Iatrogenic calcinosis cutis occurs when insoluble calcium salts deposit in cutaneous and subcutaneous tissue. Iatrogenic calcinosis cutis is a rare complication from a variety of medical interventions, most commonly due to extravasated intravenous calcium-containing solutions. We present a severe case of iatrogenic calcinosis cutis in a patient with end-stage renal disease and an elevated serum calcium-phosphate product. Iatrogenic calcinosis cutis has a wide range of clinical presentations. Either subclinical or clinically noticeable extravasations may cause mild to severe calcinosis cutis. Patients with increased serum calcium and phosphate may be at increased risk of iatrogenic calcinosis cutis. Treatment options include conservative, pharmacologic, or surgical management.
Background Cardiac manifestations of neonatal lupus include an array of structural and conduction abnormalities due to placental transference of maternal anti-SSA/Ro and anti-SSB/La autoantibodies. Late-onset neonatal lupus cardiomyopathies, occurring outside the neonatal period, is an infrequently reported manifestation with unknown pathophysiology and poorly defined treatment regimens. Due to the rarity of this condition, additional studies and case reports are required to better understand and manage late-onset neonatal lupus cardiomyopathies. Case presentation A 4-week-old female, born to a mother with known anti-SSA/Ro and anti-SSB/La autoantibodies, presents with classic cutaneous manifestations for neonatal lupus and is found to have left bundle branch block, severely dilated cardiomyopathy with an ejection fraction of 25%, and a thin echogenic dyskinetic ventricular septum. Weekly second trimester and 30-week fetal echocardiograms showed no signs of structural or conduction abnormalities. There were no histologic signs of inflammation on cardiac tissue biopsy. After a complicated hospital course, she was successfully treated with biventricular pacemaker, intravenous immunoglobulin, and plasmapheresis. Conclusions We present a case of late-onset neonatal lupus with severe dilated cardiomyopathy, a dyskinetic ventricular septum, and left bundle branch block. To our knowledge, the dyskinetic ventricular septum has never been reported and left bundle branch block is rarely reported in NL. This case further validates the need for long term cardiac follow up for patients born with NL, even if lacking cardiac manifestations in the peripartum period. We characterize a unique presentation of a rare clinical entity, highlighting the diagnostic challenges, and describe a successful treatment course.
Phosphatidylinositol-3,4-bisphosphate (PtdIns(3,4)P2) is a messenger that accumulates in platelets in a phosphoinositide 3-kinase and platelet aggregation-dependent manner. PtdIns(3,4)P2 is broken down by inositol polyphosphate 4-phosphatases, type I (INPP4A) and type II (INPP4B). These enzymes do not catalyze hydrolysis of phosphoinositides other than PtdIns(3,4)P2, and therefore provide unique means for studying the role of this lipid in platelet activation. We have found that the dominant isoform of 4-phosphatases expressed in platelets is INPP4A and we have generated radiation chimera mice with the deficiency in INPP4A restricted to hematopoietic cell lineage. Compared to wild type platelets, agonist-stimulated INPP4A-deficient platelets accumulated higher levels of PtdIns(3,4)P2. An increase in platelet aggregation in INPP4A-deficient platelets was observed with all tested agonists. To study platelet function in vivo, we performed carotid artery injury mouse thrombosis model experiments. Time to occlusion was dramatically reduced in mice with INPP4A deficiency. These data support the hypothesis that by regulating PtdIns(3,4)P2 levels, INPP4A downregulates platelet aggregation and thrombus formation. To investigate mechanisms mediating INPP4A-dependent signals, we compared levels of phosphorylated Akt and phosphorylated glycogen synthase kinase (GSK) in wild type and INPP4A-deficient platelets in response to agonist stimulation. An increase in phospho-Akt levels was observed in INPP4A-deficient platelets, suggesting that in addition to its well-characterized regulator, PtdIns(3,4,5)P3, PtdIns(3,4)P2 can promote Akt activation. Interestingly, this was not accompanied by a significant increase in phospho-GSK levels, suggesting a possible novel mechanism involved in platelet aggregation. Disclosures No relevant conflicts of interest to declare.
Background and Hypothesis: Endoscopic ultrasound (EUS) guided fine-needle biopsy (FNB) to obtain core liver specimen is shown to be effective and safe. However, prospective data is limited regarding EUS-FNB in non-malignant liver disease. This study evaluates two EUS-FNB techniques with the hypothesis that the modified wet suction (MWS) technique will produce greater pathological yield than the slow pull (SP) technique in patients with non-malignant liver disease. Experimental Design or Project Methods: In this prospective, randomized controlled trial we are evaluating efficacy and safety of EUS-FNB techniques (MWS versus SP) in patients with initial indication for an upper endoscopy plus need for a liver biopsy to assess non-malignant disease. The primary outcome is pathological yield defined as number of complete portal tracts (CPTs), specimen length, and fragmentation. Secondary outcomes include pathological yield between two specimen processing techniques, pathological yield between left versus right liver lobe biopsy, time for biopsy technique, and complications. Results: For this interim analysis, 8 patients (5 received MWS and 3 received SP) out of a projected total of 360 patients are enrolled. Independent t-test analysis reveals no statistical difference between CPTs (P=0.56), specimen length (P=0.12), and fragmentation (P=0.16). No differences are found between any secondary outcomes, and there have been no biopsy-related complications. Conclusion and Potential Impact: This underpowered interim analysis reveals no statistical difference in primary or secondary outcomes between MWS versus SP technique. The current results for both groups are consistent with specimen adequacy criteria determined by American Association for the Study of Liver Disease.
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.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.