[Predictive value of the product of plasma colchicine concentration and poisoning time for the prognosis of colchicine poisoning patients].

Objective: To investigate the predictive value of the product of first plasmacolchicine concentration and poisoning time for the prognosis of colchicine poisoning patients, and to provide a basis for early prognosis assessment. Methods: October 2021, patients with colchicine poisoning admitted in the First Affiliated Hospitol of Wenzhou Medical University from January 2017 to September 2021 were collected, including general information such as patient gender, age, oral colchicine dose, poisoning time, the first laboratory test index andplasma colchicine concentration after admission. The patients were divided into survival group and death group according to their prognosis. The differences in clinical indicators such as admission plasma colchicine concentration, blood routine, blood biochemistry, coagulation function, and blood gas analysis were compared between the two groups, and their predictive value for the prognosis of patients were analyzed. Results: A total of 23 patients with colchicine poisoning, aged 20-85 years, were included in this study, of which 15 cases (65.22%) survived and 8 cases (34.78%) died. The first plasma colchicine concentration at admision were 0.42-53.61 ng/ml. The plasma colchicine concentration and the concentration-time product were 10.08-2147.04 h·ng/ml.Compared with the survival group, the plasma colchicine concentration and the concentration-time product in the death group were significantly increased, and the differences were statistically significant (P<0.05). Univariate logistic regression analysis showed that first plasma concentration and poisoning time>132.48 h·ng/ml, high C-reactive protein, high D-dimer, high absolute value of BE were the risk factors for the prognosis of patients with colchicine poisoning (OR=12.000, 95%CI: 1.1181-128.836; OR=1.053, 95%CI: 1.009-1.098; OR=1.219, 95%CI: 1.039-1.429; OR=1.360, 95%CI: 1.1.044-1.773; P<0.05). High prothrombin time activity was protective factor affecting the prognosis of colchicine poisoning patients (OR=0.941, 95%CI: 0.892~0.993; P<0.05). ROC curve analysis showed that the areas under the curves of first plasma concentration and poisoning time, C-reactive protein, absolute value of BE, D-dimer for predicting the prognosis of patients with colchicine poisoning were 0.918, 0.888, 0.867, 0.837, respectively, and the areas under the curves of prothrombin time activityfor predicting the prognosis of patients with colchicine poisoning was 0.788 (P<0.05) . Conclusion: The product of the first plasma colchicine concentration at admission and poisoning time is closely related to the prognosis of patients with colchicine poisoning, it can be used as a predictor for early evaluation of the prognosis of poisoned patients.

[Accidental colchicine intoxication in a cross-breed dog]. / Akzidentelle Colchicinintoxikation bei einem Mischlingshund.

A 2-year old cross-breed dog presented due to acute vomiting and progressive lethargy following ingestion of the owner's anti-gout medication (colchicine, 0.35 mg/kg) 1-3 hours prior to presentation.The dog developed signs of all 3 stages of colchicine poisoning (gastrointestinal phase, multi-organ phase, recovery phase) and the clinical course was complicated by the presence of multi-organ dysfunction syndrome (MODS) and numerous negative prognostic factors.This case report describes the clinical and laboratory effects of colchicine poisoning and represents the first successful treatment of an accidental colchicine ingestion in a dog in Europe.

Accidental poisoning with autumn crocus (Colchicum autumnale): a case series.

INTRODUCTION: Colchicum autumnale (autumn crocus) is a plant that contains highly toxic alkaloid colchicine. The aim was to evaluate accidental C autumnale poisoning and assess serum troponin as a prognostic parameter. METHODS: In this study, we retrospectively included all adult patients with a history of accidental C autumnale ingestion and serum colchicine confirmation during the study period from 2000 to 2019. The medical files of enrolled patients were reviewed. Literature search of accidental ingestions of C autumnale was done. RESULTS: Over the study period of 20 years, 16 adult patients were admitted to the University Medical Centre Ljubljana due to acute colchicine poisoning after ingestion of C autumnale. They all mistakenly ingested C autumnale's leaves instead of Allium ursinum in the spring and had confirmed colchicine in serum by GC-MS or LC-MS/MS (15.5 µg/L (0.5-80 µg/L)). They developed vomiting and diarrhoea within 1-9 h after the meal. Vomiting within 2 h was associated with lethality (p=.04). Bone marrow suppression developed in 15 patients (94%). Acute myocardial injury with positive troponin I (>0.10 µg/L) developed in five patients; lethal cardiogenic shock with decreased cardiac output and hypotension occurred in four of these patients despite supportive therapy. Positive troponin I ultra (>0.10 µg/L) was associated with need for intensive support therapy (p=.01), decreased cardiac output (p=.01) and death (p=.01). The mortality was 4/16 (25%). On review, we found 58 cases; 95% cases accidently ingested leaves of C autumnale instead of A ursinum. Troponin I was reported in 3% cases. The lethality of this and reviewed cases was 35% (26/74). CONCLUSIONS: In unexplained gastroenterocolitis after ingestion of wild plants as a salad or spice in the spring, especially when wild garlic is mentioned, we should always consider C autumnale poisoning. Cardiogenic shock can be predicted by a positive serum troponin I measurement.

[A case of colchicine poisoning complicated with extra pontine myelinolysis].

To analyze the clinical presentation and the treatment process of one case of colchicine poisoning complicated with extra pontine myelinolysis and discuss its pathogenesis. Increasing the attention of hyponatremia caused by colchicine poisoning is of great significance for improving the prognosis and quality of life of patients.

[A successfully treated case of colchicine poisoning with lethal dose].

At present, there is no specific antidote for colchicine intoxication, and 0.8 mg/kg is its lethal dose. The prognosis of colchicine intoxication patients is closely related to the dosage, but the individual difference is very great. A 38-year-old man with colchicine poisoning was admitted to the Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, who had ingested 80 mg colchicine tablets (1.19 mg/kg) orally for 4 hours. He was immediately put on gastric lavage, enema, and catharsis. Continuous blood purification was performed for 34 hours and 22 minutes, with a combination of hemoperfusion (HP) and continuous veno-venous hemofiltration dialysis (CVVHDF). He also received a large dose of the glucocorticoid with 80 mg of methylprednisolone injected intravenously every 8 hours and organ function support. The patient was hospitalized for 2 weeks and discharged with improvement. The successful treatment of this case was reported for reference.

Acute Colchicine Poisoning Causes Endotoxemia via the Destruction of Intestinal Barrier Function: The Curative Effect of Endotoxin Prevention in a Murine Model.

BACKGROUND: Colchicine binds to intracellular tubulin and prevents mitosis. Colchicine is also used as an anti-inflammatory drug. Meanwhile, excess administration of medication or accidental ingestion of colchicine-containing plants can cause acute colchicine poisoning, which initially results in gastrointestinal effects that may be followed by multiorgan dysfunction. However, the mechanism of colchicine poisoning remains unclear, and there are no standard therapeutic strategies. AIMS: We focused on intestinal barrier function and attempted to reveal the underlying mechanism of colchicine poisoning using an animal model. METHODS: Colchicine was orally administered to C57Bl/6 mice. Then, we performed histopathological analysis, serum endotoxin assays, and intestinal permeability testing. Additionally, the LPS-TLR4 signaling inhibitor TAK-242 was intraperitoneally injected after colchicine administration to analyze the therapeutic effect. RESULTS: We observed villus height reduction and increased numbers of apoptotic cells in the gastrointestinal epithelium of colchicine-treated mice. Both intestinal permeability and serum endotoxin levels were higher in colchicine-treated mice than in control mice. Although colchicine-poisoned mice died within 25 h, those that also received TAK-242 treatment survived for more than 48 h. CONCLUSION: Colchicine disrupted intestinal barrier function and caused endotoxin shock. Therapeutic inhibition of LPS-TLR4 signaling might be beneficial for treating acute colchicine poisoning.

Survival of a dog with accidental colchicine overdose.

OBJECTIVE: To describe the treatment and clinical course of a dog accidentally prescribed 10 times the recommended dose of colchicine (0.3 mg/kg/d instead of 0.03 mg/kg/d). CASE SUMMARY: After glaucoma surgery, a 1-year-old male neutered Pomeranian weighing 6.8 kg was prescribed 1,000 µg colchicine twice a day per os. The dog presented to the emergency department after the first dose with vomiting and was treated as an outpatient. Two colchicine doses later, the dog represented with vomiting, ocular pain, and increased intraocular pressure. The dog's vital signs were normal, and the dog was admitted for rehydration, analgesia, and revision glaucoma surgery the next day. Two hours after revision surgery, the dog developed vomiting and diarrhea. Postoperatively, the dog was hypothermic (36.3°C), persistently hypertensive (227 mm Hg), and bradycardic (60/min). Biochemistry revealed metabolic acidosis and increased hepatic enzyme activities. Mannitol was administered for presumed cerebral edema. Later, the dog developed bradycardia due to second-degree atrioventricular heart block, which responded to atropine. Total hospitalization was 9 days. Treatment included IV fluids, IV lipid emulsion, N-acetylcysteine, activated charcoal, gastroprotectants, antiemetics, opioids, antimicrobials, and barrier nursing due to transient neutropenia. NEW OR UNIQUE INFORMATION PROVIDED: This is the first report to describe the successful treatment of a dog with colchicine overdose. The systemic effects were presumed to be secondary to colchicine toxicosis rather than diet, infection, or other drug reaction, and may have been compounded by a second anesthetic episode. Gastrointestinal signs, symptoms of cerebral edema, cardiac arrhythmias, and neutropenia were documented. One other report of colchicine overdose in a dog exists, and that patient was euthanized. This report demonstrates that complete recovery with intensive care is possible; however, the prognosis remains guarded.

Clinical outcomes after colchicine overdose: A case report.

RATIONALE: Colchicine can inhibit cell division and intracellular transport in affected organs by fixing intracellular tubulin and preventing its polymerization into microtubules. A lethal dose of colchicine is considered to be 0.8 mg/kg. The wide distribution of colchicine through 70% of the body following an overdose makes it difficult to eliminate. PATIENT CONCERNS: A 56-year-old man with a clear history of colchicine overdose was admitted to our hospital nearly 40 hours after taking 12 mg (0.17 mg/kg) of colchicine. He had a history of gout and chronic kidney disease. As the disease progressed, he showed most of the clinical manifestations and pathological features of colchicine overdose. DIAGNOSES AND INTERVENTIONS: Colchicine overdose was clear, with symptoms of multiple organ failure including primary gastrointestinal failure, bone marrow hematopoietic inhibition, rhabdomyolysis, cardiac damage, hepatocyte damage. The patient developed secondary septic shock, renal failure, circulatory failure, and respiratory failure. We performed continuous renal replacement therapy and gastric lavage, and administered norepinephrine, frozen plasma, proton-pump inhibitors, adenosylmethionine, antibiotics, granulocyte colony stimulating factor, and total parenteral nutrition. OUTCOMES: The patient rapidly developed complete hematopoietic function inhibition, gastrointestinal failure, and cardiac damage 32 hours after admission. Sustained severe infection and circulatory instability caused a progressive deterioration of respiratory function. Tracheal intubation was performed but the patient continued to deteriorate, and death occurred approximately 132 hours after admission. LESSONS: Excessive colchicine levels cause continuous organ damage due to extensive tissue distribution, eventually leading to multiple organ failure. Colchicine metabolism is delayed in patients with liver or kidney dysfunction, and even a low dose of colchicine may result in poisoning in these individuals. Early diagnosis and reduction of colchicine levels is critical to improve prognosis, and colchicine poisoning should be considered in patients with poor liver or kidney function even when the ingested dose is low.

Fatal colchicine intoxication by ingestion of Gloriosa superba tubers.

Gloriosa superba is an ornamental herb, wildly found in the tropics especially in the southern parts of India and Sri Lanka. All parts of the plants are toxic, especially the tuberous rhizomes in view of their high content of colchicines and its derivatives. We report a case of fatal ingestion of the tubers of G. superba, with an intention of deliberate self harm, leading to systemic coagulopathy and progressive multiple organ dysfunctions. The patient was managed with intralipid rescue therapy, plasmapheresis, haemodialysis and intensive care. The ease of availability makes plant poisons, a common method of deliberate self-harm in South India. This report reiterates the need for clinician's awareness of common toxidromes associated with plant poisons.

Rapid identification of Gloriosa superba and Colchicum autumnale by melting curve analysis: application to a suicide case involving massive ingestion of G. superba.

The plant species Gloriosa superba and Colchicum autumnale produce extremely poisonous colchicine as a major toxic metabolite. Almost all previous studies on colchicine poisoning have focused on drug analysis and clinical and pathological aspects. In this study, we developed a rapid, highly sensitive method to identify G. superba and C. autumnale. This method, which can distinguish between G. superba and C. autumnale using even minute amounts of plant material, is based on duplex real-time PCR in combination with melting curve analysis. To discriminate between the two genera of colchicine-containing plants, we designed new primer pairs targeting the region of the ycf15 gene, which is present in C. autumnale but not G. superba. By producing PCR amplicons with easily distinguishable melting temperatures, we were able to rapidly and accurately distinguish G. superba from C. autumnale. The new primer pairs generated no PCR amplicons from commercially available human DNA or various plant DNAs except for G. superba and C. autumnale. Sensitivity testing indicated that this assay can accurately detect less than 0.031 ng of DNA. Using our method in conjunction with colchicine drug analysis, we successfully identified G. superba in the stomach contents of a suicide victim who ingested massive quantities of a colchicine-containing plant. According to these results, duplex real-time PCR analysis is very appropriate for testing forensic samples, such as stomach contents harboring a variety of vegetables, and enables discrimination between G. superba and C. autumnale in forensic and emergency medical fields.

Two fatal intoxications by colchicine taken for saffron. Clinical, medico-legal and forensic toxicological implications.

Although fatal colchicine intoxications are rare and mostly related to suicidal intake or accidental overdose, other hypotheses should be considered when dealing with colchicine poisoning. We present a case of double, acute, and subacute, fatal colchicine intoxication in a married couple. The 70-year-old male victim suddenly died after vomiting and diarrhea. The next day his wife showed aggravating gastrointestinal symptoms and was hospitalized with a diagnosis of septic shock. A complete postmortem examination on the man was performed, together with histopathological analysis. Toxicological examination performed through liquid chromatography coupled to mass spectrometry revealed a colchicine blood peripheral concentration of 33 ng/mL. A few days after hospitalization, the woman showed a colchicine plasma concentration of 32 ng/mL. Despite veno-venous hemofiltration, she ultimately died of septic shock and multi-organ failure. Death scene investigation revealed that, a few days before the death of the male victim, the couple had collected wild saffron and had eaten a presumed saffron risotto. The integrated analysis of circumstantial, clinical, postmortem and toxicological data allowed to establish that the couple had died of a fatal accidental intoxication due to the ingestion of natural colchicine, mistaken for saffron. The death of the male was deemed caused by acute cardiovascular collapse induced by acute intoxication, while the female had suffered a subacute poisoning by antimitotic agent, resulting in immunosuppression and systemic infection. Toxicological analyses, promptly performed on the man for forensic purposes, directed the investigations and suggested the clinical diagnosis on the woman.

Epidemiology, toxicokinetics and biomarkers after self-poisoning with Gloriosa superba.

Introduction: Gloriosa superba is a flowering plant that contains colchicine. Deliberate self-poisoning with this plant in Sri Lanka is common and potentially fatal. The objective of this study was to describe the epidemiology, toxicokinetics and selected biomarkers in these patients. Materials and methods: The study consisted of three parts; epidemiologic and outcome data (n = 297), concentrations and toxicokinetics (n = 72), evaluation of urinary and serum biomarkers (n = 45). Plasma colchicine levels were measured by high-performance liquid chromatography (HPLC). We also measured serum biomarkers: creatinine (sCr), cystatin C (sCysC) and creatine kinase (CK), and urinary biomarkers: creatinine, kidney injury molecule-1 (KIM - 1), clusterin, albumin, beta-2-microglobulin (ß2M), cystatin C, neutrophil gelatinase-associated lipocalin (NGAL), osteopontin (OPN) and trefoil factor 3 (TFF3). Results: The case fatality was 10% (29/297), and death was much more common in older patients. Median concentrations of colchicine were higher in those over 65 [median 4.7 ng/mL (IQR: 1.7-6.6) vs. 1.2 (IQR: 0.2-2.7) for those <35]. Admission colchicine concentrations were highly correlated with a fatal outcome [median 7.8 ng/ml (IQR: 5.8-18.7) vs 1.2 (0-2.3) in survivors]. The area under the receiver operating characteristic curve (AUC-ROC) for uncorrected admission colchicine level was highly predictive of a fatal outcome, and this improved even further with two methods we developed to correct for the expected change with time. The best method had an AUC-ROC of 0.98 (95%CI 0.94-1.00) in predicting death, with 100% sensitivity and 96% specificity at the best cut-point. Discussion: Fatal outcomes and high concentrations were both much more common in the elderly following poisoning with Gloriosa superba. Our findings are consistent with kinetic data after medicinal colchicine ingestion. Conclusions: Gloriosa superba self-poisoning causes significant mortality. High concentration of colchicine is highly predictive of a fatal outcome. Ingestion of Gloriosa superba caused only mild acute kidney injury (AKI) and rhabdomyolysis.

Temporary Seizure in an Infant Who Had Been Exposed to G-Amino Butyric Acid Receptor Antagonist Thiocolchicoside.

Seizure is the most common presentation of neurological disorder in the pediatric emergency care setting. In evaluating the child after a first seizure, the first consideration should be determining if the seizure was provoked or unprovoked. Investigation listing the causes of the first seizure is considerably long, and adverse drug reactions must be in mind. Epileptic seizures after using thiocolchicoside (TCC) have been reported in several adult patients with epilepsy and acute brain injury. We present a previously healthy 3-month-old female infant who was admitted to the emergency department with a generalized seizure after exposure to TCC. To the best of our knowledge, this is the first case of a child who had an epileptic seizure after TCC intake via breastfeeding in the literature.

Colchicine Extract Suicidal Lethal Poisoning Confirmation Using High-Resolution Accurate Mass Spectrometry: A Case Study.

A case of suspected acute and lethal intoxication caused by colchicine has been reported. The woman was hospitalized after her suspicion of suicidal poisoning by a rare autumn crocus (Colchicum autumnale). Suspected colchicine poisoning was confirmed using a novel UHPLC method with a modern reversed-phase stationary phase with a sub 2-micron superficial porous particle size combined with a QTOF mass spectrometer. Sample preparation procedure included the addition of propiverine as internal standard, protein precipitation using methanol and solid phase extraction. High-resolution MS only and targeted MS/MS modes are reported for the qualitative analysis and screening of other potential drugs of abuse in blood samples. All Ion MS mode was used for quantitative determination of colchicine afterward. The concentration of colchicine in the blood sample was approximately 41 ng/mL, and more than 200 µg/mL of the plant extract used for the suicide.

A rare case report of heavy dose colchicine induced acute kidney injury.

BACKGROUND: Colchicine is a natural alkaloid that is mainly used for the treatment of inflammatory diseases. Effective and toxic doses are very similar, but case reports of higher colchicine doses inducing acute toxicosis is rare. CASE PRESENTATION: A 19-year-old woman was sent to the emergency room for taking 80 colchicine tablets (0.5 mg per tablet) 44 h previously. The main physical symptom was abdominal pain. Following ingestion, the patient suffered multi-system failure including renal, respiratory, circulatory, and digestive. Continuous renal replacement therapy (CRRT) and other treatment measures were used to remove metabolic wastes and poisons, and to treat other complications. Renal function was restored after a series of treatments. CONCLUSION: We report a case of an acute kidney injury induced by an overdose of colchicine. CRRT and a series of related treatments were beneficial for the treatment of colchicine poisoning.

A critically ill patient after a colchicine overdose below the lethal dose: a case report.

BACKGROUND: Although 0.8 mg/kg is considered a lethal dose of colchicine, fatal cases of patients who followed a critical disease course after an intake below this lethal dose have been reported. CASE PRESENTATION: An 18-year-old Japanese woman who had taken an overdose of prescription colchicine (15 mg; 0.2 mg/kg) was brought to our emergency out-patient department. Although her colchicine intake was below 0.8 mg/kg (considered the lethal dose), she reached a critical state and underwent three phases characterizing colchicine poisoning (gastrointestinal symptoms, multiple organ failure, and recovery). Her condition was critical, with a Sequential Organ Failure Assessment score of a maximum of 14. CONCLUSIONS: Patients might reach a critical stage after colchicine ingestion at a non-lethal dose. Thus, it might be necessary to review which dose of colchicine should be considered lethal.

Dermatologic Manifestations of Colchicine Intoxication.

Colchicine is an anti-inflammatory drug that has a narrow therapeutic index. Poisoning typically shows 3 phases with systemic symptoms. Gastrointestinal symptoms dominate in the first phase. Dermatologic manifestations usually appear, with skin eruptions in the second phase where multiorgan failure occurs and alopecia in the third phase where organ derangements resolve. Alopecia is a cardinal feature of the third phase, but there is no specifically defined eruption for toxication. Here, we report a case of colchicine intoxication in a 16-year-old girl with maculopapular/purpuric rash and alopecia.

Acute Pediatric Colchicine Toxicity is Associated with Marked Bradydysrhythmias.

BACKGROUND: Colchicine ingestion is rare but highly lethal. Patients usually die of multiorgan failure and cardiogenic shock. Colchicine is not only associated with depressed myocardial function but also with fatal heart rhythm disturbances, such as complete heart block, ventricular tachycardia, and asystole. While histologic changes of myocytes are well known, the mechanism by which colchicine affects cardiac impulse generation and conduction is not fully understood. CASE REPORT: We present a case of colchicine ingestion with sinus bradycardia, marked sinus arrhythmia, and first- and second-degree heart block. A 10-year-old previously healthy boy was brought to the emergency department for the sudden onset of dizziness, abdominal pain, and vomiting after ingesting his grandfather's colchicine and furosemide. His symptoms improved with ondansetron and intravenous normal saline. However, because of the colchicine ingestion, he was admitted to the pediatric intensive care unit for observation. He first developed PR prolongation (∼4-30 h postingestion) followed by marked sinus bradycardia and sinus arrhythmia along with second-degree heart block (∼48-60 hours postingestion). The minimum heart rate was 40 beats/min. Marked sinus arrhythmia was observed, suggesting an increase in parasympathetic activity. His heart rhythm improved initially with less sinus arrhythmia followed by resolution of heart block. He was discharged home without any sequelae. Holter monitoring 1 week after discharge showed normal heart rate variability for age. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: This case provides novel insights into how colchicine may affect the heart's electrophysiology. Colchicine may increase the parasympathetic tone enough to cause sinus bradycardia and different degrees of heart block.

Anti-colchicine Fab fragments prevent lethal colchicine toxicity in a porcine model: a pharmacokinetic and clinical study.

BACKGROUND: Colchicine poisoning is commonly lethal. Colchicine-specific Fab fragments increase rat urinary colchicine clearance and have been associated with a good outcome in one patient. We aimed to develop a porcine model of colchicine toxicity to study the pharmacokinetics and efficacy of ovine Fab. METHODS: A Göttingen minipig critical care model was established and serial blood samples taken for colchicine and Fab pharmacokinetics, clinical chemistry, and haematology. Animals were euthanised when the mean arterial pressure fell below 45 mmHg without response to vasopressor, or at study completion. RESULTS: Initial studies indicated that oral dosing produced variable pharmacokinetics and time-to-euthanasia. By contrast, intravenous infusion of 0.25 mg/kg colchicine over 1 h produced reproducible pharmacokinetics (AUC0-20 343 [SD = 21] µg/L/h), acute multi-organ injury, and cardiotoxicity requiring euthanasia a mean of 22.5 (SD = 3.2) h after dosing. A full-neutralising equimolar Fab dose given 6 h after the infusion (50% first hour, 50% next 6 h [to reduce renal-loss of unbound Fab]) produced a 7.35-fold increase in plasma colchicine (AUC0-20 2,522 [SD = 14] µg/L/h), and removed all free plasma colchicine, but did not prevent toxicity (euthanasia at 29.1 [SD = 3.4] h). Earlier administration over 1 h of the full-neutralising dose, 1 or 3 h after the colchicine, produced a 12.9-fold (AUC0-20 4,433 [SD = 607] µg/L/h) and 6.0-fold (AUC0-20 2,047 [SD = 51] µg/L/h) increase in plasma colchicine, respectively, absence of free plasma colchicine until 20 h, and survival to study end without marked cardiotoxicity. CONCLUSIONS: Colchicine-specific Fab given early, in equimolar dose, bound colchicine, eliciting its movement into the blood, and preventing severe toxicity. Clinical studies are now needed to determine how soon this antidote must be given to work in human poisoning.

Severe hypertriglyceridemia and colchicine intoxication following suicide attempt.

Colchicine overdose is uncommon but potentially life threatening. Due to its serious adverse systemic effects, overdose must be recognized and treated. We report a case of an 18-year-old female who ingested 18 mg (~0.4 mg/kg) of colchicine in a suicide attempt. The patient's clinical manifestations included abdominal cramps, vomiting, pancytopenia, hypocholesterolemia, and rhabdomyolysis. Two unique manifestations of toxicity in this patient were profound and persistent, severe hypertriglyceridemia and electrolyte imbalance, mainly hypophosphatemia, with no other evident cause except the colchicine intoxication. Following intensive supportive treatment, including ventilator support, N-acetylcysteine, granulocyte colony stimulating factor, electrolyte repletion, and zinc supplementation, the patient made a complete recovery. Colchicine intoxication is a severe, life-threatening situation that should be followed closely in intensive care units. Severe changes in body functions can rapidly develop, as previously described in the literature. To our knowledge, this extremely elevated triglyceride level has never been reported without the administration of propofol, and requires further evaluation.