Bullosis diabeticorum, or diabetic bullae, is a non-inflammatory blistering condition that is virtually diagnostic of diabetes. Diabetic bullae most often present as painless, tense, superficial bullae that occur in an acral distribution and commonly heal in 2-6 weeks without scarring, but complications such as secondary bacterial infection or hemorrhage may occur. The diagnosis of bullosis diabeticorum in a nondiabetic patient should prompt screening for diabetes. A case of recurrent bullae in a prediabetic patient is presented, with a review of the clinical features and significance of bullosis diabeticorum.
Patient: Male, 27Final Diagnosis: Bath salt induced cardiomyopathySymptoms: Agitation • fever • pedal edemaMedication: Intravenous nor-epinephrine for less than 6 hoursClinical Procedure: —Specialty: Internal medicine • cardiologyObjective:Unusual clinical courseBackground:“Bath salts” is the street name for a group of recently identified and increasingly abused stimulant synthetic cathinones that are associated with multiple systemic effects. We present a case of a patient who developed reversible dilated cardiomyopathy secondary to their use.Case Report:A 27 year old male with no past medical history was brought to emergency department with agitation. He had been inhaling and intravenously injecting “bath salts”, containing a mephedrone/Methylenedioxypyrovalerone (MDPV) combination. On presentation, he was tachycardic, hypotensive and febrile. His initial labs showed an elevated white count, creatinine and creatinine phosphokinase levels. His erythrocyte sedimentation rate; C-reactive protein; urinalysis; urine drug screen; Human Immunodeficiency Virus, hepatitis, coxsackie, and influenza serology were normal. EKG showed sinus tachycardia. An echocardiogram was done which showed dilated cardiomyopathy with an ejection fraction (EF) of 15–20% and global hypokinesia. A left heart catheterization was done and was negative for coronary artery disease. At a 20 week follow up, he had stopped abusing bath salts and was asymptomatic. A repeat echocardiogram showed an EF of 52%.Cocnlusions:Bath salts (MDPV, mephedrone) are synthetic cathinones with amphetamine/cocaine like properties with potential cardiotoxic effects. Cardiovascular manifestations reported include tachycardia, hypertension, myocardial infarction, arrhythmias and cardiac arrest. “Bath salts” can also cause severe reversible dilated cardiomyopathy. Prior to diagnosis, other causes of cardiomyopathy including ischemic, infectious, familial, immunological, metabolic and cytotoxic may need to be ruled out; as was done in our patient.
Painful crises in sickle cell disease (SCD) are associated with increased plasma cytokines levels, including endothelin-1 (ET-1). Reduced red cell magnesium content, mediated in part by increased Na + /Mg 2+ exchanger (NME) activity, contributes to erythrocyte K + loss, dehydration and sickling in SCD. However, the relationship between ET-1 and the NME in SCD has remained unexamined. We observed increased NME activity in sickle red cells incubated in the presence of 500 nM ET-1. Deoxygenation of sickle red cells, in contrast, led to decreased red cell NME activity and cellular dehydration that was reversed by the NME inhibitor, imipramine. Increased NME activity in sickle red cells was significantly blocked by pre-incubation with 100 nM BQ788, a selective blocker of ET-1 type B receptors. These results suggest an important role for ET-1 and for cellular magnesium homeostasis in SCD. Consistent with these results, we observed increased NME activity in sickle red cells of three mouse models of sickle cell disease greater than that in red cells of C57BL/J6 mice. In vivo treatment of BERK sickle transgenic mice with ET-1 receptor antagonists reduced red cell NME activity.Among patients with sickle cell disease (SCD), 5% experience 3-10 potentially lethal vaso-occlusive painful crises annually. 1,2 Vaso-occlusive crises are initiated, in part, by red cell deoxygenation and by elevated plasma levels of cytokines such as endothelin-1 (ET-1), leading to increased adhesive interactions among sickle red cells, between sickle red cells and endothelium and involving plasma factors, through mechanisms that remain incompletely understood. [3][4][5][6] ET-1 plays important roles in the disordered erythrocyte homeostasis, inflammation, vaso-occlusion, tissue injury, and pain common to the pathophysiology of SCD. 7,8 ET-1 levels are increased in SCD, 9,10 and in vivo treatment with ET-1 receptor antagonists improve hematological parameters and reduced oxidant stress in mouse models of SCD. 11 However, the mechanisms by which ET-1 receptor antagonists mediate their beneficial effects in SCD remain unclear.Dysregulated Mg 2+ levels have been reported in SCD and in patients with Type 2 diabetes, 12,13 hypertension, and stroke, all diseases with an important inflammatory component. [14][15][16] Low Mg 2+ levels are accompanied by oxidant stress, impaired vascular function and increased inflammation, all associated with the pathophysiology of SCD. 17,18 Low cellular Mg 2+ levels stimulate cytokine production in and release from endothelial cells and modulate activity of NF-κB, a master regulator of cytokine production. 19,20 Intracellular Mg 2+ regulates multiple additional activities linked to SCD, including casein kinase II (CK2), 21 PKC [22][23][24] and hypoxia-inducible factor-1 (HIF-1). 25 Thus, regulation of Mg 2+ levels has been proposed as a therapeutic target in SCD. [26][27][28] A preliminary study reported that the activity of the Na + /Mg 2+ exchanger (NME) in sickle erythrocytes was significantly reduced after 6 months of...
Delusions of parasitosis are a rare psychiatric disorder in which the patient has a fixed, false belief of being infested with parasites. The disorder is classified as primary if no cause is identified or secondary if associated with general organic conditions, psychiatric illnesses, and drugs (substance induced). Several medications have been reported in association with delusions of parasitosis, including anti-parkinsonian medications, ciprofloxacin, cetirizine, doxepin, and others. Delusions of parasitosis have not been previously reported to be associated with gabapentin use. We present the case of a patient who developed delusions of parasitosis after been initiated on gabapentin treatment for neuropathic pain and complete disappearance of symptoms after the medication was discontinued.
Activation of the mineralocorticoid receptor (MR), a critical component of the Renin-Angiotensin-Aldosterone (ALDO)-System (RAAS), has been shown to play an important role in inflammatory and vascular endothelial responses in addition to its well-described effects on sodium and water homeostasis. Activationof endothelial cells leads to, among other factors, increased endothelin-1 (ET-1) and protein disulfide isomerase (PDI) release. PDI and ET-1 contribute to vascular inflammation and are increased in patients with SCD and sickle transgenic mouse models. The MR is a member of the steroid family of nuclear receptors and transcription factors that upon activation binds to hormone response elements of edn1, the gene for ET-1, leading to increased ET-1 expression.In vivo, blockade of MR has been shown to reduce circulating ET-1 levels and ET-1 mRNA expression. However, the role of MR in SCD is unclear. We hypothesized that MR blockade in sickle transgenic mice would reduce PDI activity and improve hematological parameters and inflammation. We first studied EA.hy926 (EA) cells, a human endothelial cell line that expresses MR. We incubated EA cells with ALDO (10-8 M), an MR agonist, for 24 hr and observed a rise in PDI mRNA levels by qRT-PCR (P<0.01, n=5), an event that was blocked by pre-incubation of EA cells with 1 μM canrenoic acid (CA), an MR antagonist (P<0.05, n=5). We then measured PDI activity in the supernatant of ALDO-stimulated EA cells using a Di-E-GSSH fluorescent marker and observed a rise in PDI activity following ALDO (10-8 M) when compared to vehicle treatment (P<0.05; n=5). To test the in vivo effects of MR activation, we studied Berkeley Sickle Transgenic (BERK) mice that were randomized to receive either normal rodent chow or chow containing eplerenone (156 mg/kg per day), an MR antagonist (MRA), for 14 days. We observed significantly lower plasma PDI activity in mice treated with MRA than those on regular chow (63.7 ± 8.7 control diet to 47.9 ± 2.4 eplerenone, Relative Fluorescence Units (RFU); P<0.005, n=6 and 9, respectively). Treatment with MRA was associated with reduced plasma ET-1 and myeloperoxidase (MPO) levels in BERK mice. We also studied RBC Gardos channel activity in these mice and observed a significant reduction in clotrimazole-sensitive K+ efflux following MR blockade (2.49±0.5 control and 1.37±0.3 mmol/1013 cells x hr; P<0.04 n= 5 and 7 respectively). Consistent with these results, MR blockade was associated with increases in both erythrocyte MCV (41.3±2.5 vs 47.4±1.1 fL, P<0.03, n=7) and reticulocyte MCV (53.6.3±2.8 vs 60.1±0.6 fL, P<0.02, n=7). We also studied gene expression by qRT-PCR in heart tissue from these mice and observed that MR blockade reduced mRNA expression of: ET-1 (0.654 ± 0.233, P<0.05, n=5 and n=7); PDI (0.546 ± 0.063, P<0.01, n=5 and n=7); and Tumor Necrosis Factor Receptor Superfamily Member 1A mRNA (0.464 ± 0.061, P<0.01, n=5 and n=7). Thus, our results suggest a novel role for RAAS and, in particular, MR activation in SCD. Disclosures No relevant conflicts of interest to declare.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.