Intravenous Colchicine Research Articles

Purulent pericarditis and cardiac tamponade in HIV: a case report on a dreaded complication of streptococcus pneumoniae

Introduction and importance: Purulent pericarditis is an uncommon complication of Streptococcus pneumoniae, which commonly occurs in an immunocompromised state such as HIV and can lead to life-threatening complications such as cardiac tamponade and potentially death if untreated. Early identification, pericardiocentesis, and general measures such as antibiotics and anti-inflammatory medications can be life-saving. Case presentation: We present a case of a 64-year-old male with HIV who presented with clinical symptoms suggestive of pericarditis. Chest imaging revealed multifocal airspace diseases and moderate pericardial effusion. He had worsening lactic acidosis, and bedside point-of-care ultrasound showed pericardial effusion with features suggestive of cardiac tamponade. His lactic acidosis improved with emergency pericardiocentesis. Blood and pericardial fluid cultures revealed Streptococcus pneumoniae. He was further treated with intravenous antibiotics, colchicine, and ibuprofen. Clinical discussion: Although Streptococcus pneumoniae is a common etiology of community-acquired pneumonia (CAP), it has not been cited as the leading cause of pericarditis or pericardial effusion. In immunocompromised patients, it is necessary to consider a broad differential diagnosis as an etiology of acute chest pain, as it may be challenging to differentiate pleuritic and pericarditic chest pain from clinical presentation only. Moreover, infectious etiology of acute pericarditis and pericardial effusion should be considered in this patient population, especially those with HIV. At the same time, it is crucial to promptly identify and treat cardiac tamponade to prevent further deterioration. Conclusion: Our case provides insight into the diagnosis and management of CAP and its potential complication of purulent pericarditis and cardiac tamponade in immunocompromised patients.

A Case of Severe Cardiomyopathy Due to Covid-Induced Myocarditis, Completely Resolved after Colchicine and Immunoglobulin Therapy.

Myocarditis should be suspected in patients with acute onset cardiomyopathy with troponin leak and no evidence of ischaemia. COVID-19 myocarditis can present with arrhythmia, which could be fatal in some cases.Even though supportive management is the mainstay of treatment for COVID-19 myocarditis, there have been reports of benefits of intravenous immunotherapy (IVIG) and colchicine.More studies are warranted to explore the beneficial effects of IVIG and colchicine not just in COVID-19 myocarditis, but also in other viral causes of myocarditis he aim of this study is also to raise awareness among healthcare professionals about the Bentall procedure in patients with type A aortic dissection involving the aortic valve.

État des lieux de la maladie des emboles de cholestérol

Cholesterol crystal embolism is a systemic pathology associated with diffuse atherosclerosis. Pathophysiology corresponds to tissue necro-inflammation secondary to arteriolar occlusion associated with microembolism from atherosclerotic plaques of large diameter arteries. The clinical presentation is heterogeneous and polymorphic. Multiple organs may be the targets, but preferential damage is skin, kidneys and digestive system. It is a serious pathology, underdiagnosed, with a poor prognosis. The risk factors for developing the disease remain the same risk factors as atheroma. The factors favouring migration of microembolism remain mainly vascular interventional procedures; easy to diagnose, they oppose spontaneous embolic migrations or secondary to the introduction of antithrombotic treatment, whose diagnosis is more difficult and the prognosis more severe. The diagnosis of the disease remains mostly a diagnosis of elimination and often refers to a bundle of clinical, biological, morphological and histologic arguments. The treatment is poorly codified and the subject of few publications. It will favour both symptomatic treatment (and mainly that of pain) and complications (high blood pressure, renal insufficiency). The aetiological support remains less consensual. The treatment of atherosclerotic plaques consists, of course, in the correction of classical cardiovascular risk factors, the introduction of a statin. It will be discussed in the implementation of surgery or angioplasty to exclude potentially responsible atherosclerotic lesions. Eviction of antithrombotic therapy should be considered in terms of the benefit–risk balance, but often in favour of maintaining it. Finally, other treatments may be proposed in a case-by-case basis, such as oral or intravenous corticosteroid therapy, colchicine or LDL aphaeresis.

Whole exome sequencing in a child with acute disseminated encephalomyelitis, optic neuritis, and periodic fever syndrome: a case report

BackgroundAcute disseminated encephalomyelitis is generally preceded by an infection, and it is usually self-limiting and non-recurrent. However, when there are multiple attacks of acute disseminated encephalomyelitis followed by optic neuritis, it is defined as acute disseminated encephalomyelitis-optic neuritis. To the best of our knowledge, there are no previous reports of acute disseminated encephalomyelitis and optic neuritis preceded by autoinflammation, triggered by periodic fever syndrome.Case summaryWe report on a case of acute disseminated encephalomyelitis with optic neuritis and periodic fever syndrome in a 12-year-old Ecuadorian Hispanic boy with several relapses over the past 10 years, always preceded by autoinflammatory manifestations and without evidence of infectious processes. Whole exome sequencing was performed, and although the results were not conclusive, we found variants in genes associated with both autoinflammatory (NLRP12) and neurological (POLR3A) phenotypes that could be related to the disease pathogenesis having a polygenic rather than monogenic trait.ConclusionWe propose that an autoinflammatory basis should be pursued in patients diagnosed as having acute disseminated encephalomyelitis and no record of infections. Also, we show that our patient had a good response after 1 year of treatment with low doses of intravenous immunoglobulin and colchicine.

Safety and efficacy of intravenous Colchicine in children with Familial Mediterranean Fever.

Familial Mediterranean Fever (FMF), the most common monogenic inflammatory disease, is mainly treated by oral Colchicine. However, 5% of patients are considered non-responders and, therefore, candidates for biologic therapy. Intravenous (IV) Colchicine treatment has been shown to be effective and safe in adult patients. The objective of this study was to evaluate the safety of IV Colchicine for pediatric FMF patients in our hospital, refractory to oral Colchicine, by reviewing their medical records. Inclusion criteria were all patients with FMF who commenced treatment with IV Colchicine before the age of 18years, and received at least 6months of IV therapy. The patients completed questionnaires to assess the efficacy of the treatment. Between 2004 and 2017, 7 pediatric FMF patients receiving maximal oral Colchicine doses and deemed non-responders were treated with weekly IV Colchicine, including 38 cumulative patient years of follow-up data (a full blood count, renal and liver function tests). All patients were homozygous for the M694V genotype. Long-term follow-up showed normal laboratory results with no Colchicine-related hospital admissions or toxicity. Global health assessment and the number of disease-free days have significantly improved (P < 0.05). Prolonged IV Colchicine use is described in pediatric FMF patients for the first time, with an excellent safety profile in our population, and decrease in intensity and frequency of attacks. In the biological era, IV Colchicine, although not leading to complete remission, may be considered a second-line option in countries where anti-interleukin 1 blockers are not available, or as a third-line option in case of failure to respond to biologics.

Efficacy and safety of long-term treatment with intravenous colchicine for familial Mediterranean fever (FMF) refractory to oral colchicine.

Colchicine is the mainstay of treatment for familial Mediterranean fever (FMF). Intravenous (IV) colchicine, administered over several months, has been shown to be effective for FMF patients unresponsive to oral colchicine. The objective of this study was to evaluate the efficacy and safety of long-term IV colchicine treatment in oral colchicine-resistant FMF. We analyzed data of 15 patients with frequent FMF attacks, despite a maximal tolerated dose of oral colchicine (2-3mg/day), who were treated with weekly IV injections of 1mg of colchicine for at least 12 months. Treatment efficacy was determined by changes in frequency, duration and severity of FMF attacks. Safety was assessed according to adverse events. The mean duration of IV colchicine treatment was 5.16 ± 2.85years. Decreases were observed from pre-treatment period in the monthly mean rates of abdominal attacks (from 5.6 ± 3.7 to 1.9 ± 3.3, p = 0.0009), joint attacks (from 6.5 ± 5.1 to 1.6 ± 1.6, p = 0.01) and overall attacks (from 22.3 ± 16.2 to 7.4 ± 5.7, p = 0.002) as well as in the mean duration (from 3.8 ± 1.5 to 2.4 ± 1.1days per attack, p = 0.008) and severity of attacks (from 9.9 ± 0.3 to 5.7 ± 2.6, on a scale of 0-10, p < 0.05). The rate of adverse events was low, and they were mainly gastrointestinal. No severe or serious adverse events were recorded. Long-term treatment with IV colchicine in patients unresponsive to oral colchicine therapy is effective and safe.

Novel presentations of periodic fever syndromes: Discrepancies between genetic and clinical diagnoses.

ObjectiveThe Periodic fever syndromes (PFS) are a group of disorders of the innate immune system. We investigated patients diagnosed with PFS at the Dartmouth Hitchcock Pediatric Rheumatology Clinic.MethodsCase acquisition was performed by reviewing ICD 9/10 coded records for familial Mediterranean fever (ICD 9 277.31), laboratory test records for PFS genetic screening, and clinic records between 1/1/2011 and 12/31/2017.ResultsTwenty-seven cases had clinical evaluations including PFS genetic screening. Clinical diagnoses included familial Mediterranean fever (FMF) (10 cases), Muckle-Wells (2 cases), tumor necrosis factor receptor associated periodic syndrome (TRAPS) (4 cases), hyper IgD syndrome (HIDS) (1 case), Crohn’s Disease (1 case), systemic onset juvenile idiopathic arthritis (SoJIA) (1 case), fever of unknown origin (FUO) (1 case), periodic fever adenitis pharyngitis aphthous ulcer (PFAPA) (6 cases), and cold-induced urticaria (1 case). Fifteen cases were associated with a genetic cause. Seven of the 10 FMF cases were confirmed genetically and were either heterozygous or compound heterozygotes. Both cases of Muckle-Wells had either a compound heterozygote for CIAS 1 or a NOD gene mutation. Both TRAPS cases presented atypically with patients developing systemic lupus erythematosus (SLE) or being asymptomatic. Two patients had novel syndromes. One FMF patient had a TRNT1 gene mutation who responded to intravenous immunoglobulin (IVIg) and colchicine after failing multiple treatments. The other had SoJIA with a LPIN 2 gene mutation but responded to colchicine. Only one of the 15 genetically proven cases had classical presentation and genetics (HIDS secondary to a mevalonate kinase (MVK) gene mutation).ConclusionPFS screening was helpful in over half of the cases to develop therapeutic treatment plans. Given the atypical clinical presentations seen with genetically determined PFS, extensive genetic testing is indicated for all patients presenting with a PFS, excluding classical PFAPA syndrome.

AB0931 Anti-TNF Agents in Intractable Familial Mediterranean Fever with Axial Spondylarthropathy: Four Cases

BackgroundFamilial Mediterranean Fever (FMF) is an autoinflammatory disease characterized by recurrent attacks of fever and serositis. A relation between FMF and Ankylosing Spondylitis (AS) has been suggested in small cohort...

Management of Idiopathic Thrombocytopenic Purpura in Adult: A Review Article

Idiopathic thrombocytopenic purpiira (ITP), also known as primary immune or autoimmune thmmbocytopenic purpura, is a common cause of thrombocytopenia and bleeding complications in children and adults. It mav be confused with other causes of thrombocvtopenia and is treated with agents that varv in efjicacv, toxicity, and cost. Clinical presentation very in children and adult. In children, ITP is usually an acute, self-limited disorder that resolves spontaneously: in adults, it is typically a chronic disorder with a more insidious onset. In about one third of adults with ITP, the condition is persistent and relatively resistant to most treatments .Available evidence suggests that only about 5% of adults with chronic ITP have spontaneous remission. The principal therapeutic options for ITP include glucocorticoids, intravenous immunoglobulin and splenectomy. Other treatments have been used for refractory cases; these include intravenous anti-Rh (D), azathioprine, cyclophosphamide, danazol, vinca alkaloids, ascorbic acid, colchicine, interferon-alpha, combination chemotherapy, protein A, immunoadsorption, cyclosporine, epsilon-aminocaproic acid, plasma exchange, and accessory splenectomy. Journal of Shaheed Suhrawardy Medical College Vol 2No.1 June 2010 page 24-28 DOI: http://dx.doi.org/10.3329/jssmc.v2i1.12348

Traitement par photochimiothérapie extracorporelle de quatre cas de lupus érythémateux cutané réfractaires aux traitements conventionnels

Photopheresis is a leucopheresis procedure in which cells are photoactivated by psoralen and then irradiated by ultraviolet A. We report four cases of women with refractory cutaneous lupus erythematosus (LE) who responded to this treatment. We treated one patient with subacute LE having a contraindication to antimalarials and to thalidomide and three patients with chronic LE (lupus panniculitis, lupus tumidus and disseminated discoid LE) refractory to treatment with hydroxychloroquine, chloroquine, thalidomide and dapsone, and also, in some cases, to oral and intravenous corticosteroids, methotrexate, colchicine, acitretine, sulfasalazine, mycophenolate mofetil and intravenous immunoglobulin. Treatment consisted of two 4-hour sessions fortnightly. Only antimalarials were continued during photopheresis. Photopheresis had a positive effect on all four patients. We noticed complete remission in two patients and interruption of progression followed by partial remission in the other two after a mean delay of two to three months of treatment. All treatments other than antimalarials were stopped. Photopheresis appears to be an effective treatment option in patients with cutaneous LE. Due to its high cost, it should nevertheless remain an exceptional therapeutic option restricted to patients with cutaneous LE resistant to standard therapy.

Cell Membrane Stretch and Chest Blow‐Induced Ventricular Fibrillation: Commotio Cordis

Commotio cordis, sudden cardiac death secondary to blunt nonpenetrating chest blows in sports, is reported with increasing frequency. In a swine model, ventricular fibrillation (VF) is induced by a baseball blow to the chest, and the initiation of VF is related to the peak left ventricular (LV) pressure produced by the blow. LV pressure changes likely result in cell membrane stretch and mechanical activation of ion channels. Disruption of cell cytoskeleton that anchors the cell membrane prior to precordial blows offers the opportunity to explore whether cell membrane deformation is critical to commotio cordis. Twelve juvenile swine (mean 12.7 +/- 1.6 kg) were randomized to intravenous normal saline (control, n = 6) or 10 mg of intravenous colchicine (n = 6), which is known to depolymerize microtubules. Animals were given up to six blows timed to the vulnerable portion of the cardiac cycle with a 30 mph baseball on the chest directly over the cardiac silhouette. VF was initiated by 14 of the 29 (48%) impacts in the colchicine-treated animals compared with only 3 of 28 (11%) in the controls (P = 0.002). The peak generated LV pressure did not differ between colchicine animals (405 +/- 61 mmHg) and controls (387 +/- 115) (P = 0.47). However, animals administered colchicine were more likely to have VF generated by the chest blow at all pressures. The initiation of VF by chest blows is significantly increased by selective disruption of the cytoskeleton, suggesting that mechanical deformation of the cell membrane is fundamental to the activation of ion channels and underlies the mechanism of VF in commotio cordis.

Deaths From Intravenous Colchicine Resulting From a Compounding Pharmacy Error—Oregon and Washington, 2007

Deaths From Intravenous Colchicine Resulting From a Compounding Pharmacy Error—Oregon and Washington, 2007

Reassessing the safety of intravenous and compounded injectable colchicine in acute gout treatment

Colchicine has been used for over 2000 years. Intravenous (IV) colchicine has been used for the treatment of acute gout since the 1950s. IV and oral colchicine were ‘grandfathered’ before the 1969 FDA Phase III trials for drug toxicity became law. Data on toxic reactions are, therefore, based only on passive surveillance. The risk of toxicity with IV use depends on the total dose over a period of time, the presence of comorbid conditions and the size of individual dose. Colchicine toxicity has been compared to arsenic poisoning. Symptoms start 2 – 5 h after the toxic dose has been ingested and not uncommonly lead to death. Injections of compounded colchicine have been implicated in the deaths of several patients, several of which received off-label IV colchicine for back pain. Given that colchicine has the smallest benefit to toxicity ratio of the drugs that are used in the management of acute gout and the fact that acute gout is not life-threatening, one could make a strong case for eliminating the use of IV colchicine the treatment of acute gout.

Hazards of colchicine

We agree with Tortorici et al.[1][1] that greater safeguards are needed for the administration of intravenous colchicine.[1][1] The authors’ recommendations would indeed improve safety. We believe, however, that the safest alternative is to remove colchicine from the formulary and use alternatives

Development of Acute Gouty Attack in the Morbidly Obese Population after Bariatric Surgery

Gout is associated with increased body weight. We evaluated the prevalence of gout and acute gouty attacks in the morbidly obese population who underwent bariatric surgery. The medical records and operative reports of 1,240 patients who underwent bariatric surgery were reviewed retrospectively for weight parameters, BMI, weight loss, medical history of gout, and onset of acute gouty attacks. Of the 1,240 patients, 5 (0.4%) had been previously diagnosed with gout. 2 of these 5 had acute attacks during the postoperative period, and responded successfully to intravenous colchicine. Although rare, gout must be considered a co-morbid illness in obese and morbidly obese patients. Surgeons should be familiar with the signs and symptoms of attacks in the postoperative period, and be knowledgeable in the management.

Accidental Intravenous Colchicine Poisoning

Colchicine is a commonly used drug for the treatment of gout and other indications. Toxicity from intentional oral overdoses of colchicine has been reported. Two cases are reported here in which colchicine was given by intravenous injection, and patients presented with multiorgan toxicity. The authors tested plasma and urine colchicine levels in these patients and found them significantly elevated. Testing of the vial from which the colchicine injections were given showed that the vial was mislabeled and contained 10-fold greater concentration of drug than the labeling indicated. These patients thus received a bolus dose of 20 mg of intravenous colchicine rather than the intended 2-mg dose. An intravenous dose of this magnitude has not previously been reported.

Promoting the safe use of intravenous colchicine

Promoting the safe use of intravenous colchicine

Deaths associated with inappropriate intravenous colchicine administration

Intravenous (IV) colchicine is occasionally prescribed for the treatment of acute gouty arthritis. The Food and Drug Administration (FDA) recently received a report of death in a patient that was associated with inappropriate IV dosing of colchicine. This report prompted further investigation of other deaths associated with IV colchicine use in the FDA Adverse Event Reporting System (AERS) and the medical literature. A total of 20 deaths were identified. Eight patients were females, 11 were males, and the gender was unknown in 1. In all cases, the recommended maximum cumulative dose of 2 to 4 mg during a course of therapy was exceeded. Dose reductions are recommended in patients with renal or hepatic disease and in the elderly. All reported adverse events were associated with colchicine toxicity, including thrombocytopenia, leukopenia, pancytopenia, agranulocytosis, aplastic anemia, acute renal failure, and disseminated intravascular coagulopathy. Death occurred within 1 to 40 days after drug administration. Therapeutic guidelines exist for use of IV colchicine and these guidelines should be followed to prevent serious toxicities and death.

Investigational agents for the treatment of asthma

The approach to the treatment of asthma has changed considerably over the years. Initial treatments for asthma were designed to relieve symptoms and included epinephrine, atropine-like drugs, and inhalers such as albuterol. Subsequently, as the inflammatory processes involved in asthma were better understood, agents were developed to decrease these processes. These agents include corticosteroids, theophylline, and cromones. The precise mechanism of action of these drugs has remained unclear. Recently, however, important studies have revealed information regarding causes of asthma including the interrelationships among specific immune cells, cytokines, and other immune mediators. This knowledge has led to tailored treatment approaches and improved application of nonspecific anti-inflammatory drugs in the treatment of asthma. In addition, more specifically targeted agents have been and continue to be developed. Combinations of nonspecific and specific agents may further improve the treatment of asthma. NONSPECIFIC CONTROL OF CELLULAR INFLAMMATION Newer agents that can be categorized as nonspecific controllers of cellular inflammation include some of the newly developed inhaled corticosteroids and noncorticosteroid anti-inflammatory agents. Inhaled corticosteroids

Diagnosis and Treatment of Gout in the Intensive Care Unit

Gout is a common cause of arthritis resulting from formation of monosodium urate crystals in synovial tissues. The incidence of this condition in the critically ill population is unknown, but gout can result in short-term morbidity and it can occasionally complicate management of a patient's primary condition. The diagnosis of gout should be considered in any patient in whom acute arthritis or bursitis develops. Aspiration of the involved joint or bursa and identification of crystals using either polarized or light microscopy are mandatory. Treatment options in critically ill patients differ from the usual treatment of gout because most critically ill patients have or are at risk for renal dysfunction and gastrointestinal bleeding, thus making use of nonsteroidal anti-inflammatory agents and colchicine hazardous. Intravenous colchicine in critically ill patients should be used with extreme caution, if at all, because the risk of bone marrow toxicity and other complications are well described in this patient population. Initial regimens should include use of adrenocorticotropic hormone, intra-articular corticosteroids, or systemic steroids. Analgesics may be beneficial as primary therapy in minor cases of acute gout, and they may be useful as adjunctive therapy in more severe cases. The role of colchicine as a prophylactic agent is discussed, as are treatment options in the allograft transplant population, in which rapidly progressive gout is increasingly common.