Corticosteroids

The anti-inflammatory bet on the leak itself. ATS 2024 suggests corticosteroids for ARDS (conditional recommendation, moderate certainty) on a pooled mortality reduction, and the SCCM 2024 CIRCI update, as reported in a 2024 JAMA review, conditionally recommends low-dose steroids for ARDS due to community-acquired pneumonia, started within 24 hours of meeting severity criteria. Timing is the exam point: initiation more than 2 weeks after onset may be associated with harm, and use is aimed at moderate-to-severe disease. The nurse watches glucose, sodium, GI bleeding and neuromuscular weakness — and flags the steroid-plus-paralytic combination as an ICU-acquired-weakness risk.

Here the class is the treatment, not the cause — the exact mirror of Cushing’s syndrome, and replacement is lifelong. The 2016 Endocrine Society guideline recommends hydrocortisone 15–25 mg in two or three divided oral doses daily, with the largest dose on waking so the schedule mimics the normal diurnal cortisol curve; prednisone 3–5 mg/day is an alternative. Dexamethasone is recommended against for maintenance because dose titration is difficult and Cushingoid side effects follow. In primary disease only, the mineralocorticoid half is added — fludrocortisone, usually 0.05–0.2 mg daily, titrated to keep plasma renin in range, with the explicit instruction that patients must not restrict salt. The two rules that save lives are dose rules: sick-day dosing (double the glucocorticoid above 38 °C, triple it above 39 °C, for the 2–3 days of illness, while leaving the mineralocorticoid dose unchanged) and the crisis dose — 100 mg hydrocortisone IV or IM immediately, then 200 mg over 24 hours.

Corticosteroid injections are on the NHS list of treatments for stump and phantom pain.

Adjunct only, and increasingly debated. Methylprednisolone 80–125 mg IV (or hydrocortisone 250–500 mg IV) acutely, then oral prednisone 40–60 mg/day for 3–5 days; StatPearls frames the rationale as reducing the length or biphasic response of anaphylaxis, but WAO 2020 cites increasing evidence of no benefit in acute management — possibly harm — making routine use controversial. Whatever the verdict, a steroid never delays epinephrine.

The systemic exacerbation course: short courses for moderate-to-severe exacerbations shorten recovery, prevent relapse, and reduce hospitalization — typically prednisone 40–60 mg daily for 5–7 days (5–10 days after ED discharge to prevent early relapse). Oral and IV are equally effective, so IV is for the patient who can’t swallow, not the one who "needs it more." This is the drug for the late-phase cellular inflammation the bronchodilator can’t touch.

[Bell’s palsy] First-line — early. NINDS: "oral steroids should be started within three days of symptom onset to reduce inflammation and swelling and increase the chance of recovering facial nerve function." NHS: "a 10-day course of steroid medicine." Monitor glucose in diabetes — antihyperglycemics are "added or adjusted as necessary." Not for Lyme or Guillain-Barré facial palsy ("steroids should be avoided").

Dexamethasone for peritumoral (vasogenic) edema. "Dexamethasone, mannitol, and furosemide are used to treat the peritumoral edema associated with brain tumors." For new metastases, treating edema is "The first step," and "After the initial clinical response, which can occur rapidly, the dose may be tapered to avoid many of the adverse effects of long-term high dose steroid administration." Never stop abruptly — HPA-axis suppression. Monitor glucose and HbA1c, electrolytes and blood pressure; use caution in peptic ulcer disease; watch for infection and insomnia. On temozolomide, patients receiving steroids need particularly close monitoring for lymphopenia and PCP (label). No doses here — see the class page.

Used with steroid-sparing agents when sarcoidosis drives restrictive cardiomyopathy.

Post-op steroid eye drops treat inflammation and pain after ocular surgery — but prolonged use can raise eye pressure (monitor IOP if used 10 days or longer), delay healing and mask infection. Steroids are also a cause of posterior subcapsular cataract.

Refractory celiac disease type 1 only — not the treatment of ordinary celiac disease, which is the gluten-free diet alone.

Dexamethasone — only with an oxygen need. IDSA (9/25/2020) recommends dexamethasone for critically ill hospitalized patients and suggests it for severe (SpO2 ≤94% on room air, including patients on supplemental oxygen); it "suggests against the use of glucocorticoids" in hospitalized patients without hypoxemia requiring supplemental oxygen. NIH guidelines (archived 2024) recommend "against the use of dexamethasone (AIIa) or other systemic corticosteroids (AIII) for the treatment of COVID-19 in patients who do not require supplemental oxygen," and "Patients who are receiving corticosteroid treatment for an underlying condition should continue to receive corticosteroids." IDSA "suggests against inhaled corticosteroids" for ambulatory mild-to-moderate COVID-19.

The one class on this page that is the cause, not the treatment. Exogenous glucocorticoids are the most common source of Cushing’s syndrome, and every feature above is a magnified version of this class’s adverse-effect profile — which is why the class page and this page teach the same physiology from opposite ends. The nursing payload is the taper logic: a course under 14–21 days does not suppress the axis and needs no taper, while 3–4 weeks or more at any dose above 4–6 mg prednisone daily does, in decrements of 5–10 mg weekly above 40 mg, 2.5 mg every 1–4 weeks at 10–20 mg, and 1 mg every 4 weeks at 5 mg (2024 ESE/Endocrine Society joint guideline). Never stop abruptly — and note that the drugs used to treat endogenous Cushing’s syndrome are steroidogenesis inhibitors and receptor antagonists, an entirely different pharmacology from the steroids that caused the iatrogenic form.

Here as a cause of glaucoma, not a treatment for it. "Steroid therapy of any kind can contribute to elevated IOP; however, topical eye and periocular steroids are most likely to increase IOP," and corticosteroids are named among the causes of secondary glaucoma alongside uveitis, diabetes and eye injury. Chronic use of topical or systemic corticosteroids is on the sourced referral list — a patient on long-term steroids needs ophthalmologic monitoring, not reassurance. The mechanistic link is hiding in the genetics of the disease, and it is worth teaching because it makes the association memorable: the gene most associated with inherited open-angle glaucoma is MYOC, which encodes myocilin — a protein "expressed in the trabecular meshwork and is also known as trabecular meshwork glucocorticoid-inducible response protein." The drainage tissue that fails in glaucoma is running a protein that steroids switch on. The nursing consequence is a medication reconciliation that includes topical and inhaled products and over-the-counter preparations, since "steroid therapy of any kind" is the sourced phrase. The class page owns systemic corticosteroid pharmacology.

The role is inflammation control, and it is disease-specific rather than universal — which is where most errors are made. Generally, corticosteroids "help relieve the inflammation in the kidney and promote healing," and immunosuppression "is most useful for rapidly progressive glomerulonephritis." In RPGN they are urgent and empirical: intravenous methylprednisolone 500 mg or 1 g for a minimum of 3 doses, and in anti-GBM disease 1 g daily for 3 days followed by oral prednisolone 1 mg/kg/day (maximum 60 mg), reduced weekly to 20 mg by 6 weeks and tapered off by 6 months. In IgA nephropathy they are conditional and now second-choice: the KDIGO 2025 IgA nephropathy guideline suggests a 9-month course of targeted-release budesonide (Nefecon) for patients at risk of progression (proteinuria ≥ 0.5 g/day), and where that is unavailable, a reduced-dose systemic glucocorticoid for 6–9 months with antimicrobial prophylaxis. And in post-streptococcal glomerulonephritis they are not indicated at all: "there is no definite recommendation for the use of immunosuppressive therapies," and KDIGO’s position is that "the role of glucocorticoids and other immunosuppression is unproven." PSGN is treated supportively. Where steroids are used, monitor for opportunistic infection, which is a named and sometimes life-threatening complication.

The third of the three equally strong first-line flare options, and the one with the most routes. ACR 2020 names "glucocorticoids (ORAL, INTRAARTICULAR, OR INTRAMUSCULAR)," and the patient-facing description matches: if the pain and swelling do not improve, "you may be given steroids as tablets or an injection." The situation where they stop being one option among three and become the answer is the patient who cannot take anything by mouth — a STRONG recommendation: "For patients who may receive NPO, we STRONGLY recommend GLUCOCORTICOIDS (INTRAMUSCULAR, INTRAVENOUS, OR INTRAARTICULAR) over IL-1 inhibitors or ACTH." That is a real and common ward scenario, because postoperative status is itself a named flare precipitant. Prednisone or prednisolone is also one of the three named prophylaxis agents for the 3-to-6-month window. One disorder-side safety interaction belongs here rather than on the class page: before any intra-articular injection, be certain the joint is not septic, because "the presence of crystals in synovial fluid analysis does not rule out septic arthritis, as both conditions can coexist." The class page owns hyperglycaemia, infection risk, adrenal suppression and the taper.

Target joints. "a short course of glucocorticoids may help reduce pain and swelling from synovial inflammation, provided there are no signs of infection."

A powerful anti-inflammatory whose disorder-side cost is that it hides the disease. No source behind this page states a phospholipase-A2 mechanism, so none is asserted here, and no list of steroid-treated diseases is printed either — what is taught instead is the set of clinical consequences, which are what a nurse actually acts on. Consequence one, and it is the most important corticosteroid fact on this page: steroids blunt the fever. "During infections, fever may not be observed in… patients taking corticosteroids; instead, HYPOTHERMIA may be present." A patient on steroids who becomes infected may be normothermic or cold. Consequence two: steroids impair healing, appearing on the sourced list of medications that "can adversely affect healing" alongside anticonvulsants, antibiotics, angiogenesis inhibitors and NSAIDs. Consequence three: steroids confound the white count — demargination, "the mobilization of cells… mediated by the effects of external factors on adhesion molecules," raises the count with no infection present, and medications are on the list of causes of a leukemoid reaction above 50,000 cells/µL. Put the three together and the composite teaching point is uncomfortable but usable: in a patient on corticosteroids, the temperature, the cardinal signs AND the white count can all mislead at once. Assess the site itself, the vital-sign trend, and the patient’s function instead of any single number. The class page owns systemic corticosteroid pharmacology and tapering.

Induction only, never maintenance. Added when 5-ASA fails to achieve remission within two weeks (UC) or to break a CD flare; acute severe UC and toxic megacolon get IV methylprednisolone 60 mg daily for 3–5 days (higher doses add nothing) or hydrocortisone IV. Budesonide targets mild ileal/cecal CD and left-sided UC with less systemic exposure. Prolonged use is avoided because of osteoporosis, osteonecrosis, infection, and adrenal insufficiency — so the taper is never skipped, and inability to wean below 10 mg prednisolone within 3 months (steroid dependence, BSG 2019 definition) means escalating to steroid-sparing therapy.

Not a maintenance treatment for IPF. "Previously, corticosteroids, immunosuppressants such as azathioprine, and N -acetyl cysteine were utilized, but the current recommendation advises against their use in IPF due to findings from the PANTHER-IPF trial" (StatPearls). Acute exacerbation: high-dose corticosteroids after infection is excluded — "immunosuppression in the context of pneumonia can be fatal."

In this disease a corticosteroid is a cytotoxic drug, not an anti-inflammatory — and that reframing is the teaching point. Steroids are lymphotoxic, which is exactly why one is among the four induction agents in ALL alongside an anthracycline, vincristine and asparaginase, and why they have no equivalent role in AML induction. They also carry two supporting roles worth knowing: intravenous dexamethasone is the immediate treatment for differentiation syndrome in APL; and corticosteroid-refractory autoimmune cytopenias are one of the named triggers to begin treating a previously observed CLL. The disorder-side caution is cumulative: steroids add infection risk to a patient who is already neutropenic, so the precautions on this page matter more, not less, while they are running.

Epidural, not systemic. "Diazepam and systemic steroids provide no additional benefit" in acute radiculopathy; but "If symptoms persist beyond six weeks, transforaminal or interlaminar epidural steroid injections may be considered for short term (2 to 4 weeks) pain relief."

Prednisone as a regimen component — the "P" in R-CHOP and Pola-R-CHP.

[Sudden hearing loss] Main treatment — early. "The most common treatment for sudden deafness, especially when the cause is unknown, is corticosteroids"; intratympanic injection "was as effective as oral steroids." [Ménière’s] Intratympanic corticosteroid injections "often reduce dizziness and have little to no risk of hearing loss."

Dexamethasone can reduce early headache recurrence after an ED visit but gives no immediate relief.

Dexamethasone within regimens (the "d" in VRd) and glucocorticoids for hypercalcemia.

The acute relapse drug, not a maintenance drug: high-dose IV methylprednisolone (500–1,000 mg daily for 3–7 days, optionally with a short prednisone taper) is the preferred first-line treatment, and high-dose oral prednisone at equivalent doses gives equivalent outcomes. Steroids accelerate recovery but do not change long-term disability — the final vision after optic neuritis is no better with steroids than without — and low-dose oral prednisone alone increases recurrent optic neuritis. They are reserved for true relapses: rule out fever and infection first, because in a pseudo-relapse the target is the underlying illness. Poor response → plasma exchange, daily or alternate days for 3–7 treatments.

The first-line immunosuppressant when pyridostigmine alone does not meet goals, and the initial immunosuppressive agent of choice in ocular MG (it also cuts generalization). Benefit begins within days and most patients improve within 2–3 weeks; prednisone is the immunosuppressant of choice in pregnancy. The disorder-specific hazard is transient worsening in 25–75% when high doses start — so the dose is titrated up slowly or PLEX/IVIG is given first, and swallow and breathing are watched for the first two weeks. Many patients need long-term low-dose maintenance; taper once goals are met.

The first-line therapy, and the single highest-yield fact in this disorder. In childhood minimal change disease steroids are the primary treatment and 85 to 90% of patients are steroid-responsive, typically achieving remission within about 4 weeks — which is why a child aged 1 to 12 who is normotensive with normal renal function gets a steroid trial instead of a biopsy. Adults with minimal change nephropathy also usually respond, but remission takes two months or more, and FSGS responds far less well, with a remission rate around 30%. The disorder-side burden is the monitoring: steroid toxicity is reviewed every 3 months, calcium and vitamin D protect bone, and a yearly cataract check is advised.

The cord-rescue drug: dexamethasone 10 mg IV bolus, then 4 mg IV every 6 hours for cord compression with neurologic involvement — it shrinks the vasogenic cord edema (via VEGF downregulation) and is given immediately, buying time for surgery and/or radiation. Steroids also reduce swelling in SVC syndrome and are the specific therapy for calcitriol-mediated hypercalcemia (lymphomas), which responds well to them.

Intra-articular glucocorticoids are strongly recommended for knee and hip, and conditionally recommended for the hand. Both halves of that are corrections: the strength is strong rather than conditional at the knee and hip, and the hand direction is for rather than against. This is the third of the four cells that secondary sources commonly reverse, and it matters at the bedside because a nurse who believes ACR discourages joint injection will convey doubt about a treatment the guideline actively endorses. The disorder-side rationale is that the inflammation in osteoarthritis is real but low-grade and local — synovitis with interleukins 1-beta, 6, 15, 17 and 18 and tumor necrosis factor alpha — so a locally delivered anti-inflammatory addresses the right compartment without systemic exposure. The guideline does address injection frequency, and its answer is an explicit uncertainty rather than a limit: "a certain frequency of steroid injections may contribute to cartilage loss, but the Voting Panel was uncertain of the clinical significance of this finding, particularly since change in cartilage thickness was not associated with a worsening in pain, functioning, or other radiographic features." A separate carrier states more bluntly that repeated injections "accelerate joint damage." What no fetched source gives is a number — the familiar "no more than three or four per joint per year" is not in this evidence base. Present it as the reason injections are spaced and reassessed, not as a count. Systemic corticosteroid pharmacology and adverse effects belong to the class page.

For hypercalcemia from lymphoma or granulomatous disease — prednisone "inhibits calcitriol production and lowers calcium levels."

Second-line, and the class with the recurrence trap: corticosteroids are a second option when NSAIDs are contraindicated or fail (allergy, recent GI ulcer, anticoagulation, CKD, pregnancy beyond 20 weeks, systemic inflammatory disease), at low-to-moderate dose (prednisone 0.2–0.5 mg/kg/day) with a slow taper, because steroid use increases the risk of recurrence once therapy stops. Early or high-dose steroid exposure in idiopathic pericarditis is consistently associated with more recurrences, so the taper is very slow (for example 1.25–2.5 mg every 1–2 weeks after remission) and infection — especially TB — is excluded first. Exceptions as reported by the Italian Society of Cardiology position paper and StatPearls: they may be first-line in postpericardiotomy syndrome, are used as an adjunct in TB pericarditis only in HIV-negative patients, and rescue Dressler non-responders with a roughly 4-week taper — relapses are occasionally seen on withdrawal.

Two roles. Corticosteroids are on the list of drugs that can trigger a hypertensive crisis; and after bilateral total adrenalectomy, lifelong steroid replacement is required.

Antenatal corticosteroids are on a bleeding page for one reason: both previa and abruption cause preterm delivery, and the decision to admit and watch rather than deliver exists partly to buy time for the steroid course to work. The regimens, the gestational-age windows, the four-society disagreement at 34 to 36 6/7 weeks and the rescue-course rule are owned by the preterm-labor page — follow the link rather than reading a second, shorter version of them here. What belongs on a bleeding page is narrower and is not on that page: which bleeding patient can afford to wait for them. The disorder-side judgement is the part that matters here: in an unstable bleed, delivery is not delayed for steroids. In previa, "earlier delivery might be warranted based on individual bleeding profiles," and in abruption, fetal distress or rapid maternal decompensation can make an emergency cesarean necessary. Steroids are for the patient who can be watched. Systemic corticosteroid pharmacology, adverse effects and the glucose rise belong to the class page.

NHLBI lists corticosteroids to reduce pleural inflammation — with serious side effects on long-term use.

Antenatal corticosteroids are the reason tocolysis exists. The regimen and doses are ordered by the provider; the window is where the sources speak. The World Health Organization "recommends antenatal corticosteroids from 24 to 34 weeks EGA, including patients with PPROM, multifetal gestations, hypertensive disorders, or fetal growth restriction." Between 34 and 36 6/7 weeks sources differ: the Society for Maternal-Fetal Medicine offers a single course to patients meeting the ALPS trial criteria, WAPM-PMF suggests a 34 0/7-week cutoff, the Royal College of Obstetricians and Gynaecologists recommends offering steroids up until 34 6/7 weeks, and the World Health Organization recommends them from 24 to 34 weeks and advises against them before a planned cesarean between 34 and 36 6/7 weeks. A rescue course "may consist of either a standard 48-hour regimen described above or a single dose of betamethasone." Two contraindications belong with the late-preterm course specifically, and both collide with material elsewhere on this page. The Society for Maternal-Fetal Medicine recommends "against the use of antenatal steroids in late preterm patients with pregestational diabetes mellitus due to the risk of neonatal hypoglycemia," and the World Health Organization advises "against therapy for individuals with chorioamnionitis." So the finding that ends expectant management also withdraws the steroid, and a patient with pregestational diabetes does not get the late-preterm course. The WHO window explicitly includes patients with PPROM. What the drug buys, in the WHO evidence summary: "a 32% reduction in neonatal deaths," RDS "reduced by 35%," and "a reduction in the occurrence of cerebroventricular haemorrhage … and necrotizing enterocolitis." One practical consequence for the nurse reading labs: steroids raise the white cell count, so a rise after a dose is expected. Systemic corticosteroid pharmacology and adverse effects belong to the class page.

IVIG premedication — "occasionally hydrocortisone" for patients with reactions.

Caution, not a psoriasis or eczema treatment. Abrupt withdrawal of systemic steroids can trigger erythrodermic psoriasis; oral steroids are not usually given for atopic dermatitis because it "can flare or rebound and be more severe than before." In severe contact dermatitis only, systemic steroids "should be tapered gradually to prevent recurrences."

[GCA][PMR] The mainstay. "Corticosteroids. These anti-inflammatory medications are a mainstay of treatment for both disorders" — low to moderate doses for PMR and higher doses for GCA, then a gradual taper; "You may remain on a maintenance dose for a year or possibly longer" (NIAMS). In GCA, "Guidelines state that all patients with GCA warrant high-dose glucocorticoids as the initial treatment" (StatPearls), and "Patients with diplopia should also receive IV steroids" (StatPearls, citing ACR and BSR).

A bridge, and the guideline is emphatic that it should end. The sourced uses are narrow: bridge therapy for "a new patient with very active RA," short courses for mild flares, and intra-articular injection for a single-joint flare, with about 50% of patients requiring low-dose prednisone at some point. But ACR 2021 states it at strong strength: "Initiation of a csDMARD WITHOUT longer-term (≥3 months) glucocorticoids is STRONGLY recommended over initiation of a csDMARD with longer-term glucocorticoids," because "the toxicity associated with glucocorticoids was judged to outweigh potential benefits." Teach the bridge as a bridge, with a planned end date — not as routine chronic therapy. The disorder-specific reason is that steroids compound exactly the two comorbidities RA already carries: a 60% to 100% increased fracture risk, and independently accelerated coronary artery disease. One practical rule belongs at the bedside: perioperative glucocorticoid coverage is required above a prednisolone dose of 10 mg/day — hydrocortisone 50 mg IV before incision then 25 mg IV every 8 hours for a minor procedure, 100 mg IV before incision with an infusion for a major one.

[Scleroderma] CAUTION — can trigger renal crisis. "Corticosteroids should generally be avoided in systemic sclerosis due to the risk of precipitating scleroderma renal crisis"; if truly needed, "the lowest possible dose for the shortest duration possible." [Sjögren’s] Used for serious extraglandular disease at "the lowest dose possible"; NHS: "a short course of steroid tablets" for severe joint pain. Topical eye steroids: "infrequent use is recommended" (glaucoma, cataract, infection risk).

Treatment of immune-related adverse events — for pembrolizumab and nivolumab, NCI notes the FDA label recommends "withholding the drug and administering corticosteroids" for suspected irAEs.

Methylprednisolone (MPSS) is an option, not a standard of care — and the timing rules are exam gold. The 2017 AOSpine guideline suggests a 24-hour infusion of high-dose MPSS be offered within 8 hours of injury as a treatment option (weak recommendation, moderate evidence; pooled motor-score gain 3.88 points at 6–12 months) — and suggests not offering it after 8 hours, and never as a 48-hour infusion (NASCIS III showed significantly more severe pneumonia at 48 h). The history matters: the 2013 AANS/CNS guideline made a Level I recommendation against MPSS (not FDA-approved for SCI; harms including death outweighed unproven benefit), and 2017 bridged the conflict by splitting on timing and duration.

Controversial adjunct — not proven. "Systemic corticosteroids are commonly used to halt the progression of TEN. However, results from some studies linked corticosteroids to increased mortality incidence." They are associated "with increased risk of infection"; "The role of corticosteroids as monotherapy is still debated." Topical corticosteroid drops may be part of eye care (StatPearls, citing SDH).

The fast tool for organ-threatening inflammation — and the one with an explicit exit plan. Short courses treat ongoing or recurrent inflammatory arthritis; moderate doses treat pleuropericarditis; high-dose intravenous pulse corticosteroids treat acute lupus pneumonitis, severe or symptomatic thrombocytopenia, and inflammatory CNS manifestations; combinations with cyclophosphamide, mycophenolate or rituximab treat myocarditis, and with IVIG or rituximab treat hemolytic anemia. The taper target is a guideline number, not a preference: the ACR-based lupus-nephritis regimen tapers to approximately 5 mg/day of prednisone-equivalent by the 6-month mark, with maintenance below 7.5 mg/day if steroids are used at all. On provenance, two honest caveats: the StatPearls carrier reporting this does not name its ACR edition, and ACR has since published a 2024 lupus-nephritis guideline and a 2025 lupus guideline whose full texts are not open — their abstracts stress limiting how long glucocorticoids are used and, in nephritis, continuous therapy with pulse steroids, an oral taper and two added immunosuppressants for 3–5 years in patients who reach a complete renal response, but they give no taper number — while the same ≤ 5 mg/day-within-6-months target is independently carried by the EULAR 2023 recommendations, so the number has recent corroboration from a second society. That number exists because glucocorticoids exacerbate the accelerated atherosclerosis that already kills about half of these patients, and add osteoporosis, glaucoma, cataracts, weight gain and diabetes on top — a real cost in someone facing fifty more years of disease.

First-line for ITP, and with a treatment threshold rather than a reflex. Per the ASH ITP guidelines (2019 thresholds, unchanged in the 2026 update), corticosteroids are recommended for adults with newly diagnosed ITP and a platelet count below 30,000/μL who are asymptomatic or have only minor mucocutaneous bleeding — and for counts at or above 30,000/μL, "observation instead" is advised. That single pair of numbers prevents a great deal of unnecessary immunosuppression. They work by inhibiting autoantibody production and platelet destruction, the same two arms the disease attacks through. The disorder-side caution is duration: prednisone "for an extended duration exceeding 6 weeks" is not recommended, because in chronic paediatric ITP most mortality and morbidity come from the complications of long-term immunosuppression rather than from the platelet count. The 2026 ASH update keeps that threshold and the 6-week limit but now suggests pairing the initial corticosteroid with rituximab or a thrombopoietic agent (± IVIG) where available, rather than giving corticosteroids alone. Steroids are often paired with intravenous immunoglobulin, which is "often considered to have an augmentative effect."

Severe allergic reactions — "More severe symptoms can be treated with bronchodilators, corticosteroids, and epinephrine." In a delayed hemolytic reaction with a brisk hemoglobin fall, clinicians may consider glucocorticoids, IVIG or rituximab (StatPearls).

Maintenance and rejection treatment. IV methylprednisolone treats T-cell-mediated rejection (StatPearls). Steroids "may decrease tacrolimus concentrations." NIDDK notes appearance changes — fuller face, weight gain, acne, facial hair.

Replace or supplement the body’s own insulin to lower blood glucose. High-alert — hypoglycemia is the #1 risk.

Non-insulin agents for type 2 diabetes — each subclass targets a different broken "lever." Metformin is first-line.

Four smaller groups of type 2 diabetes drugs, each with its own lever: pioglitazone sensitizes tissues to insulin, acarbose and miglitol slow carbohydrate digestion in the gut, repaglinide and nateglinide give a short burst of insulin at meals, and pramlintide adds amylin alongside mealtime insulin. Their signature risks follow the lever: fluid retention and heart failure, gas and diarrhea, hypoglycemia with skipped meals, and severe hypoglycemia with insulin.

Glucagon is the rescue drug for severe hypoglycemia when the patient cannot safely take sugar by mouth; dasiglucagon, a glucagon analog, is used the same way. Given by injection or as a nasal powder, glucagon makes the liver release glucose from glycogen — so it works only if the liver has glycogen to give. It also relaxes the gut and is used as a diagnostic aid in radiology.

Replace thyroid hormone in hypothyroidism, or block its synthesis — or destroy the gland with radioactive iodine — in hyperthyroidism. TSH is the monitoring dial.

Fludrocortisone replaces the missing mineralocorticoid in primary adrenal insufficiency, so it retains sodium and loses potassium — watch blood pressure, swelling and potassium. Osilodrostat and metyrapone block the last step of cortisol synthesis, and mifepristone (Korlym) blocks cortisol at its receptor; all three can tip a patient into adrenal insufficiency.