Multifaceted highly targeted sequential multidrug treatment of early ambulatory high-risk SARS-CoV-2 infection (COVID-19).

The SARS-CoV-2 virus spreading across the world has led to surges of COVID-19 illness, hospitalizations, and death. The complex and multifaceted pathophysiology of life-threatening COVID-19 illness including viral mediated organ damage, cytokine storm, and thrombosis warrants early interventions to address all components of the devastating illness. In countries where therapeutic nihilism is prevalent, patients endure escalating symptoms and without early treatment can succumb to delayed in-hospital care and death. Prompt early initiation of sequenced multidrug therapy (SMDT) is a widely and currently available solution to stem the tide of hospitalizations and death. A multipronged therapeutic approach includes 1) adjuvant nutraceuticals, 2) combination intracellular anti-infective therapy, 3) inhaled/oral corticosteroids, 4) antiplatelet agents/anticoagulants, 5) supportive care including supplemental oxygen, monitoring, and telemedicine. Randomized trials of individual, novel oral therapies have not delivered tools for physicians to combat the pandemic in practice. No single therapeutic option thus far has been entirely effective and therefore a combination is required at this time. An urgent immediate pivot from single drug to SMDT regimens should be employed as a critical strategy to deal with the large numbers of acute COVID-19 patients with the aim of reducing the intensity and duration of symptoms and avoiding hospitalization and death.

Diagnosis of mast cell activation syndrome: a global "consensus-2".

The concept that disease rooted principally in chronic aberrant constitutive and reactive activation of mast cells (MCs), without the gross MC neoplasia in mastocytosis, first emerged in the 1980s, but only in the last decade has recognition of "mast cell activation syndrome" (MCAS) grown significantly. Two principal proposals for diagnostic criteria have emerged. One, originally published in 2012, is labeled by its authors as a "consensus" (re-termed here as "consensus-1"). Another sizable contingent of investigators and practitioners favor a different approach (originally published in 2011, newly termed here as "consensus-2"), resembling "consensus-1" in some respects but differing in others, leading to substantial differences between these proposals in the numbers of patients qualifying for diagnosis (and thus treatment). Overdiagnosis by "consensus-2" criteria has potential to be problematic, but underdiagnosis by "consensus-1" criteria seems the far larger problem given (1) increasing appreciation that MCAS is prevalent (up to 17% of the general population), and (2) most MCAS patients, regardless of illness duration prior to diagnosis, can eventually identify treatment yielding sustained improvement. We analyze these proposals (and others) and suggest that, until careful research provides more definitive answers, diagnosis by either proposal is valid, reasonable, and helpful.

Elevated alanine aminotransferase in current national football league players: correlation with cardiometabolic syndrome markers, obesity, and insulin resistance.

OBJECTIVES: Media reports suggest increased cardiovascular mortality in former National Football League (NFL) players. We previously demonstrated that current heavier players already have cardiometabolic syndrome markers: blood pressure (BP) >or=130/85 mm Hg, fasting glucose >or=100 mg/dL, triglycerides >or=150 mg/dL, waist circumference >or=100 cm, and high-density lipoprotein (HDL) or=30 IU/L was significantly correlated with mean body mass index (BMI), BMI >or=30 kg/m, BP >or=130/85 mm Hg, waist circumference >or=100 cm, and triglycerides-to-HDL ratio >3.5. An elevated ALT was significantly more common in linemen. CONCLUSIONS: An elevated ALT was significantly associated with visceral obesity, hypertension, cardiometabolic syndrome markers, and insulin resistance in current NFL players.

Chronic illness associated with mold and mycotoxins: is naso-sinus fungal biofilm the culprit?

It has recently been demonstrated that patients who develop chronic illness after prior exposure to water damaged buildings (WDB) and mold have the presence of mycotoxins, which can be detected in the urine. We hypothesized that the mold may be harbored internally and continue to release and/or produce mycotoxins which contribute to ongoing chronic illness. The sinuses are the most likely candidate as a site for the internal mold and mycotoxin production. In this paper, we review the literature supporting this concept.

Detection of mycotoxins in patients with chronic fatigue syndrome.

Over the past 20 years, exposure to mycotoxin producing mold has been recognized as a significant health risk. Scientific literature has demonstrated mycotoxins as possible causes of human disease in water-damaged buildings (WDB). This study was conducted to determine if selected mycotoxins could be identified in human urine from patients suffering from chronic fatigue syndrome (CFS). Patients (n = 112) with a prior diagnosis of CFS were evaluated for mold exposure and the presence of mycotoxins in their urine. Urine was tested for aflatoxins (AT), ochratoxin A (OTA) and macrocyclic trichothecenes (MT) using Enzyme Linked Immunosorbent Assays (ELISA). Urine specimens from 104 of 112 patients (93%) were positive for at least one mycotoxin (one in the equivocal range). Almost 30% of the cases had more than one mycotoxin present. OTA was the most prevalent mycotoxin detected (83%) with MT as the next most common (44%). Exposure histories indicated current and/or past exposure to WDB in over 90% of cases. Environmental testing was performed in the WDB from a subset of these patients. This testing revealed the presence of potentially mycotoxin producing mold species and mycotoxins in the environment of the WDB. Prior testing in a healthy control population with no history of exposure to a WDB or moldy environment (n = 55) by the same laboratory, utilizing the same methods, revealed no positive cases at the limits of detection.

Cardiometabolic abnormalities in current National Football League players.

Media reports suggested an increased prevalence of cardiovascular disease and premature death in former National Football League (NFL) players. The prevalence of cardiometabolic syndrome was determined in current active NFL players. The presence of cardiometabolic syndrome was defined as > or =3 of (1) blood pressure > or =130/85 mm Hg, (2) fasting glucose > or =100 mg/dl, (3) triglycerides > or =150 mg/dl, (4) waist circumference > or =100 cm, and (5) high-density lipoprotein cholesterol < or =40 mg/dl. Sixty-nine of 91 players (76%) from 1 NFL team were studied before the 2008 preseason training camp. Cardiometabolic syndrome markers, body mass index (BMI), waist-height ratio, and triglycerides/high-density lipoprotein cholesterol ratio were compared between 69 players and an age- and gender-matched reference population from NHANES (1999 to 2002) and by player position of linemen versus nonlinemen. Blood pressure > or =130/85 mm Hg, glucose > or =100 mg/dl, and BMI > or =30 kg/m(2) were significantly more prevalent in the 69 players than the NHANES cohort (28% vs 17%, p = 0.032; 19% vs 7%, p = 0.002; and 51% vs 21%, p <0.001, respectively), although cardiometabolic syndrome prevalence was similar in both groups. However, cardiometabolic syndrome prevalence, BMI > or =30 kg/m(2), and waist-height ratio >0.5 were significantly more common in the linemen versus the nonlinemen subgroup (22% vs 0%, p = 0.004; 100% vs 32%, p <0.001, and 95% vs 36%, p <0.001 respectively). In conclusion, cardiometabolic syndrome and its individual components were noted in current NFL players, particularly linemen.