Comprehensive Pharmacotherapy Reference Guide
ADA Standards of Care 2024/2025  |  ACCP Updates in Therapeutics 2025

SECTIONTOPIC
1Classification & Staging
2Screening Criteria
3Diagnostic Criteria
4Goals of Therapy
5T1D Management & Insulin Therapy
6T2D Treatment Algorithm
7Pharmacotherapy Agents – T2D (Dosing, Renal Adjustment, Monitoring)
8Management of Complications (Hypoglycemia, DKA, Nephropathy, Retinopathy, Neuropathy, CVD)
9Inpatient Diabetes Management
10Key Clinical Trials
11Oncology Special Considerations (Steroid-induced, ICI-DM, Drug Interactions)
12Clinical Pearls & Pharmacist Watchouts

  1. CLASSIFICATION & STAGING OF DIABETES 

1A. Types of Diabetes

TYPEKEY FEATURESPREVALENCENOTES
Type 1 DM (T1D)Autoimmune beta-cell destruction; absolute insulin deficiency; usually symptomatic5-10% of DMFormerly ‘insulin-dependent DM’; any age; rapid onset in children, slower in adults (LADA)
Type 2 DM (T2D)Insulin resistance + progressive beta-cell secretory defect; GI, brain, liver, kidney involvement90-95% of DMOften asymptomatic; slow onset 5-10 years; screen early; rising in pediatrics
Gestational DMGlucose intolerance during pregnancy; most common 3rd trimester1-14% of pregnancies (~4%)Screen at 24-28 wks; screen postpartum at 4-12 wks; rescreen q3yr for life
MODYGenetic defect in beta-cell function; little/no impairment in insulin actionRareOnset <25 yrs; mimics T1D or T2D; responds to sulfonylureas; often misdiagnosed
Secondary DMPancreatic disease, drug-induced, genetic syndromesVariableGlucocorticoids, atypical antipsychotics, L-asparaginase, mTOR inhibitors, ICI (see Section 11)

1B. T1D Staging (ADA)

STAGEAUTOANTIBODIESGLYCEMIASYMPTOMSCLINICAL ACTION
Stage 1Multiple Ab+NormalNoneEnroll in observational study; counsel re: symptoms
Stage 2Multiple Ab+Prediabetes rangeNoneMonitor closely; consider teplizumab (anti-CD3 mAb) to delay T1D
Stage 3Ab+ (usually)Diabetes criteriaPresentInitiate insulin therapy immediately
CLINICAL PEARL: MODY is commonly misdiagnosed as T1D or T2D. In young, non-obese patients with ‘T2D’ or atypical T1D, consider MODY testing. These patients may respond to sulfonylureas rather than insulin.

1C. Prediabetes

  • Impaired Fasting Glucose (IFG): FPG 100-125 mg/dL
  • Impaired Glucose Tolerance (IGT): 2-hr plasma glucose 140-199 mg/dL after 75-g OGTT
  • HbA1c: 5.7%-6.4%
  • Screen annually for progression to T2D if prediabetes is confirmed
  • Interventions: lifestyle (diet + exercise), metformin (especially if BMI ≥35, age <60, or history of gestational DM)

  2. SCREENING CRITERIA 

2A. T2D Screening

  • Age ≥35: Screen all; repeat q3yr if normal
  • Screen regardless of age if BMI ≥25 kg/m² (≥23 in Asian Americans) + at least ONE risk factor:
    • First-degree relative with T2D
    • High-risk ethnicity: African American, Latino, Native American, Asian American, Pacific Islander
    • History of CVD
    • HbA1c ≥5.7%, IGT, or IFG on previous testing
    • Hypertension (BP ≥130/80 or on antihypertensive therapy)
    • HDL <35 mg/dL or TG >250 mg/dL
    • History of PCOS
    • Physical inactivity
    • Severe obesity, acanthosis nigricans (insulin resistance conditions)

2B. T1D Screening

  • Symptomatic patients: Screen immediately
  • Asymptomatic high-risk: First-degree relatives with T1D; measure islet autoantibodies (GAD65, IA-2, ZnT8, IAA)
  • If screen positive: counsel on symptoms of hyperglycemia, risk of T1D; consider enrollment in observational study

2C. Gestational DM Screening

  • At first prenatal visit: screen for undiagnosed T2D in all patients with T2D risk factors
  • At 24-28 weeks gestation: 75-g OGTT (one-step) or 50-g nonfasting OGTT (two-step)
  • Post-delivery: Screen for T2D at 4-12 weeks post-delivery
  • Lifelong: Rescreen every 3 years for T2D

  3. DIAGNOSTIC CRITERIA 

3A. Diagnostic Criteria – Non-Pregnant Adults

TESTPREDIABETESDIABETESNOTES
Fasting Plasma Glucose (FPG) (≥8 hr fast)100-125 mg/dL≥126 mg/dLEasy, convenient; most reproducible
2-hr OGTT (75-g glucose)140-199 mg/dL≥200 mg/dLMore sensitive/specific than FPG; cumbersome
HbA1c5.7%-6.4%≥6.5%No fasting required; less day-to-day variability; can be inaccurate in hemoglobinopathies, hemolytic anemia, recent transfusion, pregnancy, ESRD
Random Plasma GlucoseN/A≥200 mg/dL + symptomsSymptoms: polyuria, polydipsia, unexplained weight loss
  • Unless symptoms of hyperglycemia are clearly present, DIAGNOSIS requires TWO abnormal tests – can be from the same blood draw or two separate days.
  • Two different tests (e.g., FPG + HbA1c) on the same sample count as two tests per updated ADA recommendations.

3B. Gestational DM (24-28 wks gestation)

APPROACHTESTDIAGNOSTIC THRESHOLD
One-Step75-g OGTT (fasting)Fasting ≥92 mg/dL OR 1-hr ≥180 mg/dL OR 2-hr ≥153 mg/dL (ANY one)
Two-StepStep 1: 50-g OGTT (nonfasting) Step 2 if ≥140 mg/dL: 100-g OGTT (fasting)Step 2: Use ADA 100-g OGTT diagnostic glucose criteria (Carpenter-Coustan or NDDG)
WARNING: HbA1c LIMITATIONS in Hem/Onc: Falsely LOW in hemolytic anemia, sickle cell disease, recent chemotherapy (hemolysis), post-transfusion, erythropoiesis-stimulating agents, pregnancy. Use FPG or OGTT instead. ESRD also affects HbA1c accuracy.

3C. Additional Tests to Differentiate T1D from T2D

  • C-peptide: Measure of endogenous insulin secretion. Near-zero in T1D; normal or elevated early in T2D
  • Autoantibodies: GAD65, IA-2, ZnT8, IAA, islet cell Abs – all suggest autoimmune (T1D) etiology

  4. GOALS OF THERAPY – NON-PREGNANT ADULTS 

4A. Glycemic Goals (ADA 2024)

PARAMETERGOALNOTES
HbA1c<7.0% (general)AACE/ACE recommends ≤6.5%. Less stringent (e.g., <8%) in: short life expectancy, terminal cancer, advanced complications, frail elderly, frequent hypoglycemia, extensive comorbidities
HbA1c monitoringq6mo (at goal); q3mo (above goal)More frequent if regimen change or poor control
Fasting / Pre-meal BG80-130 mg/dLTarget range for self-monitoring
Peak Post-prandial BG<180 mg/dL1-2 hrs after meal start
Time In Range (TIR)≥70% (70-180 mg/dL range)For CGM users; time below range <4%
Time Below Range<4% (<70 mg/dL)<1% for <54 mg/dL

4B. Non-Glycemic Goals

PARAMETERGOALFIRST-LINE AGENT(S)
Blood Pressure<130/80 mmHgACEi or ARB (if albuminuria present); DHP-CCB or thiazide-like diuretic
LDL – No established CVD (age 40-75)≥50% reduction or LDL <70 mg/dLModerate- to high-intensity statin
LDL – Established CVD≥50% reduction AND LDL <55 mg/dLHigh-intensity statin; add ezetimibe or PCSK9i if still above goal
Antiplatelet – Established ASCVDASA 75-162 mg/dayClopidogrel if ASA-intolerant
Antiplatelet – Primary preventionConsider if high CV riskIndividualize; discuss risk of bleeding vs. benefit
CLINICAL PEARL: Blood pressure control reduces BOTH microvascular (nephropathy, retinopathy) AND macrovascular (MI, stroke) complications. Glycemic control primarily reduces microvascular complications. This is why BP management is arguably the most impactful intervention in T2D.

  5. T1D MANAGEMENT & INSULIN THERAPY 

5A. Insulin Types – U-100 (100 units/mL)

CATEGORYDRUG(S)ONSETPEAKDURATIONADMIN TIMING
Rapid-actingAspart (NovoLog) Lispro (Humalog) Glulisine (Apidra) Inhaled insulin (Afrezza)5-15 min (inhaled: start of meal)1-3 hr (shorter for fast-acting formulations)2-5 hr5-15 min BEFORE meal (inhaled: at start of meal)
Short-actingRegular (Humulin R, Novolin R)30-60 min2-4 hr6-8 hr30 min BEFORE meal
IntermediateNPH (Humulin N, Novolin N) [CLOUDY]1-2 hr4-8 hr10-20 hrNo fixed meal relationship (given 2x/day traditionally)
Long-acting (basal)Glargine U-100 (Lantus, Basaglar) Degludec U-100 (Tresiba)1-2 hrPeakless~24 hr 24-42 hr (degludec)Once daily; any consistent time; do NOT mix

5B. Concentrated Insulins – Special Attention Required

PRODUCTCONCENTRATIONINDICATIONKEY CONSIDERATION
Glargine U-300 (Toujeo)300 units/mLT1D/T2D – high insulin requirements3x more concentrated than U-100; do NOT dose convert 1:1 from U-100; slightly longer than U-100 glargine
Degludec U-200 (Tresiba)200 units/mLT1D/T2D – high insulin requirementsPen delivers same dose in half the volume; no dose conversion needed (same units)
Lispro U-200 (Humalog KwikPen)200 units/mLT2D with high rapid-acting needsPen only; same dose in half the volume
Regular U-500 (Humulin R U-500)500 units/mLSevere insulin resistance T2D (>200 units/day)5x concentrated; HAS INTERMEDIATE-ACTING PROPERTIES (onset 30 min, duration up to 24 hr); extreme risk of confusion with U-100
WARNING: INSULIN CONCENTRATION ERRORS are a high-alert medication concern. U-300 and U-200 are NOT dose-equivalent to U-100 on a per-mL basis. U-500 regular insulin has intermediate-acting properties – do not treat as short-acting insulin. Always verify the product and concentration at every order review.

5C. Insulin Dosing Calculations for T1D (Basal-Bolus)

CALCULATIONFORMULAEXAMPLE (80 kg patient)
Total Daily Insulin (TDI)0.3-0.6 units/kg/day (typically 0.5 units/kg/day for initial estimate) 0.3 if near honeymoon phase; higher if DKA treatment80 kg × 0.5 = 40 units TDI
Basal Insulin (50% of TDI)TDI × 0.5 → give as once-daily long-acting insulin40 × 0.5 = 20 units glargine at bedtime
Total Bolus (50% of TDI)TDI × 0.5 → divide equally among 3 meals40 × 0.5 = 20 units ÷ 3 = ~7 units before each meal
Insulin-to-Carb Ratio (ICR) ‘Rule of 500’ICR = 500 ÷ TDI = grams of carbs covered by 1 unit of rapid-acting insulin500 ÷ 40 = 12.5 g carbs per 1 unit
Insulin Sensitivity Factor (ISF) ‘1800 Rule’ISF = 1800 ÷ TDI = how much 1 unit rapid-acting lowers BG (mg/dL)1800 ÷ 40 = 45 mg/dL drop per 1 unit
ISF for Regular Insulin ‘1500 Rule’ISF = 1500 ÷ TDI1500 ÷ 40 = 37.5 mg/dL drop per 1 unit regular
CLINICAL PEARL: The 1800 rule is patient-specific and more precise than sliding-scale insulin. Always document the ISF in the patient chart. If a patient’s BG is 240 and target is 120, the correction dose = (240-120)/ISF. This is your tool at bedside during pharmacy rounds.

5D. Amylin Analog – Pramlintide (Symlin)

  • Mechanism: Synthetic amylin – co-secreted with insulin; slows gastric emptying, reduces glucagon, promotes satiety
  • T1D dosing: Start 15 mcg SQ immediately before main meals; titrate by 15 mcg q3 days; max 60 mcg per meal
  • T2D dosing: Start 60 mcg SQ before main meals; titrate by 60 mcg q3-7 days; max 120 mcg per meal
  • CRITICAL: REDUCE preprandial insulin by 50% when initiating pramlintide to avoid severe hypoglycemia
  • Cannot be mixed with insulin; requires separate injection device
  • ADEs: Boxed warning – severe hypoglycemia (especially T1D); nausea, vomiting, anorexia
  • Contraindications: Gastroparesis; HbA1c >9%; hypoglycemia unawareness; poor adherence to SMBG
  • Efficacy: 0.5-1% HbA1c reduction; effective for postprandial glucose control; modest weight loss
Rx PHARMACIST WATCHOUT: Pramlintide boxed warning: SEVERE HYPOGLYCEMIA (especially in T1D). Must reduce preprandial insulin by 50% when initiating. Use prefilled pens (NOT syringe + vial) to minimize dosing errors. Cannot be mixed with insulin in same syringe. Flag this every time you see a new pramlintide order.

5E. Continuous Glucose Monitoring (CGM) & Insulin Pump

  • Real-time CGM: Continuously transmits glucose data to a display device; used with or without insulin pump
  • Intermittent CGM: Requires patient to scan the sensor to view glucose data (e.g., FreeStyle Libre)
  • Insulin pump (CSII): Continuous subcutaneous infusion; patient-specific hourly basal + bolus dosing; uses rapid-acting only
  • Hybrid closed-loop systems: Near-artificial pancreas; CGM + pump communicate to auto-adjust basal insulin in real time
  • Inhaled insulin (Afrezza): Contraindicated in asthma, COPD, lung cancer; requires baseline spirometry and q6 months, then annually

  6. T2D TREATMENT ALGORITHM (ADA 2024) 

6A. Stepwise Approach

  • Step 1 – Lifestyle + Metformin: Initial therapy for most patients with T2D (unless contraindicated)
  • Combination therapy (metformin + second agent) if baseline HbA1c is ≥1.5% above personal goal
  • When metformin is NOT first-line (prioritize disease-based selection):
    • Established ASCVD → GLP-1 RA or SGLT-2i with proven CV benefit (regardless of HbA1c)
    • Heart failure → SGLT-2i with proven HF benefit (canagliflozin, dapagliflozin, empagliflozin)
    • CKD (eGFR ≥20 + ACR ≥200 mg/g) → SGLT-2i; consider finerenone
    • Weight management → GLP-1 RA (semaglutide, dulaglutide) or SGLT-2i
    • Hypoglycemia risk → DPP-4i, GLP-1 RA, SGLT-2i, TZD
  • Cost concern → Sulfonylurea (generic glipizide/glimepiride)

6B. When to Add Injectable Therapy (ADA Guidance)

  • Preferred injectable addition: GLP-1 RA over insulin (lower hypoglycemia, weight loss, CV benefit)
  • Add early basal insulin if: HbA1c >10% OR HbA1c >2% above personal goal
  • Basal insulin initiation (T2D): 0.1-0.3 units/kg/day or 10 units QHS
  • Titration: Increase by 2-4 units or 10-15% once or twice weekly to achieve FPG target (80-130 mg/dL)
  • Add bolus insulin if: Basal dose ≥0.5 units/kg/day OR significant postprandial excursions remain
  • Initial bolus dose: 4 units or 10% of basal dose per meal

6C. Insulin Add-On Rules (Important!)

  • When ADDING bolus insulin: REDUCE or DISCONTINUE sulfonylurea/meglitinide (↑ hypoglycemia risk)
  • When ADDING basal insulin: REDUCE or DISCONTINUE TZD (↑ risk of fluid retention/edema)
  • SGLT-2i: Add if weight gain is a concern OR secondary indication exists (HF, CKD, ASCVD)
CLINICAL PEARL: ADA now de-emphasizes a purely stepwise approach. Instead, choose the second agent based on: (1) whether established CVD/HF/CKD exists (strongest factor), (2) weight/hypoglycemia concerns, (3) cost, (4) patient preference. The days of ‘metformin, then add SU’ as default are over.

  7. PHARMACOTHERAPY AGENTS – T2D 

7A. Metformin (Biguanide) – First-Line

PARAMETERDETAILS
MOAReduces hepatic gluconeogenesis; improves insulin sensitivity; reduces intestinal glucose absorption
DosingStart 500 mg QD or BID with meals; extend-release: 500-1000 mg QD. Increase weekly as tolerated. Max 2550 mg/day (commonly capped at 2000 mg)
HbA1c reduction1-2% (larger reduction with higher baseline HbA1c)
Renal DosingeGFR ≥60: No adjustment needed; monitor q3-6mo eGFR 45-59: Do NOT initiate; if already on, reduce dose 50%, monitor q3mo eGFR 30-44: Do NOT initiate; if on it, reduce dose 50%; monitor renal function closely eGFR <30: CONTRAINDICATED – discontinue
Hold/InterruptHold for iodinated contrast (if eGFR 30-60): Reinitiate 48 hrs after with confirmed normal SCr Hold perioperatively, in acute illness, hypoxia, hepatic impairment, alcohol use
Key ADEsGI (N/V/D – dose-related, limit with slow titration, take with food); Vitamin B12 ↓ (monitor periodically); Rare: lactic acidosis
BenefitsWeight neutral to modest loss; low hypoglycemia risk; UKPDS CV benefit in overweight T2D; inexpensive
ContraindicationseGFR <30; hepatic impairment; alcohol abuse; high-risk cardiovascular events or hypoxic state; age ≥80 (caution)
Rx PHARMACIST WATCHOUT: Metformin & contrast: Stop metformin at time of contrast if eGFR 30-60 mL/min. Restart 48 hours AFTER procedure only if renal function is stable. Communicate proactively with radiology/ordering team in admitted patients.

7B. Sulfonylureas (SU) – Insulin Secretagogues

AGENTINITIAL DOSEMAX DOSERENAL NOTEHALF-LIFE / DURATION
Glipizide (Glucotrol, Glucotrol XL)5 mg QD (ER: 5 mg QD)40 mg/day (ER: 20 mg; little benefit >20 mg)Preferred in elderly/CKD – hepatic metabolism, not renally cleared2-4 hr / 12-24 hr
Glimepiride (Amaryl)1-2 mg QD8 mg/dayReduce dose in renal impairment; active metabolites renally excreted5-9 hr / 24 hr
Glyburide (DiaBeta, Glynase)2.5-5 mg QD-BID20 mg/dayAVOID in elderly and CKD – active metabolites renally excreted → prolonged hypoglycemia6-12 hr / up to 24 hr
  • MOA: Bind pancreatic beta-cell receptors → membrane depolarization → insulin secretion (glucose-independent)
  • Key ADEs: Hypoglycemia (especially glyburide; prolonged), weight gain, rash, photosensitivity (rare)
  • Avoid in: Hypoglycemia unawareness; significant renal impairment (prefer glipizide); elderly (glyburide)
  • Drug interaction: AZOLE ANTIFUNGALS (fluconazole, voriconazole) inhibit CYP2C9 → ↑ SU levels → ↑ hypoglycemia risk (CRITICAL in oncology with antifungal prophylaxis)
Rx PHARMACIST WATCHOUT: Sulfonylurea + azole antifungals = HIGH hypoglycemia risk. Fluconazole, voriconazole, and other azoles inhibit CYP2C9, significantly increasing sulfonylurea plasma levels. In oncology patients on antifungal prophylaxis (e.g., fluconazole for febrile neutropenia prophylaxis), monitor BG very closely or consider switching to a different antidiabetic agent.

7C. SGLT-2 Inhibitors – Glycosurics

AGENTDOSERENAL CUTOFFSCV / RENAL BENEFITKEY ADEs / NOTES
Canagliflozin (Invokana)100 mg QD before first meal Max: 300 mgeGFR <30: Do NOT initiate eGFR 30-59: Max 100 mg eGFR <30 but on it with albuminuria >300 mg/g: Continue 100 mg (renal protection until dialysis)CANVAS: ↓ MACE (14%) CREDENCE: ↓ ESKD/renal composite ↓ HF hospitalization↑ Amputation risk (feet/legs) ↓ Bone mineral density; fracture risk Hold 3 days pre-surgery ↑ LDL (small)
Dapagliflozin (Farxiga)5 mg QD (with or without food) Max: 10 mgeGFR <25: Do NOT initiate eGFR <25 but established on 10 mg for HF/CKD: Continue until dialysisDECLARE-TIMI 58: ↓ HF hospitalization/CV death DAPA-CKD: ↓ CKD progression (including non-diabetic CKD) ↓ HF hospitalizationIndicated for HF (HFrEF and HFpEF) and CKD regardless of diabetes status Hold 3 days pre-surgery
Empagliflozin (Jardiance)10 mg QD Max: 25 mgeGFR <20: Do NOT initiate eGFR <20 but on it: Continue 10 mg for HF/CKD benefit until dialysisEMPA-REG: ↓ CV death (38%), MACE (14%), HF hospitalization (35%) EMPA-KIDNEY: ↓ CKD progression ↓ HF hospitalizationStrongest CV mortality data of class Hold 3 days pre-surgery
Ertugliflozin (Steglatro)5 mg QD Max: 15 mgDiscontinue/do NOT initiate if eGFR <45VERTIS-CV: No significant MACE benefit ↓ HF hospitalization onlyHold 4 days pre-surgery Less robust outcomes data
Bexagliflozin (Brenzavvy)20 mg QD Max: 20 mgDiscontinue/do NOT initiate if eGFR <30NO proven CV, HF, or renal outcome benefit (newest agent; trials pending)HbA1c reduction similar to class Least evidence for secondary indication
  • Class MOA: Block SGLT-2 in proximal tubule → ↑ urinary glucose excretion; HbA1c reduction declines as eGFR declines
  • Class ADEs: Genital mycotic infections (>females), UTI, increased urination, hypotension, DKA (EUGLYCEMIC), Fournier gangrene (rare), bone fractures, dehydration
  • HbA1c reduction: 0.5-0.8%
WARNING: EUGLYCEMIC DKA with SGLT-2 INHIBITORS: Blood glucose may be near-normal (140-180 mg/dL) but patient is in DKA. Always check ketones (blood beta-hydroxybutyrate) if patient on SGLT-2i presents with vomiting, nausea, abdominal pain, or shortness of breath. High-risk situations: fasting, surgery, low-carb diet, illness, alcohol, insulin dose reduction.
Rx PHARMACIST WATCHOUT: SGLT-2i pre-surgery protocol: Hold canagliflozin, dapagliflozin, empagliflozin 3 DAYS before surgery. Hold ertugliflozin 4 DAYS before surgery. This is frequently missed in oncology patients undergoing procedures. Review medication list proactively before any scheduled surgery or procedure.

7D. GLP-1 Receptor Agonists (and GIP/GLP-1 Dual Agonist)

AGENTDOSINGRENAL NOTECV OUTCOME TRIALKEY ADEs / NOTES
Exenatide BID (Byetta)5 mcg SQ BID (≤60 min before AM and PM meals) Titrate to 10 mcg BID after 1 monthCrCl <30: AVOIDEXSCEL (ER form): Non-inferior (not superior) for MACEGI dominant (N/V/D); injection-site reactions; pancreatitis; do NOT use with severe GI disease
Exenatide ER (Bydureon BCise)2 mg SQ once weekly (powder reconstituted before injection) [inject any time, regardless of meals]CrCl <30: AVOIDNon-inferior to placebo for MACE; some CV signalsWeekly; longest-acting of extended-release agents; GI less than BID form
Liraglutide (Victoza)0.6 mg SQ QD × 1 wk → 1.2 mg → max 1.8 mg/day [inject any time, regardless of meals]No dose adjustment; use caution CrCl <30LEADER: ↓ MACE 13%; ↓ CV death 22%; ↓ nephropathyApproved for CVD risk reduction; once-daily; GI ADEs common during titration
Dulaglutide (Trulicity)0.75 mg SQ weekly → 1.5 mg → 3 mg → max 4.5 mg weeklyNo dose adjustmentREWIND: ↓ MACE 12% (includes primary prevention patients)Once weekly; device auto-injects; broadest CV benefit population (primary + secondary prevention)
Semaglutide SQ (Ozempic)0.25 mg SQ weekly × 4 wks → 0.5 mg → 1 mg → max 2 mg weeklyNo dose adjustmentSUSTAIN-6: ↓ MACE 26% (largely stroke); FLOW: ↓ renal composite 24%Highest efficacy SQ GLP-1 (before tirzepatide); first GLP-1 with proven CKD benefit in FLOW trial
Semaglutide PO (Rybelsus)3 mg QD × 1 mo → 7 mg QD × 1 mo → max 14 mg QDNo dose adjustmentPIONEER 6: Non-inferior for MACEMUST take on empty stomach with ≤4 oz water, 30 min before first food/drink/medication of day. Only oral GLP-1.
Tirzepatide (Mounjaro) – GIP/GLP-12.5 mg SQ weekly → ↑ by 2.5 mg monthly → max 15 mg weeklyNo dose adjustmentSURPASS-CVOT: awaited (results expected); SURMOUNT shows robust weight/metabolic dataVERY HIGH EFFICACY: 2.0-2.3% HbA1c ↓; significant weight loss (up to 20% body weight). Dual GIP + GLP-1 agonism. Targets both fasting AND postprandial glucose.
  • Class MOA: Binds GLP-1 receptors → glucose-dependent insulin secretion, ↓ glucagon, ↓ gastric emptying, promotes satiety
  • Class ADEs: N/V/D, constipation, acid reflux, pancreatitis (rare), gallbladder disease, acute renal failure, injection-site reactions, retinopathy (semaglutide – monitor in pre-existing retinopathy)
  • Contraindications: Personal/family history of MTC (medullary thyroid carcinoma) or MEN-2 (liraglutide, semaglutide, dulaglutide, exenatide ER)
  • HbA1c reduction: 0.8-1.6% (GLP-1); 2.0-2.3% (tirzepatide)
Rx PHARMACIST WATCHOUT: GLP-1 agonist brand confusion: Victoza (liraglutide) – max 1.8 mg (for T2D). Saxenda (liraglutide) – max 3 mg (for obesity). Different products, different max doses, different indications. Ozempic (semaglutide SQ) max 2 mg (T2D); Wegovy (semaglutide SQ) max 2.4 mg (obesity). Do NOT substitute between obesity and diabetes GLP-1 products.
CLINICAL PEARL: Oncology connection: Semaglutide is the first GLP-1 RA with proven kidney benefit (FLOW trial: 24% ↓ renal composite). In oncology patients with nephrotoxicity from chemotherapy who develop T2D and CKD, semaglutide + SGLT-2i offers a powerful renoprotective combination.

7E. DPP-4 Inhibitors (Gliptins) – Weight Neutral

AGENTSTANDARD DOSERENAL DOSE ADJUSTMENTNOTES
Sitagliptin (Januvia)100 mg QDeGFR 30-44: 50 mg QD eGFR <30: 25 mg QDBest safety data; no signal for HF hospitalization; once-daily; reports of acute pancreatitis, angioedema, SJS (rare)
Saxagliptin (Onglyza)5 mg QDeGFR ≤45: 2.5 mg QDAVOID in HF (SAVOR-TIMI: ↑ HF hospitalization). Reduce to 2.5 mg with strong CYP3A4/5 inhibitors (azoles, ritonavir)
Linagliptin (Tradjenta)5 mg QDNO RENAL DOSE ADJUSTMENT NEEDED (biliary excretion; only DPP-4i without renal adjustment)Safe in any level of renal impairment; also no hepatic dose adjustment; preferred in CKD
Alogliptin (Nesina)25 mg QDCrCl 30-59: 12.5 mg QD CrCl <30: 6.25 mg QDAVOID in HF (EXAMINE trial: signal for ↑ HF hospitalization). Hepatotoxicity risk (rare)
  • Class MOA: Inhibit DPP-4 enzyme → prevent breakdown of endogenous GLP-1 → ↑ insulin secretion (glucose-dependent), ↓ glucagon
  • Class ADEs: URTI, UTI, nasopharyngitis, severe joint pain (rare but class-wide), pancreatitis (rare), headache
  • HbA1c reduction: 0.5-0.8%; weight neutral
  • Drug interaction: Saxagliptin + strong CYP3A4/5 inhibitors (azoles, clarithromycin, ritonavir): Reduce saxagliptin to 2.5 mg
Rx PHARMACIST WATCHOUT: In oncology: Saxagliptin or alogliptin + azole antifungals (ketoconazole, voriconazole) = CYP3A4/5 inhibition → ↑ saxagliptin exposure → must reduce dose to 2.5 mg. Also avoid saxagliptin/alogliptin in patients with heart failure – significant concern in cancer patients on cardiotoxic chemo.

7F. Thiazolidinediones (TZDs / Glitazones)

  • Only available agent: Pioglitazone (Actos) – 15-45 mg QD; max 45 mg
  • MOA: PPAR-gamma agonist → ↑ expression of genes for glucose metabolism → improved insulin sensitivity
  • Key ADEs: BOXED WARNING for heart failure; weight gain; peripheral edema (worse with insulin); proximal bone fractures; possible bladder cancer (dose/duration-dependent; contradictory data); macular edema
  • Contraindicated: Class III/IV HF; hepatic impairment; existing fluid retention
  • Benefits: NASH/MASH benefit; improved HDL; possible CVA benefit; durable glycemic control; low hypoglycemia risk
  • Dosage titration: Slow onset – max effect of dose change may take 8-12 weeks
  • HbA1c reduction: 0.5-1.4%

7G. Renal Dosing Quick Reference Table

DRUG CLASS / AGENTeGFR 60+eGFR 45-59eGFR 30-44eGFR 15-29eGFR <15 / Dialysis
MetforminFull doseNo new Rx Reduce 50% if on itNo new Rx Reduce 50%CONTRAINDICATEDCONTRAINDICATED
Sulfonylureas (SU)Full doseFull dose (monitor)Glipizide preferred; reduce othersGlipizide only (caution)Avoid all SU
Sitagliptin (DPP-4i)100 mg QD50 mg QD50 mg QD25 mg QD25 mg QD
Saxagliptin (DPP-4i)5 mg QD2.5 mg QD2.5 mg QD2.5 mg QDNot recommended
Linagliptin (DPP-4i)5 mg QD5 mg QD5 mg QD5 mg QD5 mg QD (no adjustment)
Alogliptin (DPP-4i)25 mg QD12.5 mg QD12.5 mg QD6.25 mg QD6.25 mg QD
Canagliflozin (SGLT-2i)100-300 mg100-300 mg100 mg only (if albuminuria>300 for renoprotection)Do not initiate (continue 100 mg if albuminuria>300)Not recommended
Dapagliflozin (SGLT-2i)5-10 mg5-10 mg5-10 mg (HF/CKD indication)Do not initiate (continue 10 mg for HF/CKD)Not recommended
Empagliflozin (SGLT-2i)10-25 mg10-25 mg10-25 mg (HF/CKD indication)Do not initiate (continue 10 mg for HF/CKD)Not recommended
GLP-1 RA (most agents)Full doseFull doseFull doseNo adjustment (most) Exenatide: AVOIDExenatide: AVOID Others: Use with caution
InsulinFull dose (↑ risk hypo at lower eGFR)Reduce dose; ↑ hypoglycemia riskReduce dose further; monitor closelyReduce dose; frequent monitoringUse with caution; reduce dose
TZD (pioglitazone)Full doseFull doseFull doseFull doseUse with caution (limited data)
Exenatide (BID/ER)Full doseFull doseUse with cautionAVOIDAVOID (CrCl <30)

  8. MANAGEMENT OF DIABETES COMPLICATIONS 

8A. Hypoglycemia

LEVELGLUCOSECLINICAL CRITERIATREATMENT
Level 1<70 but ≥54 mg/dLGlucose alert value; with OR without symptoms15-20g oral glucose (glucose tablets, 4 oz juice, 4 oz regular soda, glucose gel); recheck in 15 min; repeat if still <70 mg/dL; eat meal/snack once normalized
Level 2<54 mg/dLClinically significant hypoglycemia; requires treatment regardless of symptoms15-20g oral glucose as above; consider cause; adjust regimen
Level 3Any glucoseSevere – altered mental/physical status; REQUIRES EXTERNAL ASSISTANCEGlucagon: 1 mg SQ or IM (GlucaGen/Glucagon Emergency Kit) OR 3 mg intranasal (Baqsimi) IV dextrose (D50W 25g IV push) if no glucagon available or no response Raise BG targets for several weeks after severe event
  • Hypoglycemia Unawareness: Patient has Level 2 BG without symptoms → lost counter-regulatory response
  • Management: Relax BG targets; modify regimen to ↓ hypoglycemia risk; use CGM with low glucose alarm
  • Consider: Switching from sulfonylurea to DPP-4i, GLP-1 RA, or SGLT-2i; reduce insulin doses
WARNING: Alpha-glucosidase inhibitor users (acarbose): If hypoglycemia occurs, treat with ORAL GLUCOSE (dextrose tablets), NOT sucrose (table sugar or fruit juice). Acarbose blocks sucrose/maltose absorption. Plain dextrose tablets or IV glucose is required. This is critical patient counseling.

8B. Diabetic Ketoacidosis (DKA)

SEVERITYBETA-HYDROXYBUTYRATEVENOUS pHBICARBONATEMENTAL STATUS
Mild3.0-4.0 mEq/L>7.25 but <7.3015-18 mEq/LAlert
Moderate4.0-5.0 mEq/L7.0-7.2510-14.9 mEq/LAlert to drowsy
Severe>5.0 mEq/L<7.0<10 mEq/LStupor / coma

DKA Treatment Protocol (ADA/JDRF Consensus 2024)

  • Step 1 – FLUIDS: 0.9% NaCl (or other crystalloid). Replace ~50% of estimated fluid deficit in first 6-12 hours. Once BG <250 mg/dL: add 5% or 10% dextrose to IV fluids.
  • Step 2 – INSULIN:
    • Mild DKA (SQ option): 0.1 unit/kg SQ bolus of rapid-acting insulin → then 0.1 units/kg/hr OR 0.2 units/kg q2hr until BG <250; then 0.1 units/kg q2hr
    • Moderate-Severe DKA (IV): Regular insulin infusion at 0.1 units/kg/hr
    • Once BG <250 mg/dL: Reduce infusion to 0.05 units/kg/hr; maintain BG ~200 mg/dL until ketosis resolved
    • TRANSITION to SQ: Once DKA resolved; overlap SQ insulin and IV infusion by 1-4 hours before stopping IV
  • Step 3 – POTASSIUM: Add 10-20 mEq/L KCl to each liter IVF if K+ ≤5 mEq/L. Use higher infusion rates for K+ <3.5 mEq/L
  • HOLD INSULIN INFUSION if K+ <3.5 mEq/L – repleting K+ first is critical to prevent fatal arrhythmias
  • Step 4 – RESOLUTION CRITERIA: BG <200 mg/dL AND ketones <0.6 mEq/L AND venous pH ≥7.3 AND bicarb ≥18 mEq/L
WARNING: DKA RESOLUTION ≠ NORMAL BLOOD GLUCOSE. The criteria for DKA resolution are: pH ≥7.3 + bicarb ≥18 + ketones <0.6 mEq/L. Glucose may normalize BEFORE acidosis resolves. Continue insulin infusion until ALL three criteria are met. Many practitioners stop insulin too early.
  • Most common DKA precipitants: Infection (most common), insulin omission/nonadherence, new diagnosis T1D, DKA on SGLT-2i, steroids, MI, pancreatitis, surgery, drugs (corticosteroids – HIGH RISK IN ONCOLOGY)
ONCOLOGY PEARL: SGLT-2i-induced euglycemic DKA is particularly relevant in oncology. Cancer patients on SGLT-2i who are fasting (NPO before procedure, reduced oral intake during chemo), on a low-carb diet, or receiving insulin dose reductions are at HIGH RISK. BG may be <200 but patient is acidotic. Check blood beta-hydroxybutyrate in any patient on SGLT-2i with unexplained GI symptoms or fatigue.

8C. Diabetic Nephropathy

  • Screening: Random spot urine albumin-to-creatinine ratio (ACR) + eGFR annually; at T2D diagnosis; after 5 years in T1D
  • Normal ACR: <30 mg/g
  • Albuminuria: ACR ≥30 mg/g (confirmed with 2 of 3 specimens over 3-6 months)
  • ADA no longer uses ‘microalbuminuria’ or ‘macroalbuminuria’ – report ACR value directly
ACR (mg/g)eGFR (mL/min)RECOMMENDED INTERVENTION
≥30AnyACEi OR ARB (first-line; do NOT combine)
≥200≥20ADD SGLT-2i (canagliflozin, dapagliflozin, or empagliflozin)
≥200≥25 (CKD criteria)Consider adding finerenone (nonsteroidal MRA) per ADA
AnyDecliningDietary protein restriction as eGFR declines
AnyAny with T2D CKDSemaglutide showed ↓ renal composite in FLOW trial (add if not already on GLP-1)
  • Target: ≥30% reduction in albuminuria with therapy
  • Finerenone (Kerendia): Nonsteroidal mineralocorticoid receptor antagonist; indicated for CKD associated with T2D (FIDELIO-DKD trial: ↓ renal progression and CV events)

8D. Diabetic Retinopathy

  • Screening: Annual dilated/comprehensive eye exam at T2D diagnosis; after 5 years in T1D
  • Frequency can be reduced to q2-3 years after consistently normal exams
  • Optimize glycemia, BP, and cholesterol to prevent progression
  • Severe retinopathy treatment: Intravitreous steroids or anti-VEGF agents (e.g., ranibizumab, aflibercept) ± laser photocoagulation
  • Semaglutide caution: SUSTAIN-6 showed ↑ retinopathy complications with semaglutide vs placebo. Monitor in patients with pre-existing retinopathy.

8E. Diabetic Neuropathies

  • Screening: After 5 years in T1D; at T2D diagnosis; then annually; evaluate distal polyneuropathy (10-g monofilament, vibration, pinprick, ankle reflexes)
  • Glycemic control is primary strategy to prevent/slow progression
  • Symptomatic pharmacotherapy does NOT slow disease progression – targets pain/symptoms only
AGENT CLASSDRUG(S)DOSE / NOTESFDA-APPROVED FOR DPN?KEY CONSIDERATIONS
SNRIDuloxetine (Cymbalta)60-120 mg QD Start 30-60 mgYES (only approved SNRI for DPN)Similar efficacy to amitriptyline; better tolerability; fewer anticholinergic effects. Useful in depression + DPN comorbidity.
AnticonvulsantPregabalin (Lyrica)75-300 mg BID Start low, titrateYES (only approved anticonvulsant for DPN)Schedule V; abuse potential; dizziness, fatigue, edema. Avoid abrupt discontinuation.
AnticonvulsantGabapentin (Neurontin)300-1200 mg TID Renal dose adjustmentNO (off-label)Similar efficacy to pregabalin; less expensive; dizziness/fatigue common; renal dose adjustment required
TCAAmitriptyline DesipramineStart 25 mg QHS ↑ to effectNO (off-label)Effective but significant anticholinergic ADEs (urinary retention, constipation, dry mouth, falls); use secondary amines (desipramine, nortriptyline) for fewer effects
OpioidTapentadol ER (Nucynta ER)50-250 mg Q12HYES (only approved opioid for DPN)No head-to-head efficacy data; abuse potential; use as last resort. Schedule II.
TopicalCapsaicin 8% patch Lidocaine 5% patch/creamApply to affected areaNO (off-label)For FOCAL pain only; not for diffuse pain. Capsaicin burns transiently.
CombinationTramadol/acetaminophen (Ultracet)Tramadol 37.5mg/APAP 325mgNO (off-label)Comparable to gabapentin; Schedule IV tramadol; risk of seizures/serotonin syndrome
CLINICAL PEARL: First-line for DPN pain: Duloxetine or pregabalin (both FDA-approved). Duloxetine preferred if patient also has depression. Pregabalin preferred if pain is more severe or sleep disruption is a major complaint. TCAs are effective but use with caution in elderly and oncology patients (anticholinergic burden).

Gastroparesis Management

APPROACHOPTIONSNOTES
DietarySmall frequent meals; low-fat, low-fiber; homogenized/liquid foodNon-pharmacologic first step
Pharmacologic – ProkineticMetoclopramide 10 mg PO QID or 15 mg intranasally before meals Erythromycin 40-250 mg TID before meals (up to 1 month only)Metoclopramide: Risk of tardive dyskinesia (boxed warning); limit duration; assess risk-benefit at each visit. Erythromycin: Short-term only (tachyphylaxis); drug interactions via CYP3A4.
DeviceGastric electrical stimulation (pacemaker)Specialist referral; for refractory gastroparesis

8F. Cardiovascular Disease (CVD)

  • Most common cause of mortality and morbidity in patients with diabetes.
MANAGEMENT AREARECOMMENDATIONAGENT(S)
Blood PressureTarget: <130/80 mmHgACEi or ARB (first-line if albuminuria); DHP-CCB or thiazide-like diuretic; avoid combining ACEi + ARB
LDL – Age 40-75, no CVDModerate-intensity statin; achieve ≥50% LDL ↓ if CV risk factors present; target LDL <70 mg/dLAtorvastatin 10-20 mg or rosuvastatin 5-10 mg (moderate); atorvastatin 40-80 mg or rosuvastatin 20-40 mg (high)
LDL – Established CVDHigh-intensity statin; ≥50% LDL ↓; target LDL <55 mg/dLAtorvastatin 40-80 mg; rosuvastatin 20-40 mg; ADD ezetimibe or PCSK9i if above goal
Antiplatelet – Secondary preventionASA 75-162 mg/day (established ASCVD)Clopidogrel 75 mg/day if ASA-intolerant
Antiplatelet – Primary preventionConsider if ↑ CV risk; individualize risk-benefitASA 75-162 mg/day
GLP-1 RA / SGLT-2i for CVDADD with proven CV benefit (not all agents in class)GLP-1: liraglutide, dulaglutide, semaglutide, exenatide ER; SGLT-2i: empagliflozin, canagliflozin, dapagliflozin
HF – Add-on diabetes therapySGLT-2i with proven HF benefitCanagliflozin, dapagliflozin, empagliflozin, ertugliflozin (all except bexagliflozin)

  9. INPATIENT DIABETES MANAGEMENT (Non-Critically Ill) 

PARAMETERRECOMMENDATION
Glycemic Goal140-180 mg/dL (all hospitalized patients, non-ICU)
Initiation ThresholdInitiate insulin therapy if BG ≥180 mg/dL
Monitoring FrequencyBefore meals (AC) if eating; every 4-6 hrs if NPO or on continuous tube feeds
Preferred TreatmentBasal-bolus insulin (basal + prandial + correction). Sliding-scale insulin ALONE is NOT recommended (per ADA – insufficient for control, inappropriate in most patients)
NPO / Restricted POBasal insulin with or without correction (ISF) doses only – no prandial bolus if not eating
ICU / Critically IllContinuous IV regular insulin infusion; target 140-180 mg/dL; monitor q1-2hr
Transition from IV to SQOverlap subcutaneous basal insulin 1-4 hours BEFORE stopping IV insulin infusion to prevent rebound hyperglycemia
Oral Antidiabetic AgentsGenerally held in hospitalized patients (metformin: contrast risk, renal changes; SGLT-2i: DKA risk; GLP-1 RA: GI/gastroparesis; hold most oral agents and manage with insulin)
Discharge PlanningDischarge on pre-admission regimen if hyperglycemia was incidental; adjust regimen if hospitalization revealed poor outpatient control; ensure patient/family education, follow-up appointment, and BG monitoring supplies
Rx PHARMACIST WATCHOUT: When converting from IV insulin infusion to SQ: OVERLAP IS MANDATORY – administer basal SQ insulin at least 1-4 hours BEFORE stopping the IV infusion. Failure to overlap leads to dangerous rebound hyperglycemia (and potentially DKA in T1D). Document this handoff clearly in the chart.
CLINICAL PEARL: In oncology inpatients: Hyperglycemia is common from steroids (dexamethasone in chemotherapy regimens), stress response, and TPN. Standard inpatient glycemic target is 140-180 mg/dL. For patients receiving dexamethasone QAM, consider NPH insulin in the morning to match the steroid peak – this is the most physiologic approach for steroid-induced hyperglycemia.

  10. KEY CLINICAL TRIALS IN DIABETES PHARMACOTHERAPY 

TRIALDRUGPOPULATIONINTERVENTION vs COMPARATORKEY RESULTSNOTES
UKPDSMetforminNewly diagnosed T2D, overweight (n=1704)Metformin vs conventional diet Rx36% ↓ all-cause mortality; 32% ↓ DM-related endpoints; no excess CVD mortality (unlike SU in UGDP)Foundational trial for metformin. Demonstrated CV benefit in overweight T2D. ‘Legacy effect’ on CV outcomes post-trial.
ACCORDIntensive glycemic controlT2D with CVD or CVD risk (n=10,251)HbA1c <6.5% vs standard (7-7.9%)Intensive group: ↑ all-cause mortality (22%); ↑ CV death; ↑ hypoglycemia. NO reduction in MACE.Intensive glycemic control (<6.5%) in high-CV-risk T2D is HARMFUL. Supported less stringent targets in certain populations.
EMPA-REG OUTCOMEEmpagliflozin 10 or 25 mgT2D + established CVD (n=7,020)Empagliflozin vs placebo14% ↓ MACE; 38% ↓ CV death; 35% ↓ HF hospitalization; 39% ↓ new/worsening nephropathyLandmark trial. Strongest CV death reduction in class. Rapid separation of curves suggests hemodynamic mechanism (not just glucose lowering).
CANVASCanagliflozin 100/300 mgT2D + CVD or high CV risk (n=10,142)Canagliflozin vs placebo14% ↓ MACE; 40% ↓ HF hospitalization; ↑ amputation risk (6.3 vs 3.4/1000 pt-yrs); ↑ fracturesAmputation and fracture signals are canagliflozin-specific. CREDENCE follow-up study showed renal benefit.
DECLARE- TIMI 58Dapagliflozin 10 mgT2D with or without CVD (n=17,160)Dapagliflozin vs placeboNo significant MACE reduction in total population; 27% ↓ HF hospitalization/CV death composite; ↓ renal progressionLargest SGLT-2i CV trial. Most participants had CV risk factors (not established CVD) – supports HF/renal indication broadly.
LEADERLiraglutide 1.8 mgT2D + high CV risk (n=9,340)Liraglutide vs placebo13% ↓ MACE; 22% ↓ CV death; 15% ↓ nephropathy; 4% ↓ death from any causeFirst GLP-1 RA CV outcomes trial. Driven by reduction in CV death. Liraglutide only GLP-1 with CV death reduction (vs non-fatal MACE in others).
SUSTAIN-6Semaglutide SQT2D + high CV risk (n=3,297)Semaglutide 0.5 or 1 mg vs placebo26% ↓ MACE (primarily driven by ↓ non-fatal stroke); ↑ retinopathy complications (semaglutide group)Key semaglutide safety trial. Retinopathy risk signal – monitor closely in patients with pre-existing retinopathy. Shorter trial (2 yrs); mainly safety data.
REWINDDulaglutide 1.5 mgT2D with or without CVD (n=9,901)Dulaglutide vs placebo12% ↓ MACE; ↓ non-fatal stroke; ↓ albuminuriaBroadest GLP-1 CV population (half without established CVD). Supports use for primary CV prevention in T2D.
SURPASS-2Tirzepatide 5/10/15 mgT2D on metforminTirzepatide vs semaglutide 1 mg weeklyTirzepatide 15 mg: 2.46% ↓ HbA1c vs 1.86% semaglutide; weight ↓ -11.2 kg vs -5.5 kg; superior on all glycemic endpointsHead-to-head; tirzepatide significantly superior to semaglutide 1 mg. GI ADEs similar. SURPASS-CVOT for CV outcomes pending.
CREDENCECanagliflozin 100 mgT2D + DKD (eGFR 30-90, ACR >300 mg/g) on max RAS blockadeCanagliflozin vs placebo30% ↓ primary composite (ESKD, SCr doubling, renal/CV death); 32% ↓ ESKD; 31% ↓ HF; trial stopped early for efficacyFirst SGLT-2i trial in DKD. Supported canagliflozin for renoprotection. Efficacy seen even in eGFR 30-45 subgroup.
DAPA-CKDDapagliflozin 10 mgCKD eGFR 25-75 + ACR ≥200 mg/g (T2D AND non-diabetic CKD)Dapagliflozin vs placebo39% ↓ primary composite (sustained ↓ eGFR, ESKD, renal/CV death); consistent in diabetic + non-diabetic CKD; 29% ↓ all-cause deathFirst evidence SGLT-2i benefit extends to non-diabetic CKD. Changed practice paradigm. Trial stopped early.
EMPA-KIDNEYEmpagliflozin 10 mgCKD eGFR 20-45 OR eGFR 45+ with ACR ≥200 mg/g (T2D and non-diabetic)Empagliflozin vs placebo28% ↓ primary composite (CKD progression/CV death); benefit seen in very low eGFR (20-30) subgroup; 24% ↓ hospitalizationIncluded lowest eGFR patients of any SGLT-2i CKD trial. Supports use of empagliflozin even in advanced CKD.
FLOWSemaglutide SQ 1 mgT2D + CKD (eGFR 50-75, ACR ≥300 mg/g) on max RAS blockadeSemaglutide vs placebo24% ↓ major kidney disease composite; 21% ↓ MACE; 20% ↓ all-cause deathFirst GLP-1 RA trial with proven renal endpoint benefit. Semaglutide now recommended for CKD in T2D in combination with SGLT-2i.
FIDELIO-DKDFinerenoneT2D + DKD (eGFR 25-60 + ACR ≥300 OR eGFR 25-90 + ACR ≥30)Finerenone vs placebo18% ↓ primary renal composite; 14% ↓ secondary CV composite; ↓ albuminuriaNonsteroidal MRA with both renal and CV benefit in T2D CKD. Added to ADA recommendations for nephropathy management.

  11. ONCOLOGY SPECIAL CONSIDERATIONS 

11A. Steroid-Induced Hyperglycemia (SIH)

  • Most common cause of drug-induced hyperglycemia in oncology patients.
  • Classic pattern: Predominantly POSTPRANDIAL hyperglycemia; effects peak 4-12 hrs after steroid dose
  • Dexamethasone QAM → BG peaks in the afternoon; near-normal fasting glucose
  • Monitoring: BG AC meals + bedtime while on steroids; initiate treatment if BG >180 mg/dL
SCENARIORECOMMENDED APPROACH
New-onset hyperglycemia on once-daily AM dexamethasoneNPH insulin 0.1-0.2 units/kg with AM dexamethasone dose (mirrors steroid pharmacokinetics) OR: Add bolus (rapid-acting) insulin at lunch and dinner OR: Increase existing oral antidiabetic agents (if T2D)
Existing T2D – worsening control on steroidsIncrease existing regimen; escalate to bolus insulin if needed; basal insulin less effective alone (postprandial pattern)
High-dose steroids (e.g., RCHOP dexamethasone, high-dose dex in MM)Scheduled rapid-acting insulin AC meals + correction; may need high doses; monitor q4-6hr
Steroid taper or completionTaper insulin proportionally with steroid taper; hold glucose-lowering therapy when steroids discontinued if glucose normalizes
Stress hyperglycemia (ICU oncology patient)IV insulin infusion; target 140-180 mg/dL; q1-2hr monitoring
ONCOLOGY PEARL: In multiple myeloma (MM) regimens with dexamethasone 40 mg weekly (VRd, DRd, RVd etc.), hyperglycemia is nearly universal. The pattern is predictable: peak hyperglycemia on dex days (day 1, 8, 15, 22 of cycle). Pre-emptive NPH insulin on dexamethasone days is a practical strategy; counsel patients on hypoglycemia risk on non-dex days.

11B. Immune Checkpoint Inhibitor (ICI) – Induced Diabetes

PARAMETERDETAILS
MechanismImmune-mediated destruction of pancreatic beta cells (similar to T1D autoimmune process); uncontrolled T-cell activation
Most common agentsAnti-PD-1 (nivolumab, pembrolizumab); anti-PD-L1 (atezolizumab, durvalumab); higher incidence with combination (anti-CTLA-4 + anti-PD-1)
Incidence~1-2% with anti-PD-1/PD-L1 monotherapy; up to 2-4% with combination ICI
PresentationOften FULMINANT: DKA-like presentation; abrupt onset; absolute insulin deficiency; may occur at any cycle
DiagnosisNew hyperglycemia + low/absent C-peptide + positive autoantibodies (GAD65) in some; exclude other causes
TreatmentINSULIN THERAPY (same as T1D management); full basal-bolus regimen; likely LIFELONG
ICI continuationICI generally NOT held for ICI-DM alone (unlike other irAEs); manage diabetes with insulin and continue ICI if clinically appropriate
SteroidsSTEROIDS DO NOT RESOLVE ICI-INDUCED DIABETES (unlike most other irAEs – thyroiditis, hepatitis, etc.). This is T1D-like destruction, not inflammation-based.
CounselingEducate patient and family on T1D self-management: insulin injection, SMBG/CGM, hypoglycemia recognition and treatment, sick-day rules, MedicAlert bracelet
WARNING: ICI-induced diabetes is PERMANENT and resembles T1D. Steroids are NOT effective. Patients require lifelong insulin therapy. DKA is common at presentation. Educate oncology team: unlike most immune-related adverse events (irAEs), immunosuppression (steroids) does not reverse this complication.

11C. Drug-Induced Hyperglycemia in Oncology – Summary Table

DRUG / CLASSMECHANISMGLYCEMIC PATTERNMANAGEMENTREVERSIBILITY
Glucocorticoids (dexamethasone, prednisone, methylprednisolone)↓ insulin sensitivity; ↑ hepatic gluconeogenesis; ↑ lipolysisPredominantly postprandial (once-daily AM dosing); all-day with BID/chronic dosingNPH + meal-time insulin; titrate with steroid dose; taper insulin with steroid taperReversible upon discontinuation
L-Asparaginase (pegaspargase, asparaginase Erwinia)↓ pancreatic insulin synthesis (pancreatotoxic); ↓ plasma insulinVaries; monitor during and after therapyInsulin if BG >180 mg/dL; may be transientUsually reversible; may persist
mTOR Inhibitors (everolimus, temsirolimus)↓ insulin receptor signaling; mTOR pathway inhibition → insulin resistance; ↓ beta-cell functionElevated fasting AND postprandial glucoseOptimize oral antidiabetics; often requires insulin; avoid pioglitazone (macular edema risk)Partially reversible; may persist
Calcineurin Inhibitors (tacrolimus, cyclosporine) [Post-SCT / transplant]↓ insulin secretion (direct beta-cell toxicity); insulin resistanceFasting hyperglycemia dominantInsulin; calcineurin inhibitor dose reduction if possible; PTDM (post-transplant DM) management guidelinesPartially reversible with dose reduction
Androgen Deprivation Therapy (ADT) (GnRH agonists/antagonists)Insulin resistance; ↑ adiposity; metabolic syndromeSlow onset; metabolic syndrome patternLifestyle modification; standard T2D agents; GLP-1 RA beneficial for weight; SGLT-2iPartially reversible with discontinuation
Immune Checkpoint Inhibitors (anti-PD-1/PD-L1)Immune beta-cell destruction (T1D-like)Acute onset; DKA common; absolute insulin deficiencyInsulin (full T1D regimen); LIFELONG; steroids ineffectivePERMANENT (not reversible)
Atypical Antipsychotics (olanzapine – antiemetic)Insulin resistance; weight gain; direct beta-cell effectsPostprandial and fastingAvoid olanzapine if alternative available; standard T2D therapy if persistentReversible with discontinuation
Interferon-alpha (pegylated IFN, historical)Autoimmune beta-cell destruction (may trigger T1D-like)Acute onset; may resemble T1DInsulin therapy; treat as T1D if autoantibodies positiveVariable; may be permanent

11D. Drug Interactions Relevant to Oncology Diabetes Management

INTERACTIONCLINICAL CONCERNRECOMMENDATION
Azole antifungals (fluconazole, voriconazole, itraconazole) + SulfonylureasCYP2C9 inhibition → ↑ sulfonylurea plasma levels → severe hypoglycemiaMonitor BG closely; consider dose reduction of SU or switch to non-SU agent during antifungal course
Azole antifungals + SaxagliptinCYP3A4/5 inhibition → ↑ saxagliptin exposureREDUCE saxagliptin to 2.5 mg QD when co-administered with strong CYP3A4/5 inhibitors
Fluoroquinolones (ciprofloxacin, levofloxacin) + Any antidiabetic↑ risk of BOTH hypoglycemia AND hyperglycemia (erratic BG response)Monitor BG frequently; counsel patient; consider alternative antibiotics if possible
Beta-blockers (propranolol – used in thyroid storm/tachycardia support) + Insulin/SUMasking of tachycardia (sympathoadrenergic hypoglycemia symptoms); may blunt counter-regulatory responseCounsel patients; monitor BG; prefer selective beta-1 blockers if needed
Repaglinide + GemfibrozilCYP2C8 and OATP1B1 inhibition → up to 8x ↑ repaglinide AUC → severe hypoglycemiaCONTRAINDICATED COMBINATION – avoid gemfibrozil in any patient on repaglinide
Metformin + Iodinated Contrast (IV)Risk of contrast-induced nephropathy → ↑ metformin accumulation → lactic acidosisHold metformin at time of contrast if eGFR 30-60; restart 48 hrs post with confirmed normal SCr
Octreotide (for carcinoid/NETs/acromegaly) + Insulin/SulfonylureaOctreotide inhibits insulin AND glucagon secretion; unpredictable glycemic effectsMonitor BG closely when initiating or changing octreotide; may need to reduce insulin/SU dose
Steroids + InsulinGlucocorticoids antagonize insulin action → ↑ insulin requirementsProactive dose escalation during steroid treatment; taper insulin proportionally with steroid taper

  12. CLINICAL PEARLS & PHARMACIST WATCHOUTS 

12A. Clinical Pearls – Stepwise Mastery

CLINICAL PEARL: 1. DIAGNOSIS: Two abnormal glycemic tests required (unless classic symptoms of hyperglycemia). Can be from same blood draw (e.g., FPG + HbA1c on same day). Updated ADA recommendation – no need to wait for a second separate day if two different test types are used.
CLINICAL PEARL: 2. HbA1c LIMITATIONS: Falsely LOW in hemolytic anemia, sickle cell disease, recent blood transfusion, erythropoietin use, ESRD, pregnancy. In these patients (common in hem/onc), use FPG or 2-hr OGTT for diagnosis and monitoring.
CLINICAL PEARL: 3. GLYCEMIC TARGETS: Less stringent HbA1c targets (<8%) are appropriate in: limited life expectancy, advanced complications, terminal cancer, frail elderly with history of falls/hypoglycemia, extensive comorbidities.
CLINICAL PEARL: 4. TIME IN RANGE (TIR): ≥70% of CGM readings in 70-180 mg/dL is the glycemic quality metric. TIR is increasingly used in T1D management and correlates with microvascular outcomes.
CLINICAL PEARL: 5. METFORMIN HOLD RULE: Never hold for IV contrast if eGFR ≥60. Always hold if eGFR 30-60 at time of contrast. Restart 48 hrs post with normal creatinine. Communicate proactively with ordering team.
CLINICAL PEARL: 6. T1D BASAL-BOLUS BASICS: Basal covers fasting/overnight glucose. Bolus covers meal-related glucose. If fasting glucose is high → adjust basal. If pre-dinner glucose is high but fasting is fine → adjust morning bolus. If bedtime glucose is high → adjust dinner bolus.
CLINICAL PEARL: 7. 1800 RULE (ISF): 1800 ÷ TDI = how many mg/dL 1 unit of rapid-acting insulin drops BG. Document this in every insulin patient’s chart. It is YOUR tool for safe correction dosing.
CLINICAL PEARL: 8. SGLT-2i EUGLYCEMIC DKA: BG can be normal/near-normal. Classic DKA symptoms (N/V, abdominal pain, dyspnea) with BG <200 + ketonemia + acidosis. High-risk: fasting, perioperative, low-carb diet, reduced insulin, illness. Check ketones in any SGLT-2i patient with unexplained illness.
CLINICAL PEARL: 9. SGLT-2i CARDIO/RENAL SELECTION: Choose agent based on indication: ASCVD → empagliflozin (strongest CV death data) OR canagliflozin/dapagliflozin. HF → any (except bexagliflozin). CKD → canagliflozin, dapagliflozin, or empagliflozin (CREDENCE, DAPA-CKD, EMPA-KIDNEY). Bexagliflozin has NO proven secondary benefit.
CLINICAL PEARL: 10. GLP-1 RA vs INSULIN as first injectable in T2D: ADA PREFERS GLP-1 RA over insulin when adding injectables (better HbA1c, less hypoglycemia, weight loss). Use insulin if: extreme/symptomatic hyperglycemia, HbA1c >10%, or HbA1c >2% above goal.
CLINICAL PEARL: 11. LINAGLIPTIN advantage: Only DPP-4 inhibitor without renal or hepatic dose adjustment (biliary excretion). Go-to DPP-4i in advanced CKD when glycemic control is needed.
CLINICAL PEARL: 12. SAXAGLIPTIN/ALOGLIPTIN IN HF: Avoid – both showed ↑ HF hospitalization in outcome trials (SAVOR-TIMI, EXAMINE). In heart failure patients with diabetes, use SGLT-2i instead.
CLINICAL PEARL: 13. DKA RESOLUTION: NOT defined by normalizing blood glucose. Resolution = pH ≥7.3 + bicarb ≥18 mEq/L + beta-hydroxybutyrate <0.6 mEq/L. Glucose normalizes before acidosis resolves. Keep insulin running until all three criteria are met.
CLINICAL PEARL: 14. POTASSIUM IN DKA: If K+ <3.5 mEq/L, HOLD insulin infusion. Insulin drives K+ into cells → worsening hypokalemia → fatal arrhythmia. Replace K+ first. Continue monitoring K+ q2-4hr during DKA treatment.
CLINICAL PEARL: 15. NEPHROPATHY: ACEi OR ARB (not both) if ACR ≥30 mg/g. Add SGLT-2i if eGFR ≥20 + ACR ≥200. Add finerenone for additional reno-CV protection. Semaglutide (FLOW) offers additional kidney benefit. ADA has moved away from ‘micro-‘ and ‘macroalbuminuria’ – use ACR value only.
CLINICAL PEARL: 16. PREGABALIN vs DULOXETINE for DPN: Both FDA-approved. Duloxetine preferred if comorbid depression. Pregabalin preferred for severe pain/sleep disruption. TCAs are effective but burdensome (anticholinergic, falls, arrhythmia – be careful in elderly oncology patients).
CLINICAL PEARL: 17. GLYBURIDE IN ELDERLY/CKD: AVOID. Active renally-excreted metabolites → prolonged hypoglycemia. Glipizide is preferred (hepatically eliminated). Know the difference when reviewing medication lists.
CLINICAL PEARL: 18. STEROID-INDUCED DM (Oncology): Pattern matters. Once-daily AM dexamethasone → postprandial peak. NPH in the morning mirrors this pattern best. If BG peaks are all-day (high-dose/BID steroids), basal-bolus insulin is needed. Taper insulin with steroid taper to prevent hypoglycemia.
CLINICAL PEARL: 19. ICI DIABETES: PERMANENT insulin dependence. Steroids don’t help. Educate patient as if newly diagnosed T1D. DKA is common at presentation. ICIs are generally continued despite DM (severity-dependent). Check fasting BG at every ICI cycle.
CLINICAL PEARL: 20. PRAMLINTIDE: MUST reduce preprandial insulin by 50% at initiation. Boxed warning for severe hypoglycemia. Use prefilled pen – NOT vial/syringe. Cannot be mixed with insulin. Flag every new pramlintide order for insulin dose adjustment.

12B. Pharmacist Watchouts – Rounds, Tumor Board, Chemo Review, Counseling

Rx PHARMACIST WATCHOUT: 1. HIGH-ALERT INSULIN CONCENTRATIONS: U-300 glargine (Toujeo) and U-100 glargine (Lantus/Basaglar) are NOT interchangeable on a unit-per-volume basis – they are interchangeable on a unit-per-unit basis (same units, different volume). U-500 regular insulin has intermediate-acting properties (NOT a rapid-acting replacement). Verify product, brand, and concentration at EVERY insulin order review. Use ‘tall man’ lettering and independent double checks.
Rx PHARMACIST WATCHOUT: 2. SGLT-2i PRE-PROCEDURE PROTOCOL: Canagliflozin, dapagliflozin, empagliflozin → hold 3 DAYS before surgery/procedure. Ertugliflozin → hold 4 DAYS. Bexagliflozin → hold when eGFR drops <30. This is FREQUENTLY MISSED in cancer patients undergoing procedures. Proactively flag and communicate with surgical/procedural teams. Include in pre-procedure medication reconciliation.
Rx PHARMACIST WATCHOUT: 3. SULFONYLUREA + AZOLE ANTIFUNGALS: Fluconazole, voriconazole, posaconazole (azoles commonly used for antifungal prophylaxis in neutropenic patients) inhibit CYP2C9 → ↑ SU levels → hypoglycemia. Consider switching to a DPP-4i or GLP-1 RA, or reduce SU dose and increase BG monitoring frequency when antifungals are started.
Rx PHARMACIST WATCHOUT: 4. METFORMIN IN ONCOLOGY: (a) Hold before CT contrast if eGFR 30-60; restart 48 hrs later with confirmed normal SCr. (b) Temporarily hold during significant illness, hypotension, or dehydration (common in chemo patients). (c) Hold perioperatively. (d) Monitor B12 annually – deficiency is common and may be confused with chemotherapy neuropathy.
Rx PHARMACIST WATCHOUT: 5. DKA POTASSIUM MANAGEMENT: Monitor K+ every 2-4 hours during insulin infusion. NEVER run insulin drip if K+ <3.5 mEq/L without first replacing potassium. Clarify potassium replacement orders with the medical team at every DKA order review.
Rx PHARMACIST WATCHOUT: 6. GLP-1 RA PATIENT COUNSELING – INJECTION TECHNIQUE: Rotate injection sites (abdomen, thigh, upper arm). Oral semaglutide (Rybelsus): MUST be taken on completely empty stomach with ≤4 oz of plain water; 30 minutes must elapse before ANY food, drink (other than water), or other oral medications. Most patients and nurses are unaware of this requirement.
Rx PHARMACIST WATCHOUT: 7. INPATIENT SLIDING SCALE ALONE: Per ADA, sliding-scale insulin alone (reactive-only dosing) is NOT recommended as the sole inpatient regimen. Alert providers who order sliding-scale only; recommend scheduled basal + prandial + correction insulin. Document your recommendation.
Rx PHARMACIST WATCHOUT: 8. PRAMLINTIDE INSULIN DOSE REDUCTION: When pramlintide is newly started (inpatient or outpatient), ALL preprandial insulin doses must be reduced by 50% immediately. If this is not done, severe hypoglycemia (often severe enough to require glucagon) is likely within hours of the first dose. Review every new pramlintide order for this mandatory adjustment.
Rx PHARMACIST WATCHOUT: 9. HYPOGLYCEMIA TREATMENT WITH ACARBOSE: If a patient is on acarbose or miglitol and develops hypoglycemia, they MUST be treated with ORAL DEXTROSE (glucose tablets), NOT sucrose (juice, candy, table sugar). The alpha-glucosidase inhibitor blocks sucrose absorption. Document and educate nursing staff.
Rx PHARMACIST WATCHOUT: 10. THIAZOLIDINEDIONES (TZD) + INSULIN: Combining pioglitazone with insulin increases risk of fluid retention/edema (and HF exacerbation). When adding insulin to a regimen containing a TZD (or vice versa), reduce or discontinue the TZD. Also: TZD dose titration takes 8-12 weeks for full effect – do not escalate quickly.
Rx PHARMACIST WATCHOUT: 11. ICI-DIABETES COUNSELING: Permanent insulin dependence (T1D-like management). Educate on: how to inject insulin, SMBG or CGM use, hypoglycemia recognition and treatment (glucagon kit), sick-day rules, medical ID bracelet, endocrinology follow-up. Oncology team must be informed this irAE is not steroid-managed.
Rx PHARMACIST WATCHOUT: 12. TACROLIMUS/SIROLIMUS POST-TRANSPLANT (Post-SCT): Post-transplant diabetes mellitus (PTDM) affects 10-40% of patients. Tacrolimus is more diabetogenic than cyclosporine. Calcineurin inhibitor-induced hyperglycemia is insulin-deficient (similar to T2D but may need insulin sooner). Monitor BG closely in first 6-12 months post-SCT. Work with transplant/SCT team on dose optimization.
Rx PHARMACIST WATCHOUT: 13. REPAGLINIDE + GEMFIBROZIL: ABSOLUTE CONTRAINDICATION. Gemfibrozil inhibits both CYP2C8 and OATP1B1 → 8x increase in repaglinide AUC → severe hypoglycemia. Screen for this interaction on every patient on repaglinide. If gemfibrozil is essential, substitute a different secretagogue.
Rx PHARMACIST WATCHOUT: 14. BEXAGLIFLOZIN: Newest SGLT-2i. NO proven CV, HF, or renal outcome benefit yet (as of 2024-2025). When choosing an SGLT-2i for a secondary indication (ASCVD, HF, CKD), always choose an agent with outcome trial data (canagliflozin, dapagliflozin, or empagliflozin). Bexagliflozin is appropriate only for glucose lowering at this time.
Rx PHARMACIST WATCHOUT: 15. FLUOROQUINOLONE + ANTIDIABETICS: Fluoroquinolones (ciprofloxacin, levofloxacin) cause both hypoglycemia AND hyperglycemia, erratically. In cancer patients commonly receiving fluoroquinolones for infections, monitor BG more closely while on antibiotic therapy. No dose adjustment – clinical monitoring only.
Rx PHARMACIST WATCHOUT: 16. INTRAVENOUS-TO-SUBCUTANEOUS INSULIN TRANSITION: Overlap basal SQ insulin 1-4 hours BEFORE stopping IV insulin infusion. Failure to overlap causes rebound hyperglycemia (or DKA in T1D). Document this transition clearly in the chart and verify with nursing that the overlap timing is understood.
Rx PHARMACIST WATCHOUT: 17. SEMAGLUTIDE RETINOPATHY RISK: SUSTAIN-6 identified increased retinopathy complications with semaglutide. In patients with pre-existing diabetic retinopathy, monitor closely. Rapid improvement in HbA1c with any potent agent can transiently worsen retinopathy (early worsening phenomenon).
Rx PHARMACIST WATCHOUT: 18. INSULIN IN CKD/RENAL FAILURE: Insulin clearance decreases as renal function declines → prolonged insulin action → increased hypoglycemia risk. No formal renal dose adjustment tables exist, but lower doses and more frequent monitoring are required. Consider using shorter-acting insulins more carefully in advanced CKD.

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ADA Standards of Care 2024/2025 | ACCP Updates in Therapeutics 2025 | Hem/Onc Pharmacotherapy Specialist Edition