ABSTRACT
Cardiovascular disease, COPD, and diabetes (DM) are associated with increased complications with COVID-19. A correlation between COVID-19 and diabetic ketoacidosis (DKA) or Hyperosmolar Hyperglycemic Syndrome (HHS) has been suggested; however, the precise mechanism remains unclear. We present a case series of six patients with COVID-19 infections who were found to have DKA, HHS, or mixed picture. Wedescribe an association between COVID-19 and hyperglycemic emergencies. Six patients (50% male, 50% female, mean age 47.667 ± 18.747) were identified from November 2021 to February 2022. Comorbidities included DM (83.3%), HTN (50%), as well as ESRD, A-Fib, ISLD, HIV, and dementia (each 16.7%). Common review of systems included nausea and vomiting (50%), abdominal pain (33.3%), dyspnea (33.3%), and decreased appetite (33.3%). Additional findings were dysarthria, facial droop, generalized weakness, productive cough, myalgias, and increased urinary frequency (16.7%). Patients were diagnosed with DKA (50%), mixed process (33.3%), andHHS(16.7%). In terms of COVID-19 symptoms, most patients were asymptomatic (83.3%), with one patient developing hypoxia. The survival rate was 100%. Infections can incite DKA/HHS; yet, COVID-19 may have factors that amplify this process, in the setting of pancreatic beta-cell dysfunction from the virus itself. This may contribute to why diabetic patients have a ten times higher risk of death if they develop COVID-19. This virus binds to ACE2 receptors in the pancreas and damages the islets, ultimately decreasing insulin release. Here, we introduce cases of DKA/HHS in the setting of COVID-19, to understand the relationship between how COVID-19 infections may exacerbate diabetic complications.
ABSTRACT
The carotid sinus-arterial baroreflex is essential in maintaining blood pressure (BP) regulation. Afferent baroreflex failure (ABF) can present with labile changes in BP within seconds and can be secondary to neck surgery or radiation. We present here the first case, to our knowledge, of ABF precipitated by thyroidectomy, in a patient with active COVID-19 pneumonia, causing difficult control of severely labile BP in a critical care unit. Contributing factors included her critical illness state with upregulation of IL-6 leading to pituitary-adrenal axis alteration, her thyroidectomy further exacerbating autonomic dysfunction, as well as downregulation of ACE2 via COVID-19 infection. Management was achieved with a combination of midodrine and clonidine catered to specific BP thresholds. Additional research with a multidisciplinary approach is warranted to fully optimize the treatment of ABF in patients with neck surgery and or inflammatory conditions such as COVID-19.
ABSTRACT
Non-Hodgkin lymphoma is made from the B-cell lineage and includes extra-nodal marginal lymphomas, follicular lymphomas, mantle cell lymphoma, diffuse large B-cell lymphoma, and Burkitt lymphoma. Burkitt lymphoma is associated with Epstein Barr Virus and Human Immunodeficiency Virus. Although it is common for other B-cell lymphomas to develop in the stomach, it is less common for Burkitt lymphoma tumors to manifest there. Additionally, primary and/or secondary involvement of the duodenum, pancreas, and intestines is very rare in Burkitt lymphoma. Herein, we present a male diagnosed with extensive Burkitt lymphoma of the bone, lymph nodes, pancreas, small intestine, duodenum, and stomach.
ABSTRACT
BACKGROUND: Previously, we showed that 6ß-hydroxytestosterone (6ß-OHT), a cytochrome P450 1B1 (CYP1B1)-derived metabolite of testosterone, contributes to angiotensin II (Ang II)-induced hypertension in male mice. This study was conducted to test the hypothesis that 6ß-OHT contributes to increased vascular reactivity, endothelial dysfunction, vascular hypertrophy, and reactive oxygen species production associated with Ang II-induced hypertension. METHODS: Eight- to 10-week-old intact or castrated C57BL/6 J (Cyp1b1+/+ and Cyp1b1-/-) mice were anesthetized for implantation of a micro-osmotic pump which delivered Ang II (700 ng/kg/day) or saline for 14 days. Mice were injected with 6ß-OHT (15 µg/g b.w every third day), flutamide (8 mg/kg every day), or its vehicle. Blood pressure was measured via tail-cuff. Vascular reactivity, endothelial-dependent and endothelial-independent vasodilation, media to lumen ratio, fibrosis by collagen deposition, and reactive oxygen species production by dihydroethidium staining were determined in the isolated thoracic aorta. RESULTS: The response of thoracic aorta to phenylephrine and endothelin-1 was increased in Ang II-infused Cyp1b1+/+ mice compared to intact Cyp1b1-/- or castrated Cyp1b1+/+ and Cyp1b1-/- mice; these effects of Ang II were restored by treatment with 6ß-OHT. Ang II infusion caused endothelial dysfunction, as indicated by decreased relaxation of the aorta to acetylcholine in Cyp1b1+/+ but not Cyp1b1-/- or castrated Cyp1b1+/+ and Cyp1b1-/- mice. 6ß-OHT did not alter Ang II-induced endothelial dysfunction in Cyp1b1+/+ mice but restored it in Cyp1b1-/- or castrated Cyp1b1+/+ and Cyp1b1-/- mice. Ang II infusion increased media to lumen ratio and caused fibrosis and reactive oxygen species production in the aorta of Cyp1b1+/+ mice. These effects were minimized in the aorta of Cyp1b1-/- or castrated Cyp1b1+/+ and Cyp1b1-/- mice and restored by treatment with 6ß-OHT. Treatment with the androgen receptor antagonist flutamide reduced blood pressure and vascular hypertrophy in castrated Ang II-infused mice injected with 6ß-OHT. CONCLUSIONS: 6ß-OHT is required for the action of Ang II to increase vascular reactivity and cause endothelial dysfunction, hypertrophy, and increase in oxygen radical production. The effect of 6ß-OHT in mediating Ang II-induced hypertension and associated hypertrophy is dependent on the androgen receptor. Therefore, CYP1B1 could serve as a novel target for the development of therapeutics to treat vascular changes in hypertensive males.
