Synthetic cannabinoids: Epidemiology, pharmacodynamics, and clinical implications

Subcutaneous panniculitis-like T-cell lymphoma: definition, classification, and prognostic factors: an EORTC Cutaneous Lymphoma Group Study of 83 cases.

Cannabinoids are a group of compounds that mediate their effects through cannabinoid receptors. The discovery of Δ9-tetrahydrocannabinol (THC) as the major psychoactive principle in marijuana, as well as the identification of cannabinoid receptors and their endogenous ligands, has led to a significant growth in research aimed at understanding the physiological functions of cannabinoids. Cannabinoid receptors include CB1, which is predominantly expressed in the brain, and CB2, which is primarily found on the cells of the immune system. The fact that both CB1 and CB2 receptors have been found on immune cells suggests that cannabinoids play an important role in the regulation of the immune system. Recent studies demonstrated that administration of THC into mice triggered marked apoptosis in T cells and dendritic cells, resulting in immunosuppression. In addition, several studies showed that cannabinoids downregulate cytokine and chemokine production and, in some models, upregulate T-regulatory cells (Tregs) as a mechanism to suppress inflammatory responses. The endocannabinoid system is also involved in immunoregulation. For example, administration of endocannabinoids or use of inhibitors of enzymes that break down the endocannabinoids, led to immunosuppression and recovery from immune-mediated injury to organs such as the liver. Manipulation of endocannabinoids and/or use of exogenous cannabinoids in vivo can constitute a potent treatment modality against inflammatory disorders. This review will focus on the potential use of cannabinoids as a new class of anti-inflammatory agents against a number of inflammatory and autoimmune diseases that are primarily triggered by activated T cells or other cellular immune components.

Cannabinoids as novel anti-inflammatory drugs

Systemic scleroderma (SSc) is one of the most complex systemic autoimmune diseases. It targets the vasculature, connective tissue-producing cells (namely fibroblasts/myofibroblasts), and components of the innate and adaptive immune systems. Clinical and pathologic manifestations of SSc are the result of: (1) innate/adaptive immune system abnormalities leading to production of autoantibodies and cell-mediated autoimmunity, (2) microvascular endothelial cell/small vessel fibroproliferative vasculopathy, and (3) fibroblast dysfunction generating excessive accumulation of collagen and other matrix components in skin and internal organs. All three of these processes interact and affect each other. The disease is heterogeneous in its clinical presentation that likely reflects different genetic or triggering factor (i.e., infection or environmental toxin) influences on the immune system, vasculature, and connective tissue cells. The roles played by other ubiquitous molecular entities (such as lysophospholipids, endocannabinoids, and their diverse receptors and vitamin D) in influencing the immune system, vasculature, and connective tissue cells are just beginning to be realized and studied and may provide insights into new therapeutic approaches to treat SSc.

/pdf/pathogenesis-of-systemic-sclerosis-1gwwgxa4uy.pdf

Pathogenesis of Systemic Sclerosis.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/1469-0691.12556

Leishmaniasis in immunosuppressed individuals

A previous study of electrocardiography at rest showed that anti-Ro/SSA–positive patients with connective tissue disease (CTD) frequently had corrected QT (QTc) interval prolongation. Because QTc interval prolongation is a definite risk factor for arrhythmic sudden death in the general population, a 24-hour electrocardiographic monitoring study was performed to investigate the possible relation between QTc interval prolongation and incidence of ventricular arrhythmias as a possible expression of immunomediated electric instability of the myocardium in anti-Ro/SSA–positive patients with CTD. The study population consisted of 46 patients with CTD; 26 anti-Ro/SSA–positive and 20 anti-Ro/SSA–negative (control group) patients (Sjogren's syndrome, 9 and 3 patients; systemic lupus erythematosus, 4 and 9 patients; systemic sclerosis, 2 and 4 patients; undifferentiated CTD, 8 and 1 patients; mixed CTD, 2 and 2 patients, and polymyositis/dermatomyositis, 1 and 1 patient, respectively). All patients underwent ambulatory Holter electrocardiography to obtain 24-hour monitoring of the QTc interval and ventricular arrhythmias. With respect to the control group, anti-Ro/SSA–positive patients with CTD (1) commonly showed QTc interval prolongation (46% vs 5%), and this abnormality, when present, persisted for the 24 hours (global mean 24-hour QTc interval 440.5 ± 23.4 vs 418.2 ± 13.2 ms); (2) had a higher incidence of complex ventricular arrhythmias (i.e., Lown classes 2 to 5, 50% vs 10%) also in the absence of detectable cardiac abnormalities; and (3) in patients with CTD, there is a direct relation between global mean 24-hour QTc interval and ventricular arrhythmic load independently of age and disease duration. In conclusion, anti-Ro/SSA–positive patients with CTD seemed to have a particularly high risk of developing ventricular arrhythmias. The risk appeared related mainly to abnormalities in ventricular electrophysiologic characteristics emerging in the clinical setting as QTc interval prolongation.

Comparison of Frequency of Complex Ventricular Arrhythmias in Patients With Positive Versus Negative Anti-Ro/SSA and Connective Tissue Disease

We report a case of subcutaneous panniculitis-like T-cell lymphoma (SPTCL), associated with macrophage activation syndrome, mimicking a lupus erythematosus panniculitis (LEP). A 29-year-old woman presented with high fever, general malaise, nausea, vomiting, and subcutaneous nodules and ulcerating lesions located on the lower extremities. The histopathology showed an infiltration of the panniculus, mostly involving fat, and periadnexial and perivascular structures consistent with lymphocytic lobular panniculitis (LLP). LLP is a shared feature of LEP and SPTCL. The immunophenotyping of the cell infiltrate was crucial for a correct diagnosis.

Subcutaneous panniculitis-like T-cell lymphoma misdiagnosed as lupus erythematosus panniculitis

/pdf/mucocutaneous-leishmaniasis-in-a-patient-treated-with-anti-181gusrhp5.pdf

Mucocutaneous leishmaniasis in a patient treated with anti-TNF-α therapy

False proteinuria in patients with alkaptonuria.

A 77-year-old Caucasian man had experienced pain and progressive swelling of the left knee for 2 days prior to admission. Examination revealed an inflamed left knee joint that was aspirated, yielding 10 ml of whitish-creamy synovial fluid (fig 1A). Septic arthritis was suspected. A wet preparation under ordinary light confirmed the presence of numerous leukocytes (25 000 cells/mm3). However, further …

A whitish-creamy synovial fluid.

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