Pancreatitis aguda leve asociada a consumo de cocaína

Cerezo-Ruiz, Antonio; Rodríguez-Mancheño, Aquiles Lozano; Cortés-Rodríguez, Begoña; Rosa-Jiménez, F.

doi:10.1016/j.gastrohep.2012.01.016

Cited by 8 publications

(6 citation statements)

References 3 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The decrease in splanchnic flow would be the cause of the spectrum of gastrointestinal side effects, among which are intestinal ischemia, ischemic colitis, and hollow viscera perforation [14]. There are few reports of cocaine-induced pancreatitis in the literature [9, 10], some of which were associated with thrombotic microangiopathy as pathophysiologic mechanisms in 2 cases [11, 12]. …”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Pancreatitis Induced by Cocaine

Chapela

Paz

Ballestero

2017

Case Rep Gastroenterol

View full text Add to dashboard Cite

Pancreatitis is one of the commonest diseases of the gastrointestinal tract, characterized by epigastric pain of moderate to severe intensity, which radiates to the back, elevation of pancreatic lipase and amylase enzymes, and changes in pancreatic parenchyma in imaging methods. The most common etiologies vary, generally the most frequent being biliary lithiasis and alcohol, followed by hypertriglyceridemia. Among the less frequent causes is drug-induced pancreatitis. We report a case of acute pancreatitis caused by cocaine, rarely described in literature.

show abstract

Section: Discussionmentioning

confidence: 99%

“…The most common etiologies vary, depending on the population studied, the most frequent being biliary lithiasis and alcohol, followed by hypertriglyceridemia. Among the less frequent causes is drug-induced pancreatitis [5, 6, 7, 8], and in this subgroup, very few reports of cases induced by cocaine can be found [9, 10, 11, 12]. …”

Section: Introductionmentioning

confidence: 99%

Pancreatitis Induced by Cocaine

Chapela

Paz

Ballestero

2017

Case Rep Gastroenterol

View full text Add to dashboard Cite

show abstract

“…Gastrointestinal complications are uncommon and little documented. They include vasoconstriction and ischemia as the most common, which may result in gastrointestinal ulceration (most of times juxtapyloric, or within the first part of the duodenum [3]), infarction, perforation with intraperitoneal hemorrhage, pancreatitis, and rarer, retroperitoneal fibrosis and ischemic colitis [4][5][6][7][8][9]. As far as we know, this is the first case of acute liver failure and fulminant hepatitis caused by cocaine.…”

Section: Discussionmentioning

confidence: 99%

Cocaine-induced Fulminant Hepatitis

Roque¹,

Soy²,

Retto³

et al. 2017

J Gastrointest Dig Syst

View full text Add to dashboard Cite

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. Keywords: Fulminant hepatitis; Cocaine; Clinical case Case PresentationA 28-year-old man was admitted to our hospital on November 14, 2016 because of psychomotor agitation with fear delusions after ingesting 0.5 g of cocaine. He had no medical history of interest. As a toxic consumption history, he referred being an excigarette smoker of a pack a day, referred an ex-consumption of 10-12 alcohol units per day, and an ex-consumption of cannabis. Cocaine consumption started at 16 years old but at that time it had become sporadic. On examination in the emergency department, the patient presented a Glasgow Coma Score (GCS) of 12 with bilateral mydriasis, skin and mucous dryness, tachycardia and self-limiting temperature peak of 39.5°C. First blood test analysis showed a 51% hematocrit (43-49), 219 K/mcl platelets (150-450), 13.98 K/mcl leukocytosis (4.4-11.3), a prothrombin time (PT) of 86% (65-100), a 2.67 mg/dl creatinine (0.7-1.2), a 63 mg/dl urea (16.6-48.5), a 0.42 mg/dl total bilirubin (0.1-1.2), a 93 U/L aspartate aminotransferase (AST) (0-40), a 28 U/L alanine transaminase (ALT) (0-41), a 23 U/L gamma-glutamyltransferase (GGT) (0-60), a 97 U/L alkaline phosphatase (ALP) (40-129), a 863 U/L creatine kinase (CK) (0-190) and a high anion gap metabolic acidosis: pH 7.18, 38 mmHg pCO 2 , 39 mmHg pO 2 and 14.2 mmol/L bicarbonate. Troponin curve realized at 3 hours was flat. Toxics in urine were tested, being only positive for cocaine. Ethyleneglycol and methanol serum levels were normal and hepatitis A, B and C viruses were negative. Blood test control at 3 hours showed increasing levels of CK to 5.529 U/L and at 6 hours CK levels had arisen to 16.242 U/L, creatinine levels to 3.31 mg/dl and PT had decreased to 52%. At 24 hours, CK levels were 49.162 U/L, creatinine levels had increased to 4.79 mg/dl, platelets had fallen to 39 K/mcl and International Normalized Ratio (INR) had increased to 5.54. Brain computerized tomography (CT) scan was normal. Initial supportive treatment (such as serum therapy and bicarbonate) was initiated in the emergency room.First diagnostic approach was an acute renal failure AKIN III probably due to microangiopathy and rhabdomyolysis because of cocaine consumption. In the following hours, the patient began with a decreased level of consciousness and oligoanuria. In blood test controls, platelet levels dropped to 18 K/mcl, INR increased to 5.54, total bilirubin increased to 2.03 mg/dl, AST increased to 3.610 U/L, ALT increased to 3.287 U/L, CK levels were about 33.327 U/L and creatinine levels were still increasing to 6.44 mg/dl. A fulminant hepatic failure was diagnosed in addition to an acute renal failure, since previous abdominal ultrasound found in his clinical history showed n...

show abstract

“…Tradicionalmente se ha hecho énfasis sobre los riesgos cardiovasculares y neurológicos; no menos importante son las complicaciones gastrointestinales como ulceración, perforación gastrointestinal y colitis isquémica 17 .…”

Section: Conclusionesunclassified

Pancreatitis aguda asociada a cocaína, una complicación inusual. Serie de casos

Vásquez¹,

Mejía²,

Mejía

2023

MedUPB

View full text Add to dashboard Cite

La cocaína es una de las sustancias ilegales más consumidas y Colombia no es la excepción. Dentro de las sustancias ilegales es la segunda más consumida después del cannabis. Por su mecanismo mismo de acción, que produce aumento de aminas biógenas, se han asociado con la cocaína diferentes riesgos, tanto agudos como crónicos, y dentro de sus complicaciones se han descrito cambios comportamentales, compromiso cardiovascular y neurológico. La coingesta de cocaína y alcohol da lugar a un metabolito conocido como cocaetileno, que lleva a complicaciones cardiovasculares. Poco se ha descrito sobre el riesgo de la cocaína o la coingesta cocaína y alcohol, como un factor sumatorio, para la pancreatitis. Reportamos tres pacientes jóvenes consumidores del alcaloide que desarrollaron pancreatitis aguda, dos de ellos murieron. El objetivo de este reporte es sensibilizar a los trabajadores de la salud sobre otro riesgo para considerar en los pacientes consumidores de cocaína.

show abstract

Pancreatitis aguda leve asociada a consumo de cocaína

Cited by 8 publications

References 3 publications

Pancreatitis Induced by Cocaine

Pancreatitis Induced by Cocaine

Cocaine-induced Fulminant Hepatitis

Pancreatitis aguda asociada a cocaína, una complicación inusual. Serie de casos

Contact Info

Product

Resources

About