute crack cocaine abuse which represented 35.7% of the center's total gastroduodenal perforations requiring emergent surgery during the 4-year study period. SBO can be caused by oral ingestion of cocainefilled packets and condoms in drug smuggling [14]; however, as stated previously, SBO from cocaine's systemic toxicity has not been described prior to the present case. ...
... It has been reported that complications of the upper GT, such as duodenal perforation, happen more frequently than the lower GT complications (intestinal ischemia, gangrene and perforation). 8,9 Ischemic colitis (IC) is a medical condition in which inflammation and injury of the large intestine result from inadequate blood supply. Although uncommon in the general population, IC occurs with a greater frequency in the elderly and it is the most common form of bowel ischemia. ...
... 11,12 Generally, from drug assumption and symptom's onset there is an interval of time between 1 h and 2 days and the most common symptom is the abdominal pain, sometimes associated to a bloody diarrhea. 9 The majority of cases reported in the literature have shown ischemia of the small, than the large intestine. 13 The case reported here has been investigated following broadly accepted criteria for the investigation of numerous types of drug deaths, which include: a complete autopsy, a review of investigative findings and the identification and quantification of cocaine and/or its metabolites in biological samples collected during the autopsy 7,14 ; moreover the results Figure 1 The ascending and transverse colon show a large necrotic area, which involves the entire wall. of toxicological investigation in blood and brain samples have been considered following the interpretative value of the determination of cocaine and benzoylecgonine in blood and brain tissues and their correlation proposed by Spielher and Reed 15 and more recently reviewed by Bertol et al. 7 and the ratio of cocaine and benzoylecgonine concentrations in the blood and brain fell in the range of incidental finding rather than cocaine overdose, confirming that the correlation of blood and tissue cocaine concentrations with toxicity are not strictly related. ...
Article
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Snorting represents the most common route of administration for recreational powdered cocaine and it is considered less dangerous than other routes of intake (i.e.: intravenous; crack inhalation; etc.). A case of fulminant ischemic colitis with a fatal outcome, which occurred in a 19 year-old man after cocaine snorting, is presented. Although several cases are reported in the literature, no one has involved people aged less than 20 years. The young man showed unspecific symptoms, which began about 2 h after cocaine intake and did not allow physicians to make the diagnosis. This report may suggest doctors to treat young men, who have consumed cocaine, to take into consideration this possible complication also in young adults (teenagers) in the presence of unspecific symptoms.
... Cocaine acts by blocking reuptake of dopamine, epinephrine, and norepinephrine, leading to sympathetic nervous system stimulation and subsequent vasoconstriction. 1,16 Several other pathophysiologic mechanisms have also been proposed, including focal ischemia, 3,17 microthrombi, embolism, 12 delayed gastric emptying, 1,14 and an increase in intra-abdominal pressure due to chronic aerophagia. 9,18 A possible association with Helicobacter pylori infection has also recently been described. ...
... Cocaine acts by blocking reuptake of dopamine, epinephrine, and norepinephrine, leading to sympathetic nervous system stimulation and subsequent vasoconstriction. 1,16 Several other pathophysiologic mechanisms have also been proposed, including focal ischemia, 3,17 microthrombi, embolism, 12 delayed gastric emptying, 1,14 and an increase in intra-abdominal pressure due to chronic aerophagia. 9,18 A possible association with Helicobacter pylori infection has also recently been described. ...
... There may also be associated nausea and vomiting, as also emerged from this series. The onset of symptoms may be within an hour of drug abuse, but the presentation may be delayed by up to 48 h [28]. However, the abdominal examination of such a patient may pose difficulties in terms of both the diagnosis and treatment [18,28]. ...
... The onset of symptoms may be within an hour of drug abuse, but the presentation may be delayed by up to 48 h [28]. However, the abdominal examination of such a patient may pose difficulties in terms of both the diagnosis and treatment [18,28]. ...
Article
The purpose of this retrospective study was to describe the spectrum of medical and trauma complications associated with self-reported cocaine use. Patient databases of 23 emergency departments were searched for consultations related to cocaine use between January 2007 and December 2008. The population included 569 men (84.4%) and 105 women (15.6%): 505 (74.9%) patients were nondependent cocaine users and 169 (25.1%) were dependent cocaine users. The majority of patients (63.8%) used other drugs in combination with cocaine. Psychiatric symptoms were most frequently reported (60.9%), followed by cardiopulmonary (38.2%), gastrointestinal (22.5%), neurological (20.8%) and constitutional (17.2%) symptoms. Of psychiatric complaints, anxiety was the most common (31.5%). Sex-adjusted and age-adjusted odds ratio (OR) showed that palpitations were associated within 12 h of cocaine use [OR 2.05; 95% confidence interval (CI): 1.12-3.76], and psychotic symptoms (OR 3.05; 95% CI: 1.02-9.18) and hallucinations (OR 7.50; 95% CI: 1.12-50.31) were associated within more than 12 h of the use of cocaine. In a comparison of dependent and nondependent cocaine users, after adjusting for age and sex, cardiopulmonary symptoms (OR 1.56; 95% CI: 1.08-2.24) and paranoia (OR 2.14; 95% CI: 1.08-4.24) were associated with nondependent use of cocaine, and lethargy (OR 7.14; 95% CI: 1.55-35.56) was associated with dependent use of cocaine. The primary cause of trauma was unintentional injuries (32.4%). Sex-adjusted and age-adjusted OR showed a major risk for unintentional injuries with nondependent use of cocaine (OR 6.17; 95% CI: 1.38-42.29). The study shows that cocaine users experience diverse symptoms and may present with a wide range of physical findings.
... pone.0252853 cause abdominal complications [9], which may lead finally to splenic rupture [10][11][12], gastrointestinal perforation [13], ischemic colitis [14,15], acute renal failure [16,17], and hepatocellular necrosis [18]. Bibliographic survey led us, first of all, to macroscopic examination as well as calculation of relative weights of heart, liver, lung, brain, kidney, and spleen in rats administered cocaine. ...
Article
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The purpose of this study is to examine the effect of repeated cocaine administration on the whole body of rats. Rats (male, 6 weeks old, Sprague Dawley) were injected intraperitoneally with cocaine (50 mg/kg) once a day for 1, 3 or 7 days, and major organs (heart, liver, lung, brain, kidney, spleen) were excised from the sacrificed animals. During autopsy, we found a reduction in spleen size, but not other organs, in cocaine-administered rats as compared to control rats. This reduction became to be noticed at 3 day and easily perceived at 7 day. No marked changes were observed in other organs examined. H&E and EMG staining showed a tendency for a decrease in the number of red blood cells (RBCs) as well as an increase in collagen fibers in the spleens of rats treated repeatedly with cocaine. Transcriptome analysis indicated that repeated cocaine administration depletes RBCs from the spleen. Immunoblot analysis showed that cocaine increases the phosphorylation of myosin light chain (MYL) as well as the levels of transgelin, both of which are involved in the contraction of myofibrils. Collectively, these results show that repeated cocaine administration results in sustained contraction of the spleen, which leads to the release of RBCs from the spleen into circulation.
... A number of peripheral organs, such as the kidney, lung, and gastrointestinal tract, also contain significant dopamine concentrations in the nanomolar to micromolar range, which could significantly alter immune activity (Matt and Gaskill, 2019a). The effects of abused substances on peripheral dopamine concentrations are unknown, but abused drugs that increase CNS dopamine, such as cocaine, methamphetamine, and ethanol, are associated with significant inflammatory pathology in the periphery (Dimitrijevic et al., 2008;Lineberry and Bostwick, 2006;Tiwari et al., 2006). Thus, the effects of substance abuse could also drive inflammation in peripheral tissues through modulation of resident macrophages and other immune cells (Roy et al., 2011). ...
Article
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Induction of innate immune genes in the brain is thought to be a major factor in the development of addiction to substances of abuse. As the major component of the innate immune system in the brain, aberrant activation of myeloid cells such as macrophages and microglia due to substance use may mediate neuroinflammation and contribute to the development of addiction. All addictive drugs modulate the dopaminergic system and our previous studies have identified dopamine as a pro-inflammatory modulator of macrophage function. However, the mechanism that mediates this effect is currently unknown. Inflammatory activation of macrophages and induction of cytokine production is often mediated by the transcription factor NF-κB, and prior studies have shown that dopamine can modulate NF-κB activity in T-cells and other non-immune cell lines. Here we demonstrated that dopamine can activate NF-κB in primary human macrophages, resulting in the induction of its downstream targets including the NLRP3 inflammasome and the inflammatory cytokine IL-1β. These data also indicate that dopamine primes but does not activate the NLRP3 inflammasome in human macrophages. Activation of NF-κB was required for dopamine-mediated increases in IL-1β, as an inhibitor of NF-κB was able to abrogate the effects of dopamine on production of these cytokines. Connecting an increase in extracellular dopamine to NF-κB activation and inflammation suggests specific intracellular targets that could be used to ameliorate the inflammatory impact of dopamine in neuroinflammatory conditions associated with myeloid cell activation such as addiction.
... There is little data on the effects of drugs of abuse on peripheral dopamine concentrations, although a mouse study using positron emission tomography (PET) imaging and quantitative whole-body autoradiography (QWBAR) with [18F]FDOPA indicates that use of ketamine, cocaine and methamphetamine increase dopamine levels in the gastrointestinal tract and kidney (Yeh et al. 2014). Many of the drugs that produce increases in CNS dopamine, such as cocaine, methamphetamine, and ethanol, are associated with significant pathology in peripheral organs with higher dopamine levels, such as the lung, gut, or kidney (Dimitrijevic et al. 2008;Lineberry and Bostwick 2006;Tiwari et al. 2006). Drug induced increases in the dopamine content of these tissues could disrupt homeostatic function and/or promote inflammation through dopamine modulation of resident macrophages and other immune cells. ...
Article
Full-text available
Dopamine is well recognized as a neurotransmitter in the brain, and regulates critical functions in a variety of peripheral systems. Growing research has also shown that dopamine acts as an important regulator of immune function. Many immune cells express dopamine receptors and other dopamine related proteins, enabling them to actively respond to dopamine and suggesting that dopaminergic immunoregulation is an important part of proper immune function. A detailed understanding of the physiological concentrations of dopamine in specific regions of the human body, particularly in peripheral systems, is critical to the development of hypotheses and experiments examining the effects of physiologically relevant dopamine concentrations on immune cells. Unfortunately, the dopamine concentrations to which these immune cells would be exposed in different anatomical regions are not clear. To address this issue, this comprehensive review details the current information regarding concentrations of dopamine found in both the central nervous system and in many regions of the periphery. In addition, we discuss the immune cells present in each region, and how these could interact with dopamine in each compartment described. Finally, the review briefly addresses how changes in these dopamine concentrations could influence immune cell dysfunction in several disease states including Parkinson’s disease, multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, as well as the collection of pathologies, cognitive and motor symptoms associated with HIV infection in the central nervous system, known as NeuroHIV. These data will improve our understanding of the interactions between the dopaminergic and immune systems during both homeostatic function and in disease, clarify the effects of existing dopaminergic drugs and promote the creation of new therapeutic strategies based on manipulating immune function through dopaminergic signaling. Graphical Abstract
... The exact pathophysiology of cocaine-induced gastro duodenal injury is unclear. Cocaine over stimulates the sympathetic nervous system, causing vasoconstriction-Induced ischemia and necrosis of the mucosal wall (Tiwari, Moghal et al., 2006). ...
... The exact pathophysiology of cocaine-induced gastro duodenal injury is unclear. Cocaine over stimulates the sympathetic nervous system, causing vasoconstriction-Induced ischemia and necrosis of the mucosal wall (Tiwari, Moghal et al., 2006). ...
... The exact pathophysiology of cocaine-induced gastro duodenal injury is unclear. Cocaine over stimulates the sympathetic nervous system, causing vasoconstriction-Induced ischemia and necrosis of the mucosal wall (Tiwari, Moghal et al., 2006). ...
Article
The main objective of the current study was to evaluate the prevalence of infectious diseases in drug addicts compared to normal individuals. The study was conducted in Biotechnology Department Bacha Khan University Charsadda, KPK, Pakistan. Total 80 drug addict's blood samples including smoker, alcoholic, cocaine and cannabis users (20 of each) were collected from age range 25-50 years from local area in EDTA tube and multiple diagnostic assay were performed. Results indicated that total of 22.5% HBs, 50% HCV, 17.5% CRP, 18.5% T.B and 65% H. pylori prevalence was found in each drug category. The results suggested an interaction on the additive scale between drugs use and HBV infection, and an interaction on the multiplicative scale with HCV infection. Additional studies are required to investigate the possible biological role of drugs in the development of infectious forms of HBs, HCV, CRP, T.B and H. Pylori and effect on expression of gene and DNA of addicted individuals. There is dire need of awareness in public about the lethal effects of use of these addictive drugs.
... Focal tissue ischemia can lead more commonly to ulcerations. [6,7] As the terminal artery, vasospasm of cystic artery induced by METH is easier to cause ischemia of gallbladder. [8] Other physiopathological mechanisms of ischemia include vascular thrombosis and aortic dissection. ...
Article
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Rationale: Methamphetamine (METH) abuse is increasing rapidly all over the world and becoming a significant public health concern in China. However, abdominal complications secondary to METH abuse are usually overlooked. We describe an unusual case of gangrenous cholecystitis and small intestinal ischemia due to METH abuse. Patient concerns: In this report, a 44-year-old male patient with abdominal pain and hematochezia has a history of crystal meth abuse. Diagnosis: The patient was diagnosed as septic shock, paralytic ileus, gangrenous cholecystitis, and small intestinal ischemia due to METH abuse based on computed tomography (CT) scan, endoscopy examination, laparotomy, and pathology. Interventions: Antishock treatment, broad-spectrum antibiotics, and exploratory laparotomy were given. Outcomes: The patient survived. Six months later, he tolerated oral intake and stopped using crystal METH. Lessons: Visceral ischemia should be considered if an adult patient with a history of METH abuse is accompanied by abdominal pain and hematochezia.
... Among those who had severe liver injury, profound hypotension, hyperpyrexia, rhabdomyolysis, renal failure and disseminated intravascular coagulation was also detected, rising mortality rates up to 45% [10,13]. Either way, the mortality associated with all gastrointestinal and hepatical complications can be as high as 21%, especially in the presence of gangrenous bowel [14,15]. Clinicians must be aware of cocaine induced gastrointestinal and hepatical symptomatology, in order to astutely manage the multiple varied and serious complications affiliated with this substance abuse. ...
Article
Cocaine abuse and intoxication is a global problem leading to many medical complications that can result in significant morbidity and mortality. We present the clinical case of a young man who presented with a fulminant hepatic failure, renal failure and a duodenal ulcer related to cocaine consumption.
... Ischemic injury of the bowel caused by drug abuse has been described after cocaine intoxication and has been attributed to arterial vasospasm or vasoconstric- tion 12 . Similarly to MDPV, cocaine acts by blocking the reuptake of dopamine, epinephrine, and norepinephrine, leading to sympathetic nervous system stimulation and subsequent vasoconstriction 12 . Although any area of the colon can be affected in ischemic colitis, approximately 75% of cases involve the descending colon 13 . ...
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Background: In the recent years, a new group of designer drugs, under the brand name of bath salts has emerged as a new trend. They are mainly b-ketone amphetamine analogs and are derivatives of cathinone, a monoamine alkaloid. They are abused for psychostimulant effects. Their primary ingredient 3,4-methylenedioxypyrovalerone (MDPV), has alerted authorities worldwide due to its severe physiological and behavioral toxicities. Description of Case:We present the case of a 47-year-old man with coma, seizures, multi-organ failure and ischemic colitis after intoxication with bath salts containing MDPV. After supportive care, he had a successful outcome. To our knowledge, this report is the first to describe ischemic colitis after MDPV intoxication. Clinicians need to be especially alert since MDPV is not detected by routine screens, and its overdose can be life-threatening. Conclusion: Ischemic colitis should be recognized as a potential complication of bath salts ingestion in order to prevent unnecessary interventions, such as diagnostic laparotomy, which could worsen patient's condition. Hippokratia 2015; 19 (4): 363-365.
... The prevalence of abuse of certain prescription medicines (POM) amongst "health-club" attendees has dramatically increased in the UK [1]. The non-therapeutic use of such "medicines" was previously considered to be restricted to the professional athlete or recreational bodybuilders. ...
Article
The effects of cocaine on microbiota have been scarcely explored. Here, we investigated the gut (GM) and oral (OM) microbiota composition of cocaine use disorder (CUD) patients and the effects of repetitive transcranial magnetic stimulation (rTMS). 16S rRNA sequencing was used to characterize GM and OM, whereas PICRUST2 assessed functional changes in microbial communities, and gas-chromatography was used to evaluate fecal short and medium chain fatty acids. CUD patients reported a significant decrease in alpha diversity and modification of the abundances of several taxa in both GM and OM. Furthermore, many predicted metabolic pathways were differentially expressed in CUD patients’ stool and saliva samples, as well as reduced levels of butyric acid that appear restored to normal amounts after rTMS treatment. In conclusion, CUD patients showed a profound dysbiotic fecal and oral microbiota composition and function and rTMS-induced cocaine abstinence determined the restoration of eubiotic microbiota.
Article
Objective: Over 19 million individuals globally have a cocaine use disorder, a significant public health crisis. Cocaine has also been associated with a pro-inflammatory state and recently with imbalances in the intestinal microbiota as compared to nonuse. The objective of this pilot study was to characterize the gut microbiota and plasma metabolites in people with HIV (PWH) who use cocaine compared with those who do not. Design: Cross-sectional study. Methods: A pilot study in PWH was conducted on 25 cocaine users and 25 cocaine nonusers from the Miami Adult Studies on HIV cohort. Stool samples and blood plasma were collected. Bacterial composition was characterized using 16S rRNA sequencing. Metabolomics in plasma were determined using gas and liquid chromatography/mass spectrometry. Results: The relative abundances of the Lachnopspira genus, Oscillospira genus, Bifidobacterium adolescentis species, and Euryarchaeota phylum were significantly higher in the cocaine- using PWH compared to cocaine-nonusing PWH. Cocaine-use was associated with higher levels of several metabolites: products of dopamine catabolism (3-methoxytyrosine and 3-methoxytyramine sulfate), phenylacetate, benzoate, butyrate, and butyrylglycine. Conclusions: Cocaine use was associated with higher abundances of taxa and metabolites known to be associated with pathogenic states that include gastrointestinal conditions. Understanding key intestinal bacterial functional pathways that are altered due to cocaine use in PWH will provide a better understanding of the relationships between the host intestinal microbiome and potentially provide novel treatments to improve health.
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Cocaine, an alkaloid, is an addictive drug and its abuse as a recreational drug is on the increasing side with its associated complications. Gastrointestinal complications, after cocaine abuse, are less known and need to be addressed since the abuse is on the rise and the existing evidence is scarce. We report a case of a 22-year-old male patient who presented with abdominal pain following a cocaine injection. On examination, signs of peritonitis were noted and laparotomy revealed a 2×1 cm perforation in the distal ileum. The unhealthy intestinal segment was resected and taken out as a double-barrel ileostomy. The patient had an episode of severe lower gastrointestinal bleeding on postoperative day 6. CT and colonoscopy revealed signs of ischaemic bowel and tissue biopsy showed oedematous, inflamed and haemorrhagic bowel mucosa. The patient was managed conservatively and is doing well under follow-up in a de-addiction centre.
Article
Cocaine use causes profound vasoconstriction leading to various systemic complications. Gastrointestinal complications such as mesenteric ischaemia are difficult to recognise and may result in serious consequences if not treated promptly. We report on the case of a 47-year-old man presenting with mesenteric ischaemia on a background of acute on chronic cocaine consumption, where diagnosis was not evident until second presentation. He underwent an emergency laparotomy with small bowel resection and jejunostomy formation and made a good recovery with eventual reversal surgery. The literature on cocaine-induced bowel ischaemia shows significant variability in presentation and outcome. Laboratory investigations are non-specific, and early recognition is vital. Given the increasing recreational use of cocaine in the UK, it is imperative to have a high clinical index of suspicion for mesenteric ischaemia in patients presenting with non-specific abdominal pain, and to ensure a detailed social history covering recreational drug use is not forgotten.
Chapter
Acute and chronic gastrointestinal (GI) problems are common in the setting of alcohol, tobacco, and prescription and recreational drug use. Excessive alcohol use is associated with injury to all parts of the gastrointestinal tract. Alcohol-related liver disease, alcohol-related pancreatitis, and gastrointestinal cancer are important causes of morbidity and mortality related to excessive alcohol use. Tobacco use is associated with gastroesophageal reflux, peptic ulceration, gastrointestinal cancer, and Crohn’s disease but appears to protect against ulcerative colitis. Opioids have important effects on gastrointestinal secretion and motility. Narcotic bowel syndrome may develop in the setting of escalating doses of opioid analgesia. Cannabis use is associated with both relief of nausea and vomiting associated with chemotherapy and adverse gastrointestinal effects. Cannabinoid hyperemesis syndrome should be considered in the setting of heavy cannabis use and recurrent vomiting. The body packing syndrome is sporadically encountered at hospitals near international transport hubs and can be challenging when encountered.
Chapter
Acute and chronic gastrointestinal manifestations are common in the setting of alcohol, tobacco, prescription, and recreational drug use. Excessive alcohol use is associated with injury to all parts of the gastrointestinal tract. Within the gastrointestinal tract, alcoholic liver disease, alcoholic pancreatitis, and gastrointestinal cancer are important causes of morbidity and mortality related to excessive alcohol use. Tobacco use is associated with gastroesophageal reflux, peptic ulceration, and gastrointestinal cancer but appears to protect against ulcerative colitis. Opioids have important effects on gastrointestinal secretion and motility. Narcotic bowel syndrome may develop in the setting of escalating doses of opioid analgesia. Cannabinoid hyperemesis syndrome should be considered in the setting of heavy cannabis use and recurrent vomiting. The body packing syndrome is rare but challenging when encountered.
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The aim of this study was the assessment of histological and hormonal changes induced in the European eel from environmental concentrations of cocaine. Silver eels were exposed to 20 ng L(-1) of cocaine during 50 days; at the same time, control, vehicle control and two post-exposure recovery groups (3 and 10 days) were made. The general morphology of the skin and the intestine, and the plasma levels of prolactin, cortisol and dopamine were evaluated. In the skin, cocaine decreased the number and size of mucous cells, increased the thickness of the epidermis and altered the club cells and the basal lamina. In the intestine, cocaine increased the thickness of the epithelium and the number of mucous cells and reactivated the structure of the intestine and of the intestinal musculature. Moreover, cocaine increased plasma prolactin, cortisol and dopamine levels. These results suggest that cocaine induced histological changes, directly and/or through the hormonal changes observed. Considering the complex life cycle of the eel, the changes induced by cocaine in the skin, the intestine and the endocrine system could threaten the ability of the eel to successfully migrate and reproduce. © 2015 John Wiley & Sons Ltd.
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Pathology represents a challenge for everybody involved in drug development. Even trained pathologists with expertise in toxicological pathology have to make the difficult prediction of whether any drug induced pathology in animals is likely to occur in humans. If so, are rodents or dogs likely to be more or less sensitive to the adverse effects of drugs than patients? Do the pathology findings completely preclude giving a new drug safety to humans? In order to aide researchers with these tough decisions, the author has compiled this valuable reference.
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The new 4th edition of Histopathology of Preclinical Toxicity Studies is now completely in full color and continues to describe the pathology found in drug safety studies in laboratory animals with an evidence-based discussion of the relevance of these findings to the clinical investigation of new drugs for humans. Organized according to organ systems, this revision features a thoroughly updated bibliography and discusses new drug-induced pathologies and applicable species comparisons to aid in the preclinical safety assessment of new medicines. This updated reference is essential for those involved in drug safety evaluation, including pathologists, toxicologists and pharmacologists working in corporate, government, academic and research settings. NEW TO THE FOURTH EDITION: *This edition is in full color and features nearly 200 high-quality images *Provides extended commentary on the relevance of pathological findings and features a fully updated bibliography containing sources for further reading *Includes new content coverage on the commonly used transgenic animal models that are used in safety assessment, specific tumor types induced by drugs in rodents, and new drug-induced pathologies and lesions.
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This case highlights one of the infrequent complications of a commonly abused substance. A particular high index of suspicion of ischemic bowel is associated with cocaine abuse and should be included in the differential diagnosis of any young adult or middle-aged patient with abdominal pain and/or bloody diarrhea, particularly in the absence of other predisposing factors. To our knowledge, we report a rare case of ischemic small bowel associated with gangrene and pneumatosis intestinalis due to cocaine abuse.
Article
The long use of ephedrine, amphetamines, cocaine, LSD and more recently 3,4-methylenedioxy-N-methylamphetamine (MDMA; "Ecstasy") allows us to predict with some confidence what cardiovascular risks are likely to be associated with novel psychoactive substances (NPS). Once the probably multiple biological activities of a compound are known it is possible to define the likely risks of cardiovascular toxicity. Agonists of 5-HT(2A) receptors or alpha-adrenoceptors may cause vasoconstriction and tissue ischemia. Drugs which have agonist affinity for 5-HT(2B) receptors will probably promote heart valve fibrosis leading to heart failure. Compounds that interfere with uptake of dopamine or 5-hydroxytryptamine (5-HT) are likely to also have effects on noradrenergic neurotransmission and lead to sympathomimetic effects on the heart and vasculature. Drugs that cause dopamine release, or inhibit uptake are likely to be addictive and lead to chronic use. Other drugs (particularly the so-called empathogens) are associated with weekly usage in social settings; over time such use can lead to cardiovascular harm. Defining which of these effects NPS have is an important element of predicting the harm they may cause and informing those appointed to introduce regulations to control them.
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Recreational cocaine use in the UK is steadily rising. This review summarises some of the common clinical manifestations of cocaine use which may be encountered by acute physicians and discusses the available treatment options.
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This article describes four patients with perforated gastroduodenal ulcers related to smoking "crack" cocaine. All patients came to the hospital with acute abdominal pain; only one patient had a history of ulcer disease. Only one patient had an elevated white blood cell count, and two patients had depressed white blood cell counts. In three patients, the x ray showed that pneumoperitoneum was present. Upon surgical exploration of the abdomen, all patients were found to have extensive peritoneal contamination. Operative repair consisted of omental patching with or without primary closure of the perforation. A history of cocaine smoking should be sought in patients with unexplained abdominal pain or pneumoperitoneum. In patients with acute abdominal pain and a history of smoking cocaine, a perforated gastroduodenal ulcer may be present, despite normal or low white blood cell counts and the lack of pneumoperitoneum on x-ray examination.
Article
It is well recognized that cocaine use can be associated with serious cardiovascular complications, including myocardial infarction. Several case reports have recently linked the use of cocaine with ischemic events of the small bowel and colon. We report a case of ischemic colitis complicated by perforation in a 47-yr-old diabetic man which occurred after recreational cocaine use. The older age of the patient and underlying diabetes mellitus were unique aspects of our case, compared with others reported in the literature. The patient's history of cocaine use was not initially identified. After we obtained a negative arteriogram result, we went back to the patient and the information was revealed. The literature regarding intestinal ischemia related to cocaine and other drugs/medications is reviewed. The abuse of cocaine should be considered in the differential diagnosis of acute intestinal vascular insufficiency syndromes.
Article
In summary, we report two cases of mesenteric ischemia following cocaine abuse in young women. In such cases it is always difficult to prove a direct causal relationship between the abuse of cocaine and mesenteric ischemia. Both our patients were relatively young (in their thirties) and did not have any history of atherosclerosis, and their urine toxicity screens were positive for the use of cocaine. Cocaine-related hospital visits are on the increase. Mesenteric ischemia should be considered in the differential diagnosis when evaluating a young patient with a history of cocaine abuse presenting with an acute abdomen.
Article
To determine if a cause-effect relationship exists between crack cocaine use and duodenal ulcer perforation (DUP). A retrospective study was conducted of all patients undergoing emergency surgical management for peptic ulcer disease over a 6-year period at a large inner-city municipal teaching hospital. The hospital records of 78 consecutive patients presenting with complications of peptic ulcer disease between April 1990 and April 1996 were reviewed. Group A (n = 24) consisted of patients with confirmation of crack cocaine usage within 8 hours of clinical presentation; group B (n = 54) consisted of patients with no antecedent history of crack cocaine use. Demographic data, timing of drug use, clinical presentation, laboratory and radiographic findings, toxicology screening, operative findings, and postoperative course were compared between the two groups. Both groups revealed a similar gender distribution, tobacco use, prior peptic ulcer symptoms, and laboratory findings. Group A patients were younger (t test, P = 0.01) and more likely to present with perforation, whereas patients in group B presented with a combination of symptoms (chi square, P = 0.03). Duodenal ulcer perforation was present in 75% of patients in group A compared with 46% of patients in group B (chi square, P = 0.04). Group B patients had a significantly longer hospital stay compared with those in group A (t test, P = 0.01). Both crack cocaine and alcohol are independent predictors of duodenal ulcer perforation. Patients with recent use of crack cocaine and/or alcohol are more likely to present with duodenal perforations. Although a temporal association between crack cocaine use and duodenal ulcer perforation was demonstrated, this study does not confirm a cause-effect relationship. A prospective cohort study is needed to clarify the pathogenesis of this potential cause-effect relationship.
Article
Gastrointestinal complications of cocaine abuse occur less frequently than those of the cardiovascular and nervous systems. The clinical history and pathologic findings of three patients with cocaine-induced mesenteric ischemia are described, and the mechanism of acute and chronic cocaine-induced mesenteric ischemia is discussed. The role of preoperative angiography in detecting occlusive arterial lesions so that arterial revascularization can be carried out is emphasized. Briefly, recent intravenous cocaine use in a 45-year-old man resulted in sharply demarcated small intestinal ischemia with perforation characterized by pseudomembranous enteritis. Histologic sections of the small-bowel resection showed intraluminal fibrin and intimal hyperplasia in rare submucosal arterioles. Two women, 29 and 35 years of age, both with a 2-year history of intravenous cocaine use, presented with acute abdominal pain and had angiographic documentation of occlusion of the celiac axis and the superior mesenteric arteries. Vascular bypasses were performed in both cases. Microscopic examination of both arteries and their branches revealed total obstruction by luminal thrombus with recanalization.
Article
This is a report of 50 consecutive patients with juxtapyloric perforations after smoking "crack" cocaine (cocaine base) at one urban public hospital. Although the exact causal relation between smoking crack cocaine and a subsequent juxtapyloric perforation has not been defined, surgical services in urban public hospitals now treat significant numbers of male addicts with such perforations. This report describes the patient set, presentation, and surgical management and suggests a possible role for Helicobacter pylori in contributing to these perforations. A retrospective chart review was performed, supplemented by data from the patient log in the department of surgery. From 1994 to 1998, 50 consecutive patients (48 men, 2 women) with a mean age of 37 had epigastric pain and signs of peritonitis a median of 2 to 4 hours (but up to 48 hours) after smoking crack cocaine. A history of chronic smoking of crack as well as chronic alcohol abuse was noted in all patients; four had a prior history of presumed ulcer disease in the upper gastrointestinal tract. Free air was present on an upright abdominal x-ray in 84% of patients, and all underwent operative management. A 3- to 5-mm juxtapyloric perforation, usually in the prepyloric area, was found in all patients. Omental patch closure was used in 49 patients and falciform ligament closure in 1. Two patients underwent parietal cell vagotomy as well. In the later period of the review, antral mucosal biopsies were performed through the juxtapyloric perforation in five patients. Urease testing was positive for infection with H. pyonri in four, and these patients were prescribed appropriate antimicrobial drugs. Juxtapyloric perforations after the smoking of crack cocaine occur in a largely male population of drug addicts who are 8 to 10 years younger than the patient group that historically has perforations in the pyloroduodenal area. These perforations are usually 3 to 5 mm in diameter, and an antral mucosal biopsy for subsequent urease testing should be performed if the location and size of the ulcer allow this to be done safely. Omental patch closure is appropriate therapy for patients without a history of prior ulcer disease; antimicrobial therapy and omeprazole are prescribed when H. pylori is present.
Article
Cocaine use can result in various gastrointestinal complications, including gastric ulcerations, retroperitoneal fibrosis, visceral infarction, intestinal ischemia, and gastrointestinal tract perforation. We report cocaine-associated colonic ischemia in three patients and review the literature. Including ours, 28 cases have been reported, with a mean patient age of 32.6 years (range, 23 to 47 years); 53.5% were men and 46.5% were women. The interval between drug ingestion and onset of symptoms varied from 1 hour to 2 days. Cocaine is a potentially life-threatening cause of ischemic colitis and should be included in the differential diagnosis of any young adult or middle-aged patient with abdominal pain and bloody diarrhea, especially in the absence of estrogen use or systemic disorders that can cause thromboembolic events, such as atrial fibrillation.
Article
Crack, the free-base form of cocaine, causes pulmonary, cardiac, obstetric, neurologic, musculoskeletal, and gastrointestinal complications. As the popularity for crack use increases, it follows that the number of cocaine-related emergency department (ED) visits, hospitalizations, and deaths should increase. We report 3 cases of patients arriving to the ED with acute onset of abdominal pain after smoking crack. These patients required surgical correction of their intestinal perforations. Although the exact pathophysiology of intestinal ischemia is not known, cocaine blocks the reuptake of norepinephrine, which leads to mesenteric vasoconstriction and focal tissue ischemia that may lead to perforation. The chronologic relationship of crack consumption to gastrointestinal perforation leads us to surmise that a possible crack-related ischemic event is the cause of perforation in these patients. Physicians examining patients with abdominal pain should be aware of the potential gastrointestinal complications of crack and consider bowel ischemia whenever a cocaine abuser presents with abdominal pain.
Article
Cocaine use is common and is associated with gastrointestinal complications that can present as a surgical abdomen. We report a case of a previously healthy 25-year-old man who presented to the Emergency Department with severe abdominal pain and vomiting after using IV cocaine. Exploratory celliotomy revealed massive free intraperitoneal (IP) clotted blood with no evidence of underlying pathology. This unusual case underscores the possibility of life-threatening hemorrhage in cocaine consumers. (C) 2002 Elsevier Science Inc.
Article
Cocaine use continues to be prevalent among all races and socioeconomic groups in the United States. Patients presenting to emergency departments after cocaine ingestion frequently present with a chief complaint of chest pain. Although acute myocardial infarction is perhaps the most concerning diagnosis in this setting, there are many other potential causes of chest pain after cocaine ingestion. This article reviews the pharmacology of cocaine, as well as the etiologies and treatment of cocaine-associated chest pain, with an emphasis on this drug's range of cardiovascular effects.
Histologic spectrum of arterial and arteriolar lesions in acute and chronic cocaine-induced mesenteric ischemia: report of three cases and literature review
  • Mp Hoang
  • El Lee
  • A Anand
Hoang MP, Lee EL, Anand A. Histologic spectrum of arterial and arteriolar lesions in acute and chronic cocaine-induced mesenteric ischemia: report of three cases and literature review. Am J Surg Pathol 1998;22:1404-10