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The Trump + Covid thread


Gil Bang

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4 minutes ago, Hank Kingsley said:

Serious question for medical professionals: What happens if you take a steroid every day? 

I have zero doubt Trump will want to chase this steroid high for as long as he lives. 

 

 

Maybe Trump will break the home run record next year.

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3 minutes ago, Hank Kingsley said:

Serious question for medical professionals: What happens if you take a steroid every day? 

I have zero doubt Trump will want to chase this steroid high for as long as he lives. 

 

 

Immunosuppression is the #1 side effect

 

 

If he gets stuck by thorns from a rose bush, hes a goner

 

 

 

just joking, he’ll prolly live forever

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1 minute ago, heso said:

This was always the most likely outcome. Guy gets tested daily. The second it’s positive he’s pumped full of drugs that ordinary people can’t get, has a team of 9 doctors attending to only him. No surprise he pulls through. 

The rest of the country: you'll feel 20 years younger. 

Fuck this guy. 

FIFY

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1 minute ago, GRHorn said:

You’re right. There will be anonymous reports that he’s on the verge of being readmitted for sure. 

Well, Dr Conley for damn sure wasn’t changing his bed pan, so even if the staff seal their lips with superglue you know there are now more folks who understand the level of insanity leading the country. 

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1 hour ago, hayden_horn said:

i mean, seriously, what the actual fuck. i don't think i saw this when it was happening, but fucking christ, what were they thinking?

rose-garden-covid.jpg

they broke every fucking rule of this virus.

But it's alright now.  I learned my lesson well.

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I’m going to set aside my very one-sided bias against Loeffler for a moment and ask, is gratitude and appreciation not a thing? Even I will acknowledge that the President thanked the doctors and staff who treated him and assisted him. But this is not what is going on here and it seems a little premature and unwise to speak of a virus as if it were a person. 

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1 hour ago, Hank Kingsley said:

Here we go 

 

 

This has got to be the dumbest of his tweets.

He is actually telling people to not take "Covid" seriously. He is implying that getting infected with a life threatening disease is actually good for you. How many additional morons will get it now? Morons that don't have health care, much less access to the finest medical care facility in the world, and a team of doctors.

Go deeper: When he almost certainly relapses, this tweet will not age well. But it won't be some tweet from when Obama was pres, it will be from just a few days or weeks prior.

And then of course there is the obligatory victory lap for shit he had absolutely nothing to do with.

 

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11 minutes ago, GreenspointTexas said:

Immunosuppression is the #1 side effect

 

 

If he gets stuck by thorns from a rose bush, hes a goner

 

 

 

just joking, he’ll prolly live forever

I assume that any viruses or bacteria trying to get into Trump’s system via subcutaneous cuts or abrasions will be thwarted by the high viscosity and low flow rate of his blood. 

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19 minutes ago, Hank Kingsley said:

Serious question for medical professionals: What happens if you take a steroid every day? 

I have zero doubt Trump will want to chase this steroid high for as long as he lives. 

 

 

If you take a good dose of steroids for a long time you get much heavier. So there's that.

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2 minutes ago, henrygandorf said:

ok, i'm thinking about this in real time, but let's take a quick look...

 

mike tv - obsessed with tv

violet - ate everything, had a weight problem, talked shit to her best friends, ended up with her face being an abnormal color

veruca - spoiled little brat, wanted everything now, yelled and screamed and had tantrums when she didn't get her way

augustus - german background, also fucking fat, didn't listen to warnings from professionals and experts

charlie - really fucking poor

 

is trump a horrific yet perfectly formed amalgamation of all the wonka contestants?

 

Gotdamn.

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Chronic Systemic Steroid use.

Dermatologic effects and appearance — Many clinically relevant adverse effects of glucocorticoids on the skin and appearance that have been observed even at lower doses include skin thinning and ecchymoses, Cushingoid appearance, acne, weight gain, mild hirsutism, facial erythema, and striae. We discuss some of the major dermatologic effects in more detail below.

●Skin thinning and ecchymoses – Among the most common toxicities attributable to glucocorticoids are skin thinning and ecchymoses, even at low doses [9]. A large observational study with patient-reported data from patients with rheumatoid arthritis (RA) on glucocorticoids for at least six months reported rates of parchment-like skin and ecchymoses in 10 and 17 percent, respectively [5]. The prevalence of these effects also increased with higher doses of prednisone. In a prospective study with 80 patients, skin changes were observed in 46 percent of patients treated for three months with prednisone at doses greater than 20 mg/day [13]. The ecchymoses or purpura associated with glucocorticoid use often affects the sun-exposed areas of the dorsum of the hand and forearm and is not accompanied by palpable swelling. (See "Photoaging", section on 'Photoaging in individuals with phototypes I to IV'.)

●Cushingoid features – The development of Cushingoid features (redistribution of body fat with truncal obesity, buffalo hump, and moon face) and weight gain are dose- and duration-dependent and can develop within the first two months of therapy. A Cushingoid appearance can be quite troubling to patients and can develop even with low-dose therapy; however, it is uncommon at doses below the physiologic glucocorticoid-replacement range. Factors that may also contribute to increased weight include an increased appetite, a common side effect of glucocorticoid therapy, and an increase in food intake for symptomatic relief in patients with gastropathy or peptic ulcer disease [14]. (See 'Gastrointestinal effects' below and "Epidemiology and clinical manifestations of Cushing's syndrome", section on 'Progressive obesity'.)

●Weight gain – Several observational studies have assessed the frequency of Cushingoid features and weight gain. In an observational study of 779 patients with RA, weight gain was more frequent in patients treated with at least 5 mg/day of prednisone or equivalent for at least six months, compared with those who had not received any for at least 12 months (22.4 versus 9.5 percent) [5]. However, there was a threshold effect, such that the rate of weight gain was not increased in those who took less than 5 mg/day (8.7 percent) or further increased at doses greater than 7.5 mg/day (21.3 percent) [5]. By contrast, Cushingoid features showed a linear increase in frequency with dose rather than a threshold effect. Among patients who had received <5, 5 to 7.5, and >7.5 mg/day of prednisone or equivalent, Cushingoid features were observed in 4.3, 15.8, and 24.6 percent of patients, respectively. In another study with survey data from 2167 long-term users of glucocorticoids (mean prednisone equivalent dose ± standard deviation [SD] of 16±14 mg/day for ≥60 days), weight gain was the most common self-reported adverse effect (70 percent of patients) [8]. In those on ≤7.5 mg/day of prednisone or equivalent, increasing duration of use was significantly associated with weight gain. Also, in an analysis of four prospective trials of glucocorticoids in RA, the use of 5 to 10 mg/day of prednisone or equivalent over two years was associated with an increase of mean body weight of 4 to 8 percent [9].

Ophthalmologic effects — The risk of both cataracts and glaucoma is increased in patients on glucocorticoids and is dose-related [9]. (See "Cataract in adults" and "Open-angle glaucoma: Epidemiology, clinical presentation, and diagnosis" and "Angle-closure glaucoma".)

●Cataracts – Cataracts commonly occur after prolonged glucocorticoid use. They are usually bilateral and develop slowly. They typically occur in a posterior subcapsular location and can usually be distinguished from senile cataracts.

There may be no minimal safe dose with respect to the risk of cataract formation, although risk is dose- and time-dependent and is more common with prednisone doses greater than 10 mg/day or with medications that have been administered for more than one year [15-17]. In a study that evaluated 122 patients with RA taking a mean dose of prednisone of 8 mg/day for an average of 6.9 years, 29 percent developed cataracts compared with 18 percent of matched controls [7]. Another study of patients with RA receiving a mean dose of 6 mg of prednisone daily for a mean of six years also found cataracts more common in patients on glucocorticoids than in patients not using prednisone (15 versus 4.5 percent) [6].

●Increased intraocular pressure – Glucocorticoids can also increase intraocular pressure. This form of glaucoma occurs most commonly in patients who use glucocorticoid eye drops, although it has been observed in chronic and, to a lesser extent, acute systemic glucocorticoid use [18]. This risk of glaucoma associated with glucocorticoid use is discussed in more detail separately. (See "Open-angle glaucoma: Treatment", section on 'Glucocorticoids'.)

●Exophthalmos – Exophthalmos and swelling of the lids and ocular muscles are rare ophthalmologic complications of glucocorticoids [19,20].

A rare adverse effect of systemic, local, or even topical use of glucocorticoids is central serous chorioretinopathy [21-23]. This type of chorioretinopathy is associated with edema formation that can separate the retina from the choroid. Reduction of glucocorticoid dose is the most important element of treatment if it can be done without causing a dangerous exacerbation of the disease that is being treated with the glucocorticoids [24].

Cardiovascular effects — Glucocorticoid use has been associated with a variety of adverse cardiovascular effects including fluid retention, premature atherosclerotic disease, and arrhythmias. Cardiovascular disease risk is dose-dependent and may be low or absent in patients on low-dose glucocorticoid therapy [25].

●Fluid retention and hypertension – Higher-dose glucocorticoids may promote fluid retention, which is of particular concern to patients with underlying heart or kidney disease. This is not a problem in normal subjects because of the phenomenon of mineralocorticoid escape that prevents progressive fluid overload (see "Pathophysiology and clinical features of primary aldosteronism"). Hypertension is a known adverse effect of glucocorticoids and has been observed in up to 20 percent of patients with iatrogenic Cushing's syndrome [26]; however, it is a dose-related adverse effect and is unlikely to occur at lower doses of glucocorticoids [5,27]. Some studies have shown that long-term use of prednisone in RA patients can be associated with a higher risk of hypertension, although the data are inconsistent when low doses of glucocorticoids are used [28-30]. In patients receiving low doses of glucocorticoids (eg, 10 mg/day of prednisone), significant hypertension may be better explained by age and initial blood pressure than by the glucocorticoids themselves [31]. The mechanism by which glucocorticoid therapy can raise the blood pressure is not well understood [32,33]. (See "Epidemiology and clinical manifestations of Cushing's syndrome", section on 'Hypertension'.)

●Premature atherosclerotic disease – Glucocorticoid use has been associated with increased rates of myocardial infarction, stroke, heart failure, and all-cause mortality [25,34]. Increasing attention is being given to the increased risk of premature atherosclerosis in RA and other systemic rheumatic disease. Thus, the relative risks of cardiovascular events associated with glucocorticoid use may be confounded by the role of the underlying inflammatory disease of the vascular endothelium. In a large population-based study comparing 68,781 glucocorticoid users with 82,303 nonusers who had never been hospitalized for cardiovascular disease, patients who received glucocorticoid doses ≥7.5 mg/day were more than 2.5 times more likely than patients who did not receive glucocorticoids to experience a cardiovascular event (defined as myocardial infarction, angina, coronary revascularization, hospitalization for heart failure, transient ischemic attack [TIA], or stroke) [25]. Similarly, in another large retrospective case-control study, an increased risk of ischemic heart disease and heart failure was associated with current glucocorticoid use (adjusted odds ratios [ORs] 2.7 and 1.2, respectively) [34]. Neither of these studies included the role of disease-modifying agents or disease activity among the patients who were included who had a systemic rheumatic disease.

Studies in which the patients were limited to systemic rheumatic diseases found more variable results in terms of glucocorticoid use and cardiovascular disease risk. As an example, a prospective cohort study with 364 polymyalgia rheumatica (PMR) patients followed for a median of 7.6 years found that there was no increased risk of cardiovascular outcomes in patients treated with glucocorticoids compared with the group of patients who just received nonsteroidal antiinflammatory drugs (NSAIDs) [35]. By contrast, a large population-based study of 8384 patients with incident RA found that glucocorticoid use was associated with a 68 percent increased risk of myocardial infarction [36]. The risk of myocardial infarction increased by 13 percent for each 5 mg/day increase in glucocorticoid dose. However, the potential for unmeasured confounders and possible misclassification using administrative data limit these findings. Also, a randomized trial with 223 early RA patients followed prospectively for 10 years found an increased risk of cerebrovascular events in patients treated with prednisolone compared with those not receiving prednisolone (hazard ratio


3.7 [1.2-11.4]) [30]. However, there were no significant differences between the two treatment groups in composite cardiovascular events (which included an acute myocardial infarction or an ischemic stroke) or a first coronary event.

The development of iatrogenic Cushing's syndrome may be a marker for patients at a higher risk of cardiovascular disease. A cohort of 547 patients diagnosed with iatrogenic Cushing's syndrome in a large general practice database had a significantly greater risk of a cardiovascular event compared with patients who were receiving similar doses of glucocorticoids but who did not have a diagnosis of Cushing's syndrome and patients who did not receive glucocorticoids [37]. (See "Epidemiology and clinical manifestations of Cushing's syndrome", section on 'Cardiovascular risk'.)

●Arrhythmias – An association of glucocorticoid use with risk of atrial fibrillation and flutter has been reported several studies [38-40]. In a population-based case-control study, current glucocorticoid use was more common among 20,221 patients with atrial fibrillation or flutter compared with the 202,130 population controls (6.4 versus 2.6 percent) [40]. Currently using glucocorticoids was associated with a significant increased risk of atrial fibrillation or flutter, compared with never having used glucocorticoids (adjusted OR 1.9). Risk was increased for new users and long-term users, but not for former users (ORs 3.6, 1.7, and 1.0, respectively) and was unrelated to whether or not pulmonary or cardiovascular disease was present.

Serious adverse cardiovascular toxicities, including sudden death, have been reported in occasional patients who have been given pulse infusions of glucocorticoids (eg, 1 g/day of methylprednisolone for multiple infusions) [41]. In many of these cases, however, it was difficult to determine whether this adverse effect was more likely attributable to glucocorticoids or to the underlying disorder necessitating the therapy. Thus, cardiac monitoring is indicated in patients with significant cardiac disease who are treated with pulse glucocorticoid therapy, especially those on diuretics, the use of which may also be associated with electrolyte disturbances such as hypokalemia.

●Possible hyperlipidemia – The effect of glucocorticoids on atherosclerotic vascular disease is thought to be mediated in part by elevated nonfunctional lipoprotein levels. However, studies analyzing this issue have had mixed results, and beneficial effects of glucocorticoids on dyslipidemia have also been observed. In one report, moderate- to low-dose prednisone (20 mg/day tapered to 5 mg/day over three months) had no significant adverse effect on lipoprotein levels if other risk factors were taken into account [42]. Another observational study concluded that glucocorticoid use was associated with a more favorable lipid profile in older adults (≥60 years) [43]. Studies in patients with systemic lupus erythematosus (SLE) have indicated that the adverse effects of glucocorticoids on lipid profiles are dose-dependent, occurring only at prednisone doses greater than 10 mg/day [44-46]. Interpretation of these data is complicated by the difficulty of distinguishing effects due to disease activity from effects directly related to the medications themselves [47]. A rodent study found that the combination of prednisone and atorvastatin improves the lipid profile better than either drug alone; however, we are unaware of direct data in humans.

Glucocorticoids may act by leading sequentially to peripheral insulin resistance, hyperinsulinemia, and increased hepatic very low-density lipoprotein (VLDL) synthesis. However, glucocorticoid-induced reduction in corticotropin (ACTH) release also contributes to the lipid changes. In one report, for example, the administration of ACTH for three weeks to nine hyperlipidemic, glucocorticoid-treated patients (five of whom were transplant recipients) led to substantial reductions in total and low-density lipoprotein (LDL) cholesterol and triglycerides and to an increase in high-density lipoprotein (HDL) cholesterol [48]. ACTH may act, in part, by upregulating LDL-receptor activity.

Gastrointestinal effects — Glucocorticoids increase the risk for adverse gastrointestinal effects, such as gastritis, ulcer formation, and gastrointestinal bleeding. The estimated relative risks of glucocorticoids alone for gastrointestinal adverse effects vary from 1.1 (not significant) to 1.5 (marginally significant) [49,50]. However, the combination of glucocorticoids and NSAIDs results in a synergistic increase in the incidence of gastrointestinal events as shown by the following findings from two meta-analyses:

●Glucocorticoid use is associated with a nearly twofold increased risk of a gastrointestinal adverse effect among patients also taking NSAIDs when compared with those who use NSAIDs alone [51].

●The use of NSAIDs and glucocorticoids is associated with a fourfold increased risk of a gastrointestinal adverse effect compared with nonuse of either drug [50].

Whether substitution of a selective cyclooxygenase (COX)-2 inhibitor for a nonselective NSAID would lower this risk is unclear.

In addition to upper gastrointestinal morbidity, other complications associated with glucocorticoid use include visceral perforation [52-54] and hepatic steatosis (fatty liver) that can rarely lead to systemic fat embolism or cirrhosis [55,56]. Although glucocorticoids have also been implicated in causing acute pancreatitis [57-59], other studies, particularly in patients with SLE, have shown that the disease is causative, rather than the drugs, and that the drugs may be beneficial therapeutically [60,61]. However, the role of glucocorticoids in causing acute pancreatitis remains uncertain. (See "Etiology of acute pancreatitis".)

Glucocorticoids may mask the symptoms of serious gastrointestinal disease, an effect that may account, in part, for the increased risk of perforated sigmoid diverticular abscess associated with their use [54].

Bone and muscle effects

●Osteoporosis – Osteoporosis is a well-known adverse effect of glucocorticoid use and is discussed in detail elsewhere. (See "Clinical features and evaluation of glucocorticoid-induced osteoporosis" and "Prevention and treatment of glucocorticoid-induced osteoporosis".)

●Osteonecrosis – Osteonecrosis (avascular or ischemic necrosis of bone) has also been associated with glucocorticoid use, particularly with high doses of glucocorticoids. Glucocorticoid-induced osteonecrosis is discussed separately.

●Myopathy – Myopathy is an infrequent complication of glucocorticoid therapy. It presents as painless proximal motor weakness in both the upper and lower extremities. Glucocorticoid-induced myopathy is discussed in detail separately. (See "Glucocorticoid-induced myopathy".)

More acute and severe weakness noted in critically ill patients has been attributed at least in part to the use of glucocorticoids. Variously referred to as critical illness myopathy and acute quadriplegic myopathy, it has also been suspected to be due to an interaction between glucocorticoids and neuromuscular blocking agents. This is discussed in more detail elsewhere. (See "Neuromuscular weakness related to critical illness", section on 'Critical illness myopathy'.)

Neuropsychiatric effects — Glucocorticoids induce a range of psychiatric and cognitive symptoms, which depend upon dose and duration of therapy [62]. In most patients, these symptoms are mild and reversible, but emotional lability, hypomania, mania, depression, psychosis, delirium, confusion, or disorientation (which are more common in older patients), and cognitive changes including memory deficits may occur [63,64]. Disturbances in sleep are reported, especially with split doses or evening dosing that may interfere with the normal pattern of diurnal cortisol production. Akathisia (motor restlessness) is a common glucocorticoid side effect. The risk of developing a given neuropsychiatric disorder following glucocorticoid therapy may be increased among patients with a past history of that condition [64]. Older patients may be at higher risk for depression, mania, delirium, confusion, or disorientation [64]. We describe several conditions in more depth below:

●Mood disorders – Patients receiving glucocorticoids often experience an improved sense of well-being within several days of starting the medications; mild euphoria or anxiety may also be seen [63,65,66]. Hypomanic reactions and activated states are more common early in therapy than is depression, but the prevalence of depression is greater in patients on more longstanding therapy, even on low to moderate doses [63,65,67]. Patients with a family history of depression or alcoholism are at increased risk for affective diseases when given glucocorticoids [68].

More severe psychiatric symptoms can occur within a few days in patients receiving high doses of glucocorticoids. As an example, in one prospective but uncontrolled study of 50 patients receiving over 75 to 100 mg of prednisone or equivalent for greater than a week for various ophthalmologic indications, hypomanic symptoms were induced in approximately 30 percent, and depressive symptoms in approximately 10 percent, of patients by the end of one week [69]. No patient became overtly psychotic, demented, or delirious.

●Psychosis – Psychosis can occur but does so almost exclusively at doses of prednisone above 20 mg/day given for a prolonged period [9,70,71]. Approximately 10 percent of patients have persistent symptoms that may require treatment despite reduction of glucocorticoid dose [72]. Response to antipsychotic drug treatment is typically complete and occurs within two weeks of initiation of neuroleptics. Hypoalbuminemia may be a risk factor for glucocorticoid-induced psychosis in patients with SLE [73]. Patients with SLE who are on higher glucocorticoid doses present a particular problem since it is often difficult to differentiate psychosis due to prednisone from neuropsychiatric lupus, which may require high-dose glucocorticoid treatment. (See "Neuropsychiatric manifestations of systemic lupus erythematosus" and "Clinical manifestations, differential diagnosis, and initial management of psychosis in adults", section on 'Substance-induced psychoses'.)

●Memory impairment – Memory impairment has been associated with glucocorticoid use. As an example, a cohort study of 115 RA patients found that glucocorticoid use was a predictor of poor cognition when controlling for depression, disease severity and duration, and C-reactive protein (CRP) level [74]. Another report found that patients treated with prednisone doses of 5 to 40 mg/day for at least one year had a partial loss of explicit memory; older patients were more susceptible to memory impairment with less protracted treatment [62,75]. The effect on memory began as early as three months after the initiation of therapy. Approximately 1 percent of patients may be affected by more severe and persisting cognitive disturbances beginning during glucocorticoid treatment; this has been termed steroid dementia. In some patients, this condition may not remit for between 1 and 11 months after discontinuing the medication.

●Other symptoms – In a retrospective analysis involving 372,696 patients in general practices in the United Kingdom, there was a five- to sevenfold increased risk of completed or attempted suicide among patients receiving glucocorticoids, compared with patients with the same diagnoses who were not receiving such medications; however, the absolute risk was extremely low, approximating 0.1 cases per 100 patient-years of therapy [64]. Younger patients were at higher risk. The observational nature of the study and potential for unknown confounding variables limit study interpretation.

Rare cases of pseudotumor cerebri have been associated with glucocorticoid use, although higher doses are often effective in alleviating this generally self-limiting disorder [76]. Akathisia can occur even in patients taking low doses. An increased risk of panic disorder may be present [64].

Metabolic and endocrine effects

●Hyperglycemia – Systemic glucocorticoids cause a dose-dependent, usually mild, increase in fasting glucose levels and a greater increase in postprandial values in patients without preexisting diabetes mellitus, but the development of de novo diabetes in a patient with initially normal glucose tolerance is uncommon [77]. In a case-control study of Medicaid recipients, the relative risk of developing hyperglycemia requiring glucose-lowering therapy increased progressively with increasing glucocorticoid dose [78]. The relative risk increased from 1.8 in patients treated with the equivalent of less than 10 mg/day of prednisone to 10.3 in those with the equivalent of more than 30 mg/day of prednisone [78]. Risk factors for new-onset hyperglycemia during glucocorticoid therapy are thought to be the same as those for other patients, including a family history of diabetes, increased age, obesity, and a history of gestational diabetes [79]. Transient hyperglycemia can also occur after intraarticular glucocorticoid therapy. (See "Comorbidities that impact management of osteoarthritis", section on 'Diabetes mellitus'.)

Patients with diabetes mellitus or glucose intolerance exhibit higher blood glucose levels while taking glucocorticoids, leading to increased difficulty with glycemic control. In addition, new-onset hyperglycemia or, rarely, a nonketotic hyperosmolar state or diabetic ketoacidosis develops without warning in patients with early subclinical diabetes or glucose intolerance [29,77,78].

The mechanism by which glucocorticoids cause hyperglycemia is multifactorial, including augmentation of hepatic gluconeogenesis, inhibition of glucose uptake in adipose tissue, and alteration of receptor and postreceptor functions [1,80-82]. It is also possible that some underlying disorders for which glucocorticoids are used, such as RA, may independently predispose to a higher rate of glucose intolerance [83].

●Hypothalamic-pituitary-adrenal axis suppression – Administration of exogenous glucocorticoids can suppress the hypothalamic-pituitary-adrenal (HPA) axis. Abrupt cessation or rapid withdrawal of glucocorticoids in such patients may cause symptoms of adrenal insufficiency. The approach to withdrawal of glucocorticoids, HPA axis suppression, and the clinical manifestations of adrenal insufficiency are presented separately [84]. (See "Glucocorticoid withdrawal" and "Pharmacologic use of glucocorticoids", section on 'HPA axis suppression' and "Clinical manifestations of adrenal insufficiency in adults".)

Immune system effects — Systemic glucocorticoids have many effects upon innate and acquired immunity that predispose to infection, resulting in a dose-dependent increase in the risk of infection, especially with common bacterial, viral, and fungal pathogens. Glucocorticoids may be associated with a greater infection risk among patients with RA, compared with other antirheumatic medications, such as the anti-tumor necrosis factor (TNF)-alpha agents [85]. In one large study of RA patients, current and recent doses were most strongly associated with such risk, but the data also suggested a cumulative risk effect from doses taken during the preceding two to three years [86]. The risk of infection with glucocorticoid therapy and the mechanisms underlying such risk are discussed in more detail elsewhere. (See "Glucocorticoid effects on the immune system".)

In addition to glucocorticoid dose, factors influencing infection risk include the underlying disorder, the presence of concomitant immunosuppressive therapies, hospitalizations, lymphopenia, and diabetes mellitus [85,87]. Older patients and those with lower functional status are also at higher risk for infection. In addition, patients taking glucocorticoids may not manifest signs and symptoms of infection as clearly, due to the inhibition of cytokine release and associated reduction in inflammatory and febrile responses. This can impair early recognition of infection. (See "Glucocorticoid effects on the immune system", section on 'Infection risk' and "Glucocorticoid effects on the immune system".)

Inhaled and topical glucocorticoids are usually not implicated in increased risk of systemic infections, in contrast to the effects seen with systemic agents. The side effects of inhaled and topical glucocorticoids are reviewed elsewhere. (See "Major side effects of inhaled glucocorticoids" and "Topical corticosteroids: Use and adverse effects", section on 'Adverse effects'.)

Hematologic effects — Pharmacologic doses of glucocorticoids often result in an increased white blood cell count (leukocytosis) that is due primarily to an increase in neutrophils (neutrophilia). This phenomenon is due to a decreased proportion of neutrophils that are adhering to the endothelium. This effect of glucocorticoids is discussed in detail elsewhere. (See "Approach to the patient with neutrophilia", section on 'Medications'.)

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1 minute ago, henrygandorf said:

ok, i'm thinking about this in real time, but let's take a quick look...

 

mike tv - obsessed with tv

violet - ate everything, had a weight problem, talked shit to her best friends, ended up with her face being an abnormal color

veruca - spoiled little brat, wanted everything now, yelled and screamed and had tantrums when she didn't get her way

augustus - german background, also fucking fat, didn't listen to warnings from professionals and experts

charlie - really fucking poor

 

is trump a horrific yet perfectly formed amalgamation of all the wonka contestants?

Worse. Trump is Wonka himself. Whips the world into an unhealthy consumerism frenzy that caused mobs in the streets. The select few that are chosen by pure fate are then subjected to a quick horror show, followed by each person meeting a horrible end that exemplifies their worst qualities. He then leaves the horror show to be inherited by the sole survivor who was originally going to assist in Wonka's destruction but in the end had a change of heart because Wonka was able to use the deaths, that he caused by the way, as evidence of how people are awful and that Charlie should continue his evil works as Wonka retires without consequence.

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9 minutes ago, High Plains Drifter said:

 

This has got to be the dumbest of his tweets.

He is actually telling people to not take "Covid" seriously. He is implying that getting infected with a life threatening disease is actually good for you. How many additional morons will get it now? Morons that don't have health care, much less access to the finest medical care facility in the world, and a team of doctors.

Go deeper: When he almost certainly relapses, this tweet will not age well. But it won't be some tweet from when Obama was pres, it will be from just a few days or weeks prior.

And then of course there is the obligatory victory lap for shit he had absolutely nothing to do with.

 

he's just disgusting. a disgusting human being. 

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4 minutes ago, 4th&Five said:

 

this tweet is really vintage trump.

if you wanted to seem human and possibly get more votes, you should be straightforward and honest, and most of all, introspective and humbled.  you tell people that looking mortality in the face and being lucky enough to come out of it is harrowing and has really taught him a lot.  that he understands how scary it is, and how lucky he is that america gives him access to next-level medical procedures, expertise, drugs, etc.  you explain that your work here is not done, and you believe that fighting through this has given you purpose, and that purpose is to be the best president you can be, and really help people.  this would've been what most of the country wanted/needed to hear if they would consider voting for him.

but no.  of course not.  he comes out saying "this disease is lame, i don't see the big deal, i'm basically a superhero, peace out dumb hospital lol".  you know who likes talk like this?  his stupid fucking base.  so once again, when given the opportunity (he's had so many) to appeal to all of america, he says fuck it, and plays to his base.

this is why he will absolutely still get wrecked in a month.  we should all be very glad he played it this way.  just like covid could've handed him reelection (in march), getting the disease really could've worked for him.

alas.

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1 hour ago, bad_teammate said:

Stop telling yourselves he's dying. You aren't that lucky. The world isn't going to deliver the ending you want. This pig is going to live and thrive for 15+ more years. The narrative demands it.

Just hope the narrative doesn't demand his second term.

george rr martin thinks 2020 is ridiculous, agrees with this take

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3 hours ago, workswithseed said:

No, I'm not. Trump never told people that they couldn't see thier relatives. If you're going to lay blame, you might want to do it to the person who actually implemented it.

Negged for being obtuse. You know that the point isn't that people couldn't visit relatives due to contagion. The point is that Trump doesn't care that he's contagious nor does he care about whom he may infect, so he arranges a little Sunday drive. He exposes at least two people and likely many more. 

But you know that. You're either choosing to be a dick, or you're just a liar for President Liar.

Be best.

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jr has a moment of clarity between lines:

Quote

Sources said Donald Trump Jr. is deeply upset by his father’s decision to drive around Walter Reed National Military Medical Center last night with members of the Secret Service while he was infected with COVID-19. “Don Jr. thinks Trump is acting crazy,” one of the sources told me. The stunt outraged medical experts, including an attending physician at Walter Reed. 

https://www.vanityfair.com/news/2020/10/don-jr-thinks-trump-is-acting-crazy-presidents-covid-joyride-has-family-divided

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12 minutes ago, henrygandorf said:

ok, i'm thinking about this in real time, but let's take a quick look...

 

mike tv - obsessed with tv

violet - ate everything, had a weight problem, talked shit to her best friends, ended up with her face being an abnormal color

veruca - spoiled little brat, wanted everything now, yelled and screamed and had tantrums when she didn't get her way

augustus - german background, also fucking fat, didn't listen to warnings from professionals and experts

charlie - really fucking poor

 

is trump a horrific yet perfectly formed amalgamation of all the wonka contestants?

It’s a cross species mutation from the Oompa Loompas, the little orange men. They try not to talk about it....

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1 hour ago, Hank Kingsley said:

Here we go 

 

Fuck this guy. If there was ever an example of a guy who only cares about himself.

What happens if someone dies (completely unnecessarily) from this super spreader event? ie: Chris Christie, ,some low level staffer, white house worker?

but no fears, President Trump feels 20 years younger!

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39 minutes ago, Mrs Whiggins said:

@ChiTownDoc is the opinion I place the most confidence in when it comes to assessment from afar. If he says it looks a certain way, then I  keep that it mind when listening to the talking heads fronting the President. 

Appreciate it but I just say what I think is going on based on the info we have.  That's the problem with this administration.  Even the info we have on covid itself seems to be partial and being given with a political lean (see CDC issues). 

Re Trump:  Seeing the President walking to the chopper like he was I had a hard time believing he was desaturating below 88% O2 (the level at which I insist on supplemental O2).  Also like I said, this seemed like just a precaution after how he walked to the heli.  Anyone desaturating (resp failure) isn't putting on a suit and going to stroll 50 yards without showing issues. 

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Just now, texas08 said:

I though this dumb motherfucker had “learned a lot” regarding Covid the past couple of days...

What a reckless piece of excrement this fuckhead is.

He learned that he's ok.  That's all he fucking needs.  He's probably going to be even less cautious now.  Fucking mess. 

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1) failure to say when his last negative test tells me he was positive at the debates on Tuesday

2) He pushed for his own release for the optics, gambling hard he won’t need to be re-admitted. Sick and in a hospital, he knows the election is fucked, so he did everything possible to get out, even while still receiving treatment. 
 

3) The doctors are covering up a pneumonia diagnosis. 

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  • immamac changed the title to The Trump + Covid thread


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