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1.
J Cardiothorac Surg ; 19(1): 177, 2024 Apr 04.
Article in English | MEDLINE | ID: mdl-38575949

ABSTRACT

BACKGROUND: Hyperparathyroidism (HPT) is a disease caused by hypersecretion of one or more parathyroid glands, it can be associated with ectopic mediastinal parathyroid glands (MEPA) in 2% of cases. The use of video-assisted thoracoscopic surgery (VATS) for the surgical resection of these glands is a safe, cost-effective, and low morbidity option for patients with MEPA. We report a case series of patients with this disease managed with VATS, the first in Mexico and Latinamerica. METHODS: From 2008 to 2022, a retrospective study involving patients with MEPA and treated by VATS approach was performed in a tertiary hospital in Mexico city. Relevant biochemical and clinical variables such as imaging studies, pre and postoperative laboratory results, surgical strategy, outcomes and pathological analysis were analyzed. RESULTS: Four cases of mediastinal parathyroid adenomas causing HPT were included. All patients were female with a median age of 52.5 years-old (range 46-59 years), half of the patients had primary HPT and the others tertiary HPT after kidney transplant. 75% of cases had a MEPA in the medium mediastinum, all had a preoperative positive SPECT-CT 99mTc Sestamibi scan. Mean preoperative PTH was 621.3pg/mL (182-1382pg/mL). All patients successfully underwent parathyroidectomy with a VATS approach, no deaths were reported. CONCLUSIONS: VATS is a minimally invasive surgery that provides adequate access to mediastinal located glands, optimal visualization of mediastinal structures and has a high resection success rate with less complications and morbidity than open approaches.


Subject(s)
Parathyroid Neoplasms , Humans , Female , Middle Aged , Male , Parathyroid Neoplasms/diagnostic imaging , Parathyroid Neoplasms/surgery , Parathyroid Neoplasms/pathology , Mediastinum/surgery , Retrospective Studies , Parathyroid Glands/surgery , Parathyroid Glands/pathology , Parathyroidectomy/methods , Technetium Tc 99m Sestamibi
2.
Preprint in English | medRxiv | ID: ppmedrxiv-21266111

ABSTRACT

Patients with COVID-19 may develop abnormal inflammatory response and lymphopenia, followed in some cases by delayed-onset syndromes, often long-lasting after the initial SARS-CoV-2 infection. As viral infections may activate human endogenous retroviral elements (HERV), we studied the effect of SARS-CoV-2 on HERV-W and HERV-K envelope (ENV) expression, known to be involved in immunological and neurological pathogenesis of human diseases. Our results have showed that the exposure to SARS-CoV-2 virus activates early HERV-W and K transcription but only HERV-W ENV protein expression, in an infection- and ACE2-independent way within peripheral blood mononuclear cell cultures from one-third of healthy donors. Moreover, HERV-W ENV protein was significantly increased in serum and plasma of COVID-19 patients, correlating with its expression in CD3+ lymphocytes and with disease severity. Finally, HERV-W ENV was found expressed in post-mortem tissues of lungs, heart, brain olfactory bulb and nasal mucosa from acute COVID-19 patients in cell-types relevant for COVID-19-associated pathogenesis within affected organs, but different from those expressing of SARS-CoV-2 antigens. Altogether, the present study revealed that SARS-CoV-2 can induce HERV-W ENV expression in cells from individuals with symptomatic and severe COVID-19. Our data suggest that HERV-W ENV is likely to be involved in pathogenic features underlying symptoms of acute and post-acute COVID. It highlights the importance to further understand patients genetic susceptibility to HERV-W activation and the relevance of this pathogenic element as a prognostic marker and a therapeutic target in COVID-19 associated syndromes. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=144 SRC="FIGDIR/small/21266111v2_ufig1.gif" ALT="Figure 1"> View larger version (68K): org.highwire.dtl.DTLVardef@1be71a1org.highwire.dtl.DTLVardef@1621b8org.highwire.dtl.DTLVardef@fff085org.highwire.dtl.DTLVardef@107cb0c_HPS_FORMAT_FIGEXP M_FIG C_FIG

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