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Journal articles on the topic 'Necrosis'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 June 2025

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1

Jeican, Ionuț Isaia, Patricia Inișca, Bogdan Alexandru Gheban, Vlad Anton, Costel Vasile Siserman, Codrin Rebeleanu, Maria Aluaș, Carmen Bianca Crivii, Silviu Albu, and Veronica Trombitaș. "Asymptomatic Esophageal Necrosis in a Patient with Recent COVID-19: The First Case Diagnosed through Autopsy." Medicina 59, no. 1 (January 12, 2023): 154. http://dx.doi.org/10.3390/medicina59010154.

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Acute esophageal necrosis is a rare condition, characterized by a distinctive endoscopic/necropsic image–circumferential black area of the esophagus. This paper presents a case of a 78-year-old patient with recent history of a severe form of COVID-19 (2 months previously), with multiple comorbidities, which presents sudden death in hospital. Anatomic-pathological autopsy showed extensive esophageal necrosis, pulmonary thromboses, and coronarian and aortic atherosclerosis. The histopathological examination revealed necrosis of the esophageal mucosa and phlegmonous inflammation extended to the mediastinum, chronic pneumonia with pulmonary fibrosis, viral myocarditis, papillary muscle necrosis, and pericoronary neuritis. Thromboses and necroses were identified also in the liver, pancreas, and adrenal glands. Post-COVID-19 thromboses can manifest late, affecting various vascular territories, including esophageal ones. Their clinical picture may be diminished or absent in elderly and/or diabetic patients.

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2

Yamasaki, K., and C. Itakura. "Aseptic necrosis of bone in ICR mice." Laboratory Animals 22, no. 1 (January 1, 1988): 51–53. http://dx.doi.org/10.1258/002367788780746601.

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Aseptic bone necrosis was observed in the tibia of 23 ICR mice. Histological changes were characterized by a loss of marrow tissue with proliferation of connective tissue and bone necrosis with empty osteocytic lacunae. Focal necrosis was confined beneath the articular cartilage. Extensive necrosis was present in half or all of the epiphysis. Massive necrosis was noted in the diaphysis of one animal. It was considered that focal necrosis might be related to degenerative osteoarthritis, and that extensive and massive necroses might have been caused by a disturbance of the blood supply.

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3

Maher, Névile, J. Piot, Sylvie Bastien, Jessica Vallance, Patrice Rey, and Lucia Guérin-Dubrana. "Wood necrosis in esca-affected vines: types, relationships and possible links with foliar symptom expression." OENO One 46, no. 1 (March 31, 2012): 15. http://dx.doi.org/10.20870/oeno-one.2012.46.1.1507.

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<p style="text-align: justify;"><strong>Aims</strong>: Esca disease of grapevine is characterised by foliar symptoms associated with the development of various internal wood necroses. The aims of the present study are to determine the type and the quantity of necroses in the various woody compartments of vines, the relationships between them and the links between necroses and severity of foliar symptoms.</p><p style="text-align: justify;"><strong>Methods and results</strong>: Symptomatic and asymptomatic vines cv Cabernet- Sauvignon were cross-sectioned to quantify the different types of internal necrosis in the scions (cordons, heads, and trunks) and rootstocks. Five necrosis « variables » were accounted for: central necrosis, sectorial necrosis, mixed necrosis, white rot, altered perimeter and in addition to the variable healing cone. In the scion, for all types of necrosis variables, a significant correlation between compartments was found. Vines with acute foliar form of esca had very advanced peripheral tissue degradations in the xylem and cambial zones. Chronic foliar expression of esca was associated with quantity of internal necroses higher than those obtained for asymptomatic vines. A logistic model indicated that white rot in the cordons was the best predictor for the chronic form of esca.</p><p style="text-align: justify;"><strong>Conclusion</strong>: Necroses formed a continuum within the plant. The scion is like a single unit with a volume of necroses useful to determine the health status of vines.</p><p style="text-align: justify;"><strong>Significance and impact of the study</strong>: A quantitative analysis of vine internal necroses would open up new possibilities for esca-epidemic approaches.</p>

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4

Tejido Sandoval, C., F. Baiocchi Ureta, and S. Zarraquiños Martínez. "Acute esophageal necrosis." Revista Andaluza de Patología Digestiva 44, no. 1 (March 3, 2021): 30–32. http://dx.doi.org/10.37352/2021441.8.

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Resumen La necrosis esofágica aguda es una patología infrecuente y frecuentemente infradiagnosticada. Es importante su sospecha para realizar un diagnóstico y tratamiento precoces. La manifestación más frecuente es la hemorragia digestiva alta. Presentamos el caso de un paciente con necrosis esofágica aguda a consecuencia del desarrollo de una cetoacidosis diabética.

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5

Cicák, A., and I. Mihál. "Can artificial wounding of beech stems induce necroses?" Journal of Forest Science 51, No. 12 (January 10, 2012): 559–63. http://dx.doi.org/10.17221/4588-jfs.

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The paper presents data on the induction of necroses after small injuries to beech stems caused by electrodes during measuring cambium electric resistance. Altogether 121 beech stems of tree class 1&ndash;3 (according to Kraft) were evaluated. Among 2,904 mechanical injuries in 121 stems evaluated (24 per stem), 155 injuries induced necroses, hence each 19<sup>th</sup> injury induced necrosis. Most stems (33.06%) showed one necrosis, few stems (4.96%) showed even four necroses. 28.93% of stems did not show any necrosis. In order to prevent the infection of wounds and subsequent induction of necroses the authors recommend to treat any wounds with a suitable fungicide after using an equipment causing even negligible wounds of stems.

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6

Wang, Michael X., Timothy Morgan, William Lungo, Lina Wang, Gloria Z. Sze, and Samuel W. French. "“Piecemeal” Necrosis: Renamed Troxis Necrosis." Experimental and Molecular Pathology 71, no. 2 (October 2001): 137–46. http://dx.doi.org/10.1006/exmp.2001.2397.

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7

Kerschbaumer, Johannes, Matthias Demetz, Aleksandrs Krigers, Meinhard Nevinny-Stickel, Claudius Thomé, and Christian F. Freyschlag. "Risk Factors for Radiation Necrosis in Patients Undergoing Cranial Stereotactic Radiosurgery." Cancers 13, no. 19 (September 22, 2021): 4736. http://dx.doi.org/10.3390/cancers13194736.

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Purpose: single-staged stereotactic radiosurgery (SRS) is an established part of the multimodal treatment in neuro-oncology. Radiation necrosis after high-dose irradiation is a known complication, but there is a lack of evidence about the risk factors. The aim of this study was to evaluate possible risk factors for radiation necrosis in patients undergoing radiosurgery. Methods: patients treated with radiosurgery between January 2004 and November 2020 were retrospectively analyzed. The clinical data, imaging and medication were gathered from electronic patient records. The largest diameter of the tumors was measured using MRI scans in T1 weighted imaging with gadolinium and the edema in T2 weighted sequences. The diagnosis of a radiation necrosis was established analyzing imaging criteria combined with clinical course or pathologically confirmed by subsequent surgical intervention. Patients developing radiation necrosis detected after SRS were compared to patients without evidence of an overshooting irradiation reaction. Results: 388 patients were included retrospectively, 61 (15.7%) of whom developed a radiation necrosis. Median follow-up was 24 (6–62) months with a radiation necrosis after 8 (6–12) months. The most frequent tumors were metastases in 47.2% of the cases, followed by acoustic neuromas in 32.2% and meningiomas in 13.4%. Seventy-three (18.9%) patients already underwent one or more previous radiosurgical procedures for different lesions. The mean largest diameter of the tumors amounted to 16.3 mm (±6.1 mm). The median—80%—isodose administered was 16 (14–25) Gy. Of the radiation necroses, 25 (43.1%) required treatment, in 23 (39.7%) thereof, medical treatment was applied and in 2 (3.4%) cases, debulking surgery was performed. In this study, significantly more radiation necroses arose in patients with higher doses (HR 1.3 [CI 1.2; 1.5], p < 0.001) leading to a risk increment of over 180% between a radiation isodose of 14 and 20 Gy. The maximum diameter was a second significant risk factor (p = 0.028) with an HR of 1065 for every 1 mm increase in multivariate analysis. Conclusion: large diameter and high doses were reliable independent risk factors leading to more frequent radiation necroses, regardless of tumor type in patients undergoing radiosurgery. Alternative therapeutic procedures may be considered in lesions with large volume and an expected high radiation doses due to the increased risk of developing radiation necrosis.

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8

Prasad, Dr C. S. B. R. "New insights into programmed necrosis." JOURNAL OF CLINICAL AND BIOMEDICAL SCIENCES 04, no. 4 (December 15, 2014): 339–40. http://dx.doi.org/10.58739/jcbs/v04i4.11.

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9

Schjødt, Mette Soelberg, Rikke Bech, and Anne Braae Olesen. "Acral Necrosis in a COVID-19-Infected Man Treated with Botulinum Toxin Type A." Case Reports in Dermatology 13, no. 3 (December 27, 2021): 568–73. http://dx.doi.org/10.1159/000520589.

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COVID-19 has been associated with acral ischemia and digital necrosis. Standard treatment of acral ischemia and digital or acral necrosis includes ongoing therapy with vasodilators and anticoagulants. However, these treatments are not always efficient to avoid the progression of necroses, which in the worst case can lead to amputation. Here, we report a case in which interdigital Botox® (botulinum toxin type A) nerve cord injection stopped the progression of acral necroses arising from an underlying vasculopathy due to COVID-19. Moreover, Botox® injection eliminated inflammation in the affected acral area within 2 weeks. This is the first case report to suggest Botox® injection as a new and improving treatment for acral necroses due to COVID-19.

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10

Monika, Kwiatkowska, and Izmaiłow Romana. "Ovules, Female Gametophytes and Embryos are More Sensitive to Heavy Metal Pollution than Anthers and Pollen of Cardaminopsis Arenosa (L.) Hayek (Brassicaceae), A Member of Calamine Flora." Acta Biologica Cracoviensia s. Botanica 56, no. 1 (September 11, 2014): 128–37. http://dx.doi.org/10.2478/abcsb-2014-0015.

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Abstract Reproductive processes including male and female lines, embryo and endosperm development were studied in Cardaminopsis arenosa (syn. Arabidopsis arenosa) growing on two metalliferous sites (Bukowno and Bolesław, S. Poland), rich in Zn, Pb, Cd and other metals. Disturbances of developmental processes and necroses observed in anthers and ovules influenced plant fertility and seed set of plants from both metal-polluted sites. In anthers, disturbances and necrosis during male meiosis and pollen development occurred at low frequency (4-5%). Pollen grain viability was very high, reaching over 90%. In ovules the frequency of abnormal meiosis, female gametophyte developmental disturbances and necrosis was high, 23.5-28% depending on site. The polluted environment also affected embryo and endosperm. Necrosis of whole generative structures decreased plant fertility. This study indicates that the range of disturbances and necroses in embryological structures and processes (at gametophyte level) gives a set of useful characters to determine plant tolerance to stress, complementary to many tolerance characters at the sporophyte level of plant ontogenesis.

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11

Thomas, Austin, Athira Jayan, Yusuf Chang, Reese Svetgoff, Saumil Datar, Vinayak Memula, Michael Huang, Laura Winikka, and Jeffrey Chen. "Pembrolizumab-associated acral necrosis and esophageal necrosis." Current Problems in Cancer: Case Reports 8 (December 2022): 100193. http://dx.doi.org/10.1016/j.cpccr.2022.100193.

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12

Siegal, Deborah M., Richard J. Cook, and Theodore E. Warkentin. "Acute Hepatic Necrosis and Ischemic Limb Necrosis." New England Journal of Medicine 367, no. 9 (August 30, 2012): 879–81. http://dx.doi.org/10.1056/nejmc1207074.

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13

Barros, L. F., T. Hermosilla, and J. Castro. "Necrotic volume increase and the early physiology of necrosis." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 130, no. 3 (October 2001): 401–9. http://dx.doi.org/10.1016/s1095-6433(01)00438-x.

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14

A, Bajaj. "The Cadaverous Carnage- Aseptic Bone Necrosis." Haematology International Journal 5, no. 1 (2021): 1–6. http://dx.doi.org/10.23880/hij-16000182.

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Aseptic necrosis is a commonly discerned degenerative condition of the bone characteristically constituted of deteriorated cellular components. Generally, the condition arises secondary to discontinuity of subchondral vascular effusion. The disorder is additionally designated as avascular necrosis, osteonecrosis or ischemic bone necrosis and no bone is exempt. Specific sites incriminated are the tibial tuberosity as encountered in Osgood-Schlatter’s disease or proximal femoral epiphysis as denominated in Legg-Calve’-Perthes disease.

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15

Slaoui, Aziz. "Potassium Permanganate Necrosis of the Vagina." Women Health Care and Issues 5, no. 3 (May 4, 2022): 01–03. http://dx.doi.org/10.31579/2642-9756/117.

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A 19-year-old woman was referred to our emergency department for massive vaginal hemorrhage following an attempted clandestine abortion by intravaginal instillation of potassium permanganate crystals. Primigravida, she was 7 weeks pregnant and had no particular pathological history. Upon admission, she was in hemorrhagic shock with blood pressure at 7/3 mmHg and tachycardia at 152 bpm. Pelvic examination revealed active bleeding from the right vaginal wall. The cervix and vulva were normal. Mechanical hemostasis using a sterile gauze pad mounted on a long forceps was directly applied at the same time as the resuscitative management. After 3 minutes of compression, hemostasis was achieved and vaginal necrotic lesions appeared

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16

HOKOISHI, Mariko, Misuzu MARUYAMA, Shinji MURAKAMI, and Koji HASHIMOTO. "A Case of Encapsulated Fat Necrosis." Nishi Nihon Hifuka 66, no. 5 (2004): 451–53. http://dx.doi.org/10.2336/nishinihonhifu.66.451.

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17

Sari Dogan, Fatma, Alev Eceviz, Gulsah Sasak, and Ali Riza Odabas. "Acute Tubuler Necrosis Related to Rhabdomyolysis." Turkish Nephrology Dialysis Transplantation 23, no. 2 (May 6, 2014): 150–52. http://dx.doi.org/10.5262/tndt.2014.1002.13.

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18

Kibatala, Mtagi, Asmaa Thena, Mikaly Msangi, Nancy Mugabisho, and Gilbert Kwesi. "Subcutaneous Fat Necrosis in a Newborn." International Journal of Science and Research (IJSR) 11, no. 8 (August 5, 2022): 442–44. http://dx.doi.org/10.21275/sr22727203615.

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19

Boukerrouche, Mohammed oussama. "Gastric Conduit Necrosis in Esophageal Surgery." International Journal of Cell Biology and Physiology 05, no. 01 (January 1, 2022): 01–05. http://dx.doi.org/10.55640/ijcbp-511.

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This study aims to investigate the occurrence, risk factors, clinical presentation, and management of gastric conduit necrosis following esophageal reconstruction, providing insights into its impact on patient outcomes and strategies for prevention and treatment. A retrospective analysis was conducted on patients who underwent esophageal reconstruction with gastric conduit creation between January 2010 and December 2023. Clinical records, including surgical notes, postoperative outcomes, and follow-up data, were reviewed to identify cases of gastric conduit necrosis. Risk factors such as surgical techniques, preoperative conditions, and postoperative complications were analyzed. Management approaches, including surgical interventions and conservative treatments, were also assessed. Gastric conduit necrosis was identified in X% of the patients undergoing esophageal reconstruction. Risk factors included advanced age, diabetes mellitus, and prolonged ischemia time. Clinical presentation varied from mild symptoms, such as abdominal pain and fever, to severe complications requiring emergent surgical intervention. Early detection through imaging and endoscopy was crucial for effective management. Treatment often involved surgical debridement and, in severe cases, conduit replacement. Postoperative recovery and long-term outcomes were generally favorable with timely intervention, although some patients experienced significant morbidity. Gastric conduit necrosis is a serious complication following esophageal reconstruction, with identifiable risk factors that can guide preventive measures. Early recognition and intervention are critical for improving patient outcomes. This study highlights the importance of vigilant postoperative monitoring and the need for tailored management strategies to address this complex issue effectively. Further research is needed to refine preventive strategies and enhance treatment protocols to reduce the incidence and impact of gastric conduit necrosis.

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20

Tomifuji, Masayuki, Koji Araki, Hiroshi Suzuki, Yoshihiro Miyagawa, Shingo Tanaka, Yuya Tanaka, and Akihiro Shiotani. "Laryngeal Necrosis." Nihon Kikan Shokudoka Gakkai Kaiho 67, no. 4 (2016): 256–63. http://dx.doi.org/10.2468/jbes.67.256.

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21

Jardón Gómez, Alejandro, Ana Cristina King, and Carlos Pacheco Díaz. "Necrosis avascular." Revista de la Facultad de Medicina 63, no. 2 (March 10, 2020): 18–23. http://dx.doi.org/10.22201/fm.24484865e.2020.63.2.03.

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The clinical presentation of a proximal femoral fracture is completely different between young and adult patients. Unlike closed proximal femoral fractures, the incidence of exposed fractures is found in the young population between 15 and 30 years of age. Osteonecrosis of the femoral head is one the complications we can find in this type of fractures. Avascular necrosis (AVN or osteonecrosis) is defined as the interruption of blood supply to the femoral head due to trauma, infectionalcohol or steroid use, resulting in bone necrosis, joint collapse and osteoarthrosis. The treatment will depend on the clinical presentation, age of the patient and when the diagnosis is made. This is a case report of a 16-year-old patient with a gunshot wound on the hip. Surgical cleansing and closed reduction plus internal fixation with a nail in the center of the spine were performed. A 3-year clinical and radiographic follow up was made, observing the evolution of the fracture and the subsequent avascular necrosis that the patient presented. Key words: Proximal femoral fracture; hip; avascular necrosis (AVN, osteonecrosis); open fracture; osteoarthritis.

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22

Chattopadhyay, Sudipta, and Puvana Chandra. "Putaminal Necrosis." New England Journal of Medicine 356, no. 22 (May 31, 2007): e23. http://dx.doi.org/10.1056/nejmicm060009.

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23

Isenmann, Rainer, Markus BÜChler, Waldemar Uhl, Peter Malfertheiner, Markus Martini, and Hans G. Beger. "Pancreatic Necrosis." Pancreas 8, no. 3 (May 1993): 358–61. http://dx.doi.org/10.1097/00006676-199305000-00012.

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24

O'Brien, Timothy J. "Cetrimide Necrosis." Australasian Journal of Dermatology 34, no. 3 (December 1993): 118. http://dx.doi.org/10.1111/j.1440-0960.1993.tb00879.x.

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25

Housholder-Hughes, Susan D. "SKIN NECROSIS." AJN, American Journal of Nursing 104, no. 10 (October 2004): 16. http://dx.doi.org/10.1097/00000446-200410000-00008.

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26

Gottlieb, Amy G., Santosh Pandipati, Karlotta M. Davis, and Ronald S. Gibbs. "Uterine Necrosis." Obstetrics & Gynecology 112, no. 2, Part 2 (August 2008): 429–31. http://dx.doi.org/10.1097/aog.0b013e31817b0781.

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27

Balotti, Richard F., Richard J. Malone, and Robert J. Schanzer. "Warfarin Necrosis." American Journal of Physical Medicine & Rehabilitation 88, no. 4 (April 2009): 263. http://dx.doi.org/10.1097/phm.0b013e31819c5a04.

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28

Berbis, P. "Necrosis cutáneas." EMC - Dermatología 41, no. 1 (January 2007): 1–16. http://dx.doi.org/10.1016/s1761-2896(07)70370-9.

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29

Rosales-Castillo, Antonio, Antonio García-Sánchez, and José Mario Sabio. "Scalp necrosis." Medicina Clínica (English Edition) 148, no. 11 (June 2017): e61. http://dx.doi.org/10.1016/j.medcle.2017.05.008.

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30

Uzdensky, A. B. "Controlled Necrosis." Biochemistry (Moscow) Supplement Series A: Membrane and Cell Biology 4, no. 1 (March 2010): 3–12. http://dx.doi.org/10.1134/s1990747810010022.

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31

Kroemer, Guido. "Regulated necrosis." Seminars in Cell & Developmental Biology 35 (November 2014): 1. http://dx.doi.org/10.1016/j.semcdb.2014.08.005.

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32

Canteli, Begoña, Fermín Saez, Antonio de los Ríos, and Carmen Alvarez. "Fat necrosis." Skeletal Radiology 25, no. 3 (April 4, 1996): 305–7. http://dx.doi.org/10.1007/s002560050086.

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33

Dutner, Joseph M., Robert W. Herold, James P. Wilson, Megan E. Bunting, Jason S. Bullock, Daniel D. Dunham, and Thomas M. Johnson. "Fracture necrosis." Journal of the American Dental Association 151, no. 6 (June 2020): 454–63. http://dx.doi.org/10.1016/j.adaj.2020.01.024.

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34

&NA;. "Aseptic Necrosis." Journal of Clinical Rheumatology 18, no. 3 (April 2012): 163. http://dx.doi.org/10.1097/rhu.0b013e318252df82.

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35

Fogo, Agnes. "Cortical Necrosis." American Journal of Kidney Diseases 41, no. 1 (January 2003): E27—E28. http://dx.doi.org/10.1053/s0272-6386(13)90050-0.

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36

Branum, Gene, John Galloway, Wendy Hirchowitz, Morris Fendley, and John Hunter. "Pancreatic Necrosis." Annals of Surgery 227, no. 6 (June 1998): 870–77. http://dx.doi.org/10.1097/00000658-199806000-00010.

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37

Carabelli, Robert A., and Marilyn Goldman. "Avascular Necrosis." Physical Therapy 67, no. 4 (April 1, 1987): 542–44. http://dx.doi.org/10.1093/ptj/67.4.542.

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38

VAN DE WIELE, CHRISTOPHE, RUDÍ ANDRÉ DIERCKX, L. NOENS, and M. SIMONS. "Aseptic Necrosis." Clinical Nuclear Medicine 22, no. 2 (February 1997): 101–3. http://dx.doi.org/10.1097/00003072-199702000-00006.

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39

McKnight, J. T. "Warfarin necrosis." Archives of Family Medicine 1, no. 1 (September 1, 1992): 105–8. http://dx.doi.org/10.1001/archfami.1.1.105.

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40

Whitmore, S. Elizabeth. "Cutaneous Necrosis." Archives of Dermatology 132, no. 3 (March 1, 1996): 343. http://dx.doi.org/10.1001/archderm.1996.03890270119019.

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41

Boccaletti, V. P. "Penile Necrosis." Archives of Dermatology 136, no. 2 (February 1, 2000): 259—c—264. http://dx.doi.org/10.1001/archderm.136.2.259-c.

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42

Handayani, Melina, and Muhammad Bayu Rizaldy, Sp.OT. "Avascular Necrosis." Jurnal Kedokteran Diponegoro (Diponegoro Medical Journal) 12, no. 5 (August 31, 2023): 326–29. http://dx.doi.org/10.14710/dmj.v12i5.38551.

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Osteonecrosis can be defined as bone cell death resulting from impaired blood flow to the bone due to traumatic or non-traumatic events. Case Presentation: We present a case in which a 62-year-old female came to the Orthopedic Surgery Polyclinic with complaints of pain in her groin. The pain is intermittent and worsens when the patient moves his legs. This makes it difficult for patients to sit and have pain when walking, so they need a cane as a tool. This complaint has been felt for ± 1.5 years and has been getting worse since this 1 month. During the pain the patient said he was taking pain relievers but his complaints did not decrease. On local examination in the left Hip Joint region, it was found that on look examination there was no visible deformity, swelling and skin color that was the same as the surrounding area. On examination of the feel found positive tenderness. On AP pelvic X-ray examination, there was a fracture of the left femoral head with superior displacement. Treatment for this patient includes non-surgical and surgical (total hip replacement). Conclusion: The patient was diagnosed with Avascular necrosis.

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43

Azzi, Alain J., Gabriel Bouhadana, Fanyi Meng, and Peter G. Davison. "Spontaneous necrosis of a single digit: watershed necrosis." Case Reports in Plastic Surgery and Hand Surgery 8, no. 1 (January 1, 2021): 8–11. http://dx.doi.org/10.1080/23320885.2021.1874385.

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44

Koçer, Uğur, Yiğit Özer Tiftikcioğlu, Hasan Mete Aksoy, and Önder Karaaslan. "Skin and Soft Tissue Necrosis following Hymenoptera Sting." Journal of Cutaneous Medicine and Surgery 7, no. 2 (March 2003): 133–35. http://dx.doi.org/10.1177/120347540300700207.

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Background: All kinds of bees, wasps, and hornets are members of the hymenoptera order. Local hypersensitivity reactions after bee stings are very common and well studied. However, tissue necroses following untreated bee stings are extremely rare and they are not well documented. Objective: Two extremely rare cases of extensive skin and soft tissue necrosis following hymenoptera stings are presented. Current literature and treatment options are discussed. Conclusions: Local skin reactions following bee stings may result in severe complications such as tissue necrosis if left untreated. Skin grafting following surgical debridement is an adequate and practical treatment modality for such cases.

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45

Chawla, Sakshi, Amresh Kumar Saxena, and Sanjay Kumar. "Assessment of Ossicular Necrosis in Tubotympanic (Mucosal) Type of Chronic Otitis Media." Journal of Evolution of Medical and Dental Sciences 10, no. 36 (September 6, 2021): 3127–31. http://dx.doi.org/10.14260/jemds/2021/637.

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BACKGROUND We wanted to study the preoperative clinical, audiological, radiological findings & compare them with the perioperative findings of ossicular necrosis. METHODS 100 patients were clinically diagnosed as mucosal chronic otitis media (COM). They underwent a thorough clinical, audiological & radiological examination. X-ray mastoid Schuller's view on both sides was done in all patients & HRCT temporal bone was done in 51 patients. They were then posted for surgery & findings were compared with the perioperative ossicular necrosis. RESULTS 42 patients had ossicular defects perioperatively. Incus was found to be the most commonly necrosed ossicle & malleus was the most resistant ossicle. There was a positive association found between duration of disease, posterior perforations, large central & subtotal perforations, polypoidal middle ear mucosa, granulations over margins of perforations & audiological findings with the perioperative ossicular defects. HRCT was the most reliable investigation to predict ossicular necrosis. CONCLUSIONS From the study, it was concluded that all patients with mucosal COM can be assessed preoperatively for ossicular erosion. HRCT gives us a preoperative picture of the extent of ossicular necrosis & helps the surgeon in planning the surgical intervention. KEY WORDS COM, HRCT, Ossicular Necrosis, Mucosal, PTA

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46

Hernádez Serratos, Midori Jocelyn, Germán Isauro Garrido Fariñas, Mireya Juárez Ramírez, Jorge Luis Tórtora Pérez, Elein Hernández Trujillo, and Víctor Manuel Díaz Sánchez. "Descripción de hallazgos histopatológicos en corderos intoxicados con selenio por bolos intrarruminales." Archivos Latinoamericanos de Producción Animal 31, Suplemento (June 15, 2023): 357–62. http://dx.doi.org/10.53588/alpa.310560.

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El selenio es un micronutriente esencial para los rumiantes, participa en el funcionamiento óptimo de proteínas y enzimas que pueden combatir el estrés oxidante en el organismo. Sin embargo, su toxicidad está documentada en diferentes especies. El objetivo del presente trabajo fue describir los hallazgos histopatológicos en corderos intoxicados con selenio administrado a través de bolos intrarruminales. 4 corderos de 3 meses de edad y 15 kg promedio suplementados con selenio mediante bolos intrarruminales murieron intoxicados. Los principales hallazgos a la necropsia fueron edema pulmonar, necrosis, hemorragia e hiperqueratosis en retículo-rumen. La histopatología de los órganos mostró congestión de capilares alveolares, hemorragia, edema y membranas hialinas en pulmón; zonas de hemorragia en parénquima hepático, sinusoides hepáticos congestionados, degeneración y necrosis de hepatocitos, degeneración lipídica hepatocelular; retículo con zonas de necrosis, denegeración de la mucosa y zonas de hiperplasia, además de hiperqueratosis; múltiples áreas de degeneración y necrosis de fibras musculares cardíacas; zonas de hemorragia y congestión en parénquima renal, degeneración y necrosis tubular. Este estudio se evidenciaron las principales lesiones relacionas a la intoxicación con selenio en corderos sumplementados con el mineral mediante bolos intrarruminales.

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Paquet, Philippe. "Macrophages and Tumor Necrosis Factor a in Toxic Epidermal Necrolysis." Archives of Dermatology 130, no. 5 (May 1, 1994): 605. http://dx.doi.org/10.1001/archderm.1994.01690050073012.

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Paquet, P. "Macrophages and tumor necrosis factor alpha in toxic epidermal necrolysis." Archives of Dermatology 130, no. 5 (May 1, 1994): 605–8. http://dx.doi.org/10.1001/archderm.130.5.605.

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Hua, Minh, Leonardo Pasalic, Robert Lindeman, Philip Hogg, and Vivien M. Chen. "Procoagulant Role Of Necrotic Platelets Demonstrated Using Novel Platelet Necrosis Marker." Blood 122, no. 21 (November 15, 2013): 3512. http://dx.doi.org/10.1182/blood.v122.21.3512.3512.

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Abstract Strong agonist stimulation generates a platelet subpopulation characterized by phosphatidylserine (PS) exposure, loss of mitochondrial membrane potential and high fibrinogen retention. This population is proposed to be procoagulant, dependent on formation of the mitochondrial permeability transition pore (mPTP) with a distinct role from activated aggregratory platelets. These platelets have features of necrosis. The functional relevance of necrotic platelets in vivo is unknown due to lack of a suitable marker for these platelets. We show that a novel small molecule cellular necrosis marker, GSAO1, labels a procoagulant platelet subpopulation with features of necrosis and use it to explore the functional role of these platelets. We demonstrated using flow cytometry analysis of washed human platelets that fluorescently tagged GSAO labels a subpopulation of P-selectin positive platelets after thrombin and collagen stimulation with features of necrosis: high annexin V binding, calcein loss and dependence on exogenous calcium. This population is not dependent on the intrinsic apoptosis pathway as there was no change with pancaspase inhibition using ZVADFMK prior to dual agonist stimulation (p=0.567, n=5). In contrast, inhibition of mPTP formation through cyclophilin-D inhibition with cyclosporine A significantly inhibited GSAO+ve platelet generation (p<0.001, n=5), confirming dependence on the mitochondrial necrosis pathway. Mass spectrometry analysis of biotin-GSAO labelled proteins from platelets after streptavidin pull down identified thromboxane A synthase (TBXAS-1) as the major binding ligand after dual stimulation. Binding to TBXAS-1 was abrogated by dithiol alkylation, showing the mechanism of retention of GSAO in necrotic platelets is via covalent cross linking of closely-spaced cysteine thiols in the ligand. This allows persistent signal from the probe within the necrotic platelet with no evidence of washout. GSAO+ve platelets correlated with procoagulant potential as measured by peak and endogenous thrombin potential in the calibrated automated thrombogram (CAT) assay. Linear regression analysis showed a significant relationship between % change in GSAO+ve platelets and % change in peak thrombin after treatment with cyclosporine A or in absence of exogenous calcium (R2=0.648, p<0.01), indicating that GSAO identifies a procoagulant subpopulation. In contrast, no relationship was seen between P-selectin and peak thrombin values (R2=0.002). Inhibition of platelet activation by aspirin had no effect on the generation of GSAO+ve platelets indicating a potential uncoupling between platelet activation and necrosis pathways. After establishing that the imaging compound does not affect platelet function and coagulation in vitro, or thrombus formation in vivo, we went on to investigate the presence of GSAO+ve necrotic platelets in thrombus formation in a collagen dependent (ferric chloride) and collagen independent (laser injury) murine model of thrombosis. Confocal intravital imaging of the cremaster arterioles with fluorescent GSAO and tagged-CD42b demonstrated GSAO+ve platelets in the occlusive platelet aggregate after initiation with 10% ferric chloride. The GSAO+ve aggregating platelets specifically colabeled with calcium sensing dye rhodamine 2 indicating high sustained intracellular calcium, consistent with a necrotic phenotype. There was no signal with active site replaced control GSCA. In contrast, the laser injury model showed minimal staining with GSAO three minutes post laser injury. Using a novel platelet necrosis marker, we are able to demonstrate that necrotic platelets are procoagulant and present in the occlusive ferric chloride model and not in the non-occlusive laser injury model of thrombosis. This suggests excess platelet necrosis may be a key driving factor underlying pathological occlusive thrombi. GSAO is a promising tool for understanding factors that potentiate platelet necrosis which may offer attractive anti-thrombotic targets. 1. Park D, Don AS, Massamiri T, et al. Noninvasive imaging of cell death using an hsp90 ligand. J Am Chem Soc. 2011;133(9):2832-2835. Disclosures: No relevant conflicts of interest to declare.

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Robertson, Paul A. "Tumor Necrosis Factor Induces Hemorrhagic Necrosis of a Sarcoma." Annals of Internal Medicine 111, no. 8 (October 15, 1989): 682. http://dx.doi.org/10.7326/0003-4819-111-8-682.

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