Hypoparathyroidism is usually caused by postsurgical or autoimmune damage to the parathyroid gland. We present the case of a 46-year-old Hispanic male with no significant past medical history who was admitted to the hospital with hypoxic respiratory failure due to coronavirus disease 2019 (COVID-19) infection and had a prolonged hospital course. He was incidentally found to have hyperphosphatemia and low parathyroid hormone (PTH) levels. During the second month of hospitalization, his phosphorus levels rose to 6.9 mg/dL (normal range: 2.4-4.7 mg/dl). His PTH levels were found to be at 8 pg/mL. Vitamin D levels obtained were also low (7 ng/dL), phosphorus was at 5.8 mg/dL with albumin of 2.9 g/dL, and calcium level was normal at 9.2 mg/dl. Parathyroid hormone-related peptide (PTHrP) level was low at 10. Malignancy and genetic causes were ruled out. The patient was started on 50,000 units of ergocalciferol once a week. He was also started on calcium acetate 1,334 mg three times a day for hyperphosphatemia. Phosphorus levels remained elevated, and sevelamer was added on discharge after he was weaned off oxygen and cleared by physical therapy. No explanation for persistent hyperphosphatemia and hypoparathyroidism was found. To date, there have been some reports linking severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to widespread tissue injury; however, there have been no reports so far on the effect of the parathyroid gland. Further studies are necessary to elaborate and to confirm the causative relationship between SARS-CoV-2 and hyperphosphatemia.
Reports of complications as a result of COVID-19 infection are emerging since the virus became a pandemic. Although not fully understood, reports show that the COVID-19 virus has shown acute pericardial involvement resulting from this infection. It can cause a wide range of manifestations from minimal effusion to large effusion with tamponade; however, there is little or no data on an indolent course of COVID-19 infection and its resulting manifestations. Here we describe a patient who had minimal disease symptoms for weeks, resulting in sizeable pericardial effusion formation.
Naloxone-induced noncardiogenic pulmonary edema is a rare but reported entity that can occur following naloxone use in the reversal of opioid overdose. Proposed mechanisms include an adrenergic crisis secondary to catecholamine surge which causes more volume shift to pulmonary vasculature, subsequently leading to pulmonary edema. It appears to be more common when higher doses of naloxone are used. We present a case of a patient with opioid overdose came with altered mental status developed early features of pulmonary edema following the administration of multiple doses of naloxone. She responded well with the administration of diuretics and oxygen supplementation. Her oxygen requirements improved and didn't require mechanical ventilation.
Ventricular septal defect (VSD) is a rare but lethal complication of myocardial infarction. We present a case of a 65-year-old male who presented with a history of progressive shortness of breath associated with productive cough. Physical examination was significant for crepitation in both lower lung fields and bilateral lower extremity edema. Chest X-ray revealed bilateral reticular opacities with small bilateral pleural effusions. Polymerase chain reaction (PCR) for COVID was positive. Echo showed a left ventricular ejection fraction (LVEF) of 30-35%, ischemic cardiomyopathy, and muscular ventricular septal defects with left to right shunting and severely elevated pulmonary artery systolic pressure. Overtime during the hospital course, he developed respiratory and fulminant hepatic failure. Our patient had VSD due to an undiagnosed old myocardial infarction (MI). Initially heart failure was compensated and treated with medical management. Later on, he developed respiratory complications related to COVID-19 infection as well as hepatic failure in addition to a cardiomyopathy which made him a poor surgical candidate leading to death.
Heart failure is a complex clinical syndrome associated with high mortality and morbidity, creating a major public healthcare problem. It has a variety of etiologies, including substance abuse. Cocaine-induced cardiotoxicity is caused by direct effects of inhibition of sodium channels and indirect effects by inhibiting catecholamine uptake leading to increased sympathetic activity. Management is through the cessation of cocaine use and implantation of guideline-directed medical therapy for heart failure with the exception of beta-blockers as their safe usage is still controversial due to the risk of the unopposed alpha-adrenergic activity. Dexmedetomidine (Precedex) and Benzodiazepines (i.e., midazolam) are options for patients that demonstrate signs and symptoms of acute cocaine intoxication. If the actions of benzodiazepines fail to achieve hemodynamic stability, nitroglycerin may be used (especially in patients with cocaine-associated chest pain and hypertension). Cardiac transplantation is recommended for those who have demonstrated severe cardiovascular disease from cocaine. We present a 43-year-old male with a long-standing history of cocaine use who developed cardiomyopathy and severe acute decompensated heart failure found to have an ejection fraction of <20% admitted to the intensive care unit. He required inotropic support with milrinone and mechanical ventilation. He was later extubated and then discharged with an outpatient evaluation for a cardiac transplant.
Rothia species are gram positive, round to rod-shaped bacteria that are normally oral and respiratory tract flora. They were first isolated in 1967 from dental caries. We present a 69-year -old male with no risk factors for aforementioned bacteria however was found to have thickened anterior leaflet of the mitral valve with a small isoechoic lesion consistent with vegetation on Transthoracic echocardiogram. Blood cultures grew pan sensitive Rothia dentocariosa. Patient was treated with long-term antibiotics. This case adds to the limited number of cases of Rothia dentocariosa Endocarditis.
The rapid emergence of coronavirus disease 2019 has become the biggest healthcare crisis of the last century, resulting in thousands of deaths worldwide. There have been studies that evaluated the role of angiotensin-converting enzyme (ACE) inhibitors (ACEi) and angiotensin receptor blockers (ARBs) in treating patients with COVID-19. However, the prior use of diuretics and their effect on mortality in this setting remains unknown. The aim of the study was to evaluate the effect of diuretics in patients admitted with COVID-19. The current study was conducted between March 15, 2020, and April 30, 2020, during the COVID-19 pandemic in three different hospitals in Northern New Jersey, USA. The primary outcome was survival or in-hospital mortality from COVID-19 from the day of admission. The secondary outcome was severe or non-severe illness from COVID-19. This retrospective study included a total of 313 patients with a median age of 61.3 ± 14.6 years. There was a total of 68 patients taking diuretics at home and 245 patients who were not taking diuretics. There was a total of 39 (57.35%) deaths in patients taking diuretics as compared to 93 (37.96%) deaths in patients not taking diuretics (p-value 0.0042). Also, 54 (79.41%) patients who took diuretics had severe COVID-19 illness as compared to 116 (47.35%) who did not take diuretics (pvalue <.0001). However, after adjusting for the confounding factors, there was no difference in mortality or severity of illness in COVID-19 patients taking diuretics at the time of admission. In conclusion, there was no effect of the baseline use of diuretics in the prognosis of COVID-19.
Lemierre's syndrome is a rare but potentially severe complication of bacterial infections that usually affects previously healthy adolescents and young adults. It commonly presents as septic thrombophlebitis of the internal jugular vein and bacteremia following a recent oropharyngeal infection. The most commonly isolated organisms are Fusobacterium necrophorum, followed by Fusobacterium nucleatum and other anaerobes. Atypical Lemierre's syndrome is characterized by thrombophlebitis at sites distant from the head and neck veins and is far less encountered than typical Lemierre's syndrome. Here, we present a case of an elderly African American female with pylephlebitis, a rare abdominal variant of Lemierre's syndrome with extensive portal vein, splenic vein, and mesenteric vein thrombosis following perforated diverticulitis and resultant F. nucleatum bacteremia. She demonstrated complete recovery following appropriate long-term intravenous antibiotics and anticoagulation. This case calls attention to the re-emergence of the rare manifestation of this forgotten disease and highlights improved outcomes with prompt recognition and early treatment.
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.