Diabetes Mellitus Type 2: Drug Therapy

Therapeutic goal and treatment recommendations

  • Individualized HbA1c target corridor of 6.5-7.5% (48-58 mmol/mol).
  • HbA1c target value close to 6.5%, only if this can be achieved by lifestyle changes and/or metformin! (DEGAM)
    • Individual target should be in the lower range of the HbA1c target corridor or even below if necessary:
      • Short duration of diabetes; moderately elevated HbA1c levels to date; no cardiovascular damage; and/or
      • Target achievable without side effects (hypoglycemia/ hypoglycemia, weight gain).
    • Individual target should be rather in the upper range of the HbA1c target corridor or even above if necessary:
      • Long-standing poorly controlled diabetes and / or
      • Pre-existing cardiovascular damage/pre-existing conditions and difficult adjustability (with increased risk of hypoglycemia/low blood sugar) or
      • Comorbidities (concomitant diseases), life expectancy, or concomitant circumstances that do not justify the effort and risk compared with the benefit of achieving a low HbA1c target
    • American College of Physicians (ACP): an HbA1c target of 7-8% should be aimed for in most patients.
  • Lower fasting glucose (fasting blood glucose) serum levels between 100-125 mg/dl (5.6-6.9 mmol/L).
  • Lowering postprandial (“after a meal”) serum glucose level 180 mg/dl (10.0 mmol/L) (2h pp)
  • Therapy of existing hyperlipoproteinemia and dyslipoproteinemia (dyslipidemia):
    • Total cholesterol < 180 mg/dl (< 4.7 mmol(L) [see below Hypercholesterolemia/drug therapy: lipid target values and lipid-lowering therapy in patients with diabetes mellitus].
    • LDL < 100 mg/dl (< 2.6 mmol/L); in CHD < 70 mg/dl (< 1.8 mmol/L).
    • HDL
      • Men: > 40 mg/dl (> 1.1 mmol/L)
      • Women: > 50 mg/dl (> 1.3 mmol/L)
    • Triglycerides < 150 mg/dl (< 1.7 mmol/L)
  • Therapy of hypertension according to ESH/ESC guideline (European Society of Hypertension (ESH)/European Society of Cardiology (ESC); Barcelona, 2018):
    • Blood pressure of ≤ 140/90 mmHg; systolic blood pressure in relation to age:
      • Age 18-65: 130-120 mmHg
      • Age > 65-79: 140-120 mmHg
      • Age ≥ 80: 140-130 mmHg
    • Diastolic blood pressure: primary therapeutic goal of < 90 mmHg; regardless of age and concomitant morbidity, aim for a blood pressure target range of 80-70 mmHg.
    • Blood pressure limit: 120/70 mmHg
  • If necessary, therapy of hyperuricemia (increase in uric acid levels in the blood; gout).
  • Ggf therapy of hyperkalemia (excess potassium).
  • Weight reduction to normal weight – Sustained weight loss reduces insulin resistance, which reduces the need for antidiabetic drugs, including insulin.
  • Increase physical activity (about 150 min / week).
  • Nicotine renunciation
  • See also under “Further therapy”.

* * * An analysis of the Swedish Diabetes Registry of 187,106 type 2 diabetic patients challenges current recommendations: blood pressure of 110 to 119 mmHg was less likely to result in nonfatal acute myocardial infarction (-24%), less likely to result in myocardial infarction (-15%), less likely to result in nonfatal cardiovascular disease (-18%), and less likely to result in any cardiovascular disease (-18%) and less likely to result in nonfatal coronary artery disease (-12%). However, a J-curve was seen for the end points of myocardial infarction and all-cause mortality: patients were 20% more likely to develop heart failure and had a 28% increased risk of mortality at blood pressure levels of 110 to 119 mmHg. Notice.

  • Drug-naïve patients at high to very high cardiovascular risk should be treated with an SGLT2 inhibitor or a GLP-1 receptor antagonist (liraglutide, semaglutide, dulaglutide) regardless of HbA1c level.
  • Treatment-induced neuropathy (peripheral nervous system disorders) develops in diabetic patients as a result of treatment for diabetes (Engl.”Treatment-induced neuropathy in diabetes”, TIND), with acute onset neuropathy or symptoms of autonomic nervous system damage, if HbA1c was rapidly reduced above 2 percent within 3 months (62% vs. 4.3%, when HbA1c had decreased less than 2 percent within 3 months). The faster and the greater the reduction in HbA1c, the greater the risk of diabetic retinopathy (retinal disease) and microalbuminuria (warning signs of kidney disease).
  • Patients with MODY diabetes usually do not require insulin, but are treated with dietary measures and antidiabetic drugs (sulfonylureas).
  • Patients with latent autoimmune diabetes in adulthood (LADA) are treated largely like patients with type 2 diabetes mellitus, but usually need insulin earlier than type 2 diabetics without antibodies.
  • Short-term intensive insulin therapy (SIIT) can restore beta-cell function by reducing glucose toxicity in patients with newly diagnosed type 2 diabetes and thus also restore insulin sensitivity. Insulin therapy was administered for 14 days with either insulin lispro or insulin aspart via an insulin pump. The goal of SIIT was a fasting glucose (fasting blood glucose) < 6.0 mmol/L (108 mg/dl) and a 2-hour value < 8 mmol/L (144 mg/dl): after one year, 56 patients (58.9%) had a normal metabolic situation.In patients with type 2 diabetes, if the HbA1c value is high, the practice recommendations of the German Diabetes Society give a recommendation for initial insulin therapy .
  • National Care Guideline Type 2 Diabetes (Status: 2020): type 2 diabetics with existing clinically relevant atherosclerosis should (at HbA1c > 7) already be treated primarily with a combination of metformin and either a GLP-1 receptor agonist or a SGLT2 blocker.

Therapy recommendations according to stepwise plan

Start therapy with stage 1. If the target HbA1c has not been reached after three to six months, the measures of the next stage are implemented.

Stage Measures
1 Training, nutritional counseling, exercise
2 Metformin [CI if creatinine clearance: < 30 mL/min; or intolerance] If metformin CI:

  • DPP-4 inhibitor
  • Insulin (often long-acting insulin)
  • SGLT-2 inhibitor
  • Sulfonylurea/Glinides
  • Glucosidase inhibitors
  • Pioglitazone
3 Combination of metformin and insulin/glibenclamide/DPP-4 inhibitor; GLP-1 receptor agonist, SGLT-2 inhibitor, pioglitazone, if appropriate.
4 Intensification of insulin therapyIn obesity + metformin.

Procedure Notes:

  • Procedure, the stages described below, depends on the individual HbA1c target and non-achievement of the target after 3 to 6 months.
  • Monotherapy: if the HBa1c value exceeds the target corridor → dual combination with another antidiabetic drug (according to DDG/DGIM):
    • DPP-4 inhibitor
    • GLP-1 receptor agonist
    • Glucosidase inhibitor
    • Insulin (often long-acting insulin)
    • Gliflozines (SGLT-2 inhibitors; SGLT-2 blockers)Note: The lower the renal function, the lower the effect of SGLT-2 inhibitors.
    • Sulfonylurea/Glinide [the combination of metformin and sulfonlyureas (glibenclamide) may potentially increase cardiovascular mortality]
    • Pioglitazone
  • Dual combination: if the HBa1c value exceeds the target corridor → triple combination or insulin therapy* with a maximum of one antidiabetic drug (according to DDG/DGIM): intensive insulin and combination therapy (according to DDG/DGIM):In addition to oral antidiabetic drugs (especially metformin; possibly DPP-4 inhibitor, SGLT-2 inhibitor):
    • Delayed-release insulin or
    • Long-acting insulin + GLP-1 receptor agonist or
    • Preprandial short-acting insulin (SIT) or
    • Conventional insulin therapy (CT) or
    • Intensified insulin therapy (ICT, CSII)

* Insulin is rarely used as first-line therapy. In such cases, the following is usually present: advanced age, HbA1c ≥ 10%, neurological and renal vascular complications, multimorbidity multiple disease) and polypharmacy (> 6 prescribed drugs).

“Management of hyperglycemia in type 2 diabetes” according to the ADA* and EASD* * consensus guideline [see Guidelines: 4 below]

Measures
Training, nutritional counseling, exercise
  • Metformin [(first-line agent)
  • Escalation of treatment if the patient also has atherosclerotic cardiovascular disease (ASCVD), chronic kidney disease, and/or heart failure.

Notice:

  • If a patient with ASCVD or renal disease is already achieving their HbA1c goal without GLP-1 agonists or SGLT2 inhibitors, a switch to one of these agents should be made if multiple therapies are used.
  • In the case of monotherapy, the individual HbA1c target should be questioned and possibly lowered additionally or it should be reviewed every three months. In both cases, one of the above antidiabetic drugs would then be added if necessary
  • For patients without the three mentioned sequelae, it is recommended according to the present preferences.

Note: If injection therapy is being considered, a GLP-1 agonist is preferentially recommended

* American Diabetes Association (ADA) * * European Association for the Study of Diabetes (EASD).

Antidiabetic drugs and age

The following antidiabetic agents can be used in the elderly:

  • Metformin (first-line therapy)
  • DPP4 inhibitors; advantages: Advantages in treatment adherence, risk of hypoglycemia, body weight, and higher-grade renal insufficiency.
  • GLP-1 analogs (GLP-1 receptor agonist); advantages: low risk of hypoglycemia, weight loss; liraglutide: reduced cardiovascular morbidity and mortality.
  • Gliflozines (SGLT-2 inhibitors; SGLT-2 blockers).

Further notes

  • In type 2 diabetic patients with additional chronic kidney disease, impaired liver function, or heart failure, therapy with metformin is associated with reduced all-cause mortality (22% lower mortality risk compared with those patients not taking metformin).

Agents (main indication)

  • Biguanides: metformin [first-line therapy!]
  • Note: Switching to a sulfonylurea is associated with an increased risk of cardiovascular disease (myocardial infarction (13.2 versus 5.0 per 1,000 person-years), apoplexy) for patients with type 2 diabetes who do not achieve adequate glycemic control on metformin therapy; less risky than sulfonylurea treatment alone is combining the sulfonylurea with metformin.
  • Sulfonylureas; target groups: Combination partner for metformin or in contraindications (contraindications) or intolerance of metformin.
    • Hypoglycemia when taking sulfonylureas and antibiotics (ciprofloxacin, clarithromycin, levofloxacin, trimethoprim/sulfamethazole).
    • Caveat. The risk of cardiovascular disease (especially myocardial infarction (heart attack) and apoplexy (stroke)) is 21 percent higher during therapy with sulfonylureas than during metformin therapy!
    • A meta-analysis of 20 cohort and observational studies involving several 100,000 patients showed a doubling of all-cause mortality (total mortality) in patients taking sulfonylureas.
    • There is no relevant difference in cardiovascular safety between linagliptin (DPP4 inhibitor) and the sulfonylurea glimepiride: the primary combined study endpoint (cardiovascular death, nonfatal myocardial infarction, or stroke) occurred almost equally frequently in both groups (linagliptin n = 356, glimepiride n = 363), corresponding to a hazard ratio of 0.98 (95.47% CI 0.84-1.14).

    Note: “Sulfonylureas and overly strict glycemic control should be avoided in elderly, frail type 2 diabetics with rheumatoid arthritis because of the high risk of hypoglycemia.”

  • Glinides; Target groups: Glinides (sulfonamide urea analogues) have advantages over sulfonylureas in irregular or unreliable food intake and renal insufficiency; furthermore, higher flexibility than sulfonylureas due tothe faster onset of action and shorter duration of action.
  • Gliflozine (SGLT-2 inhibitors; SGLT-2 blockers) Target groups: with metformin not sufficiently adjusted hypoglycemia (hypoglycemia)-prone patient with weight problems.
  • Glitazones (thiazolidinediones); target groups: higher-grade renal insufficiency (kidney weakness) or combination partners in particularly hypoglycemia-prone patients.
  • Alpha-glucosidase inhibitors; target groups: early adjusted type 2 diabetes or combination partners.
  • Incretin mimetics (GLP-1 receptor agonists); target groups: hypoglycemia-prone patient with weight problems who is not adequately controlled with metformin
    • The LEADER trial of 9,340 high-risk patients with type 2 diabetes showed that liraglutide therapy reduced the incidence rate for the combined events of cardiovascular death, nonfatal myocardial infarction (heart attack), and nonfatal apoplexy (stroke) from 14.9 (placebo) to 13 percent over the median study period of 3.8 years. Crucial to this was the significant decrease in cardiovascular mortality (mortality) from 6 (placebo) to 4.7 percent (relative risk reduction: 22 percent).
    • In an authoritative endpoint study, liraglutide delayed the onset of permanent macroproteinemia (>300 mg albumin/d).
    • A “real-world” data analysis in obese diabetic patients showed that liraglutide lowered blood glucose and body weight more than basal insulin. After 12 months, body weight had decreased by 6.0 kg in the liraglutide group compared with 1.6 kg in the insulin group.
    • Of three newer antidiabetic drugs GLP-1 agonists, DPP-4 inhibitors, and SGLT-2 inhibitors, SGLT-2 inhibitors reduced mortality risk (risk of death) by 12%, ranking second.
    • The oral formulation of the GLP-1 agonist semaglutide nearly halved the mortality rate and the rate of cardiovascular death in type II diabetic patients at high cardiovascular risk. For the primary combined study endpoint – cardiovascular (heart-related) death, myocardial infarction (heart attack), apoplexy (stroke) – only a non-significant risk reduction of 21 percent was achieved.
  • Dipeptidyl peptidase 4 inhibitors (DPP-4 inhibitors; DPP-4 inhibitors; gliptins); target groups: hypoglycemia-prone patient with weight problems not adequately controlled with metforminGliptins (DPP4 inhibitors) have an insulinotropic effect, but they exert this effect only when blood glucose is elevated, so that severe hypoglycemia is almost completely avoided as a result.
    • DPP-4 inhibitors can potentially cause severe joint pain
    • Alogliptin: FDA warns of heart failure risk (risk of heart failure); alogliptin is safe even in acute coronary syndrome
    • Caveat: combination therapy of DPP-4 inhibitors and sulfonylureas leads to a 52% increased risk of hypoglycemia
    • EMA warns of possible toe amputations after taking the SGLT2 inhibitor canangliflozin.The U.S. Food and Drug Administration (FDA) concludes in a new assessment of the antidiabetic drug that the risk of amputation during treatment with canagliflozin is not as high as previously thought after all.
  • Gliflozine (SGLT-2 inhibitors; SGLT-2 blockers); target population: hypoglycemic (hypoglycemia)-prone patient with weight problems not adequately controlled with metformin.
    • Sitagliptin plus metformin: Evidence of partly unquantifiable, partly substantial additional benefit compared with sulfonylureas (IQWiG, 2016).
    • Dapagliflozin: In chronic heart failure (heart failure), hospital admissions for worsening heart failure and cardiovascular mortality (heart- and vascular-related mortality rates) were significantly reduced according to the DAPA-HF study; the same applies to patients without diabetes mellitus.
    • Patients with chronic renal insufficiency benefit significantly from dapagliflozin.
    • With dapagliflozin, bladder carcinoma occurred in 0.16% of patients compared with 0.03% in controls. Mammary carcinoma (breast cancer) was diagnosed in 0.4% of dapagliflozin patients compared with 0.22% in controls.
    • U.S. Food and Drug Administration warns of possible occurrence of severe ketoacidosis (severe metabolic derailment) during therapy with SGLT2 inhibitors such as canagliflozin, dapagliflozin, and empagliflozin
    • AkdÄ Drug Safety Mail | 07-2017|: Information of the BfArM on SGLT-2 inhibitors: possibly increased risk of lower limb amputations.
    • FDA warns of Fournier’s gangrene (necrotizing fasciitis (lat. Fasciitis necroticans) of the perineum; bacterially triggered, very violent (foudroyant) infectious disease of the subcutis and fascia) due to SGLT2 inhibitors.
    • Empagliflozin reduced cardiovascular mortality (cardiovascular)-related mortality) in high-risk patients with type 2 diabetes in one study: cardiovascular-related death, myocardial infarction (heart attack), and apoplexy/stroke (primary composite endpoint) were significantly reduced by additive treatment with empagliflozin, ie. i.e., by 14% compared to placebo (10.5 versus 12.1%)Furthermore, empagliflozin also reduced heart failure (heart failure) risk in diabetic patients with cardiovascular disease, and this was independent of whether heart failure was already present.
    • For people with type 2 diabetes and previous cardiovascular disease, the GBA (Federal Joint Committee) certifies a considerable additional benefit for empagliflozin. The basis is the EMPA-REG OUT-COME study.
    • Of three newer antidiabetic drugs GLP-1 agonists, DPP-4 inhibitors and SGLT-2 inhibitors reduce the risk of mortality by 20% and are thus in first place.
    • Empagliflozin and canagliflozin have nephroprotective effects.

Renal function-dependent* and -independent antidiabetic agents

Group Renal function dependent Renal function independent
Antidiabetic Gliquidone* Gliclacid* Glibenclamide* Glimepride* (hydroxymetabolite) Sitagliptin Metformin* * Repaglinide Rosiglitazone Nateglinide* * * pioglitazone saxagliptin* * * *

* Sulfonylureas are contraindicated from CKD stages 4 to 5* * Creatinine clearance < 60 mL/min; in the presence of stage I to II renal insufficiency after CKD, monitoring of retention parameters (min. two – to four times a year) is required during metformin therapy! * * * Dose adjustment in CKD stages 4 to 5* * * * Saxagliptin can be used up to CKD stage 5In patients with renal insufficiency, insulin therapy must often be used.

Adjuvant therapy

  • Dehydroepiandrosterone (DHEA) – to prevent oxidative stress and the formation of “advanced glycation endproducts” (AGEs). AGEs are advanced glycation endproducts; these are the result of a non-enzymatic reaction of carbohydrates with proteins.The intake of 50 mg DHEA resulted in decreased oxidative stress (measured were decreased levels of reactive oxidative species (ROS), increased levels of glutathione and vitamin E; serum pentosidine levels were decreased by half, indicating a reduction in AGEs. These results present in the aggregate, compared to the placebo group). This indicates that the cellular damage induced by hyperglycemia may be reduced by DHEAS therapy.
  • Andropause therapy – in the context of diabetes therapy in men – is an important supportive measure.Testosterone is an important modulator of insulin sensitivity: testosterone increases insulin sensitivity!Testosterone substitution, by men with decreased testosterone serum levels and type 2 diabetes mellitus, leads to:Decrease in fasting insulin serum levels.
    • Decrease in serum glucose level.
    • Decrease in HbA1c
    • Insulin therapy

Initiation of insulin therapy in type 2 patients:

  • In the advanced stage of the disease
  • Inadequate metabolic control under oral antidiabetic drugs.
  • Acute metabolic derailments (see below).

Primarily, a combination of basal insulin and metformin is considered.Note the following study result: In terms of person-years, all-cause mortality rates were increased three- to fivefold in the insulin-sulfonylurea combination compared with the insulin-metformin group. The combination of basal insulin plus GLP-1-RA is more beneficial than insulin alone: this reduces the variability of blood glucose levels as well as the risk of hypoglycemia. Pharmacokinetics of common insulin analogues.

Active ingredient Onset of action Maximum effect Duration of action Indication Special features
Short-acting insulins
Normal insulin 15-30 min 2 h 5-7 h ICT, PT,i.v. therapy <30 min injection-eating interval
Aspartate 12-8 min 30-90 min 3-5 h ICT No splash-eat distance
Lispro 15-30 min 30-90 min 3-5 h
Glulisine 12-30 min 30-90 min 3-5 h
Fast aspart 5-8 min 30-90 min 3-5 h
Delayed-release insulin* – long-acting insulin analogues
Intermediate-acting insulin 45-90 min 4-10 h Max 24 h Type 2 therapy 30-60 min spray-eat interval
Long-term insulin(zinc supension) 2-4 h 7-20 h 28-36 h ICT 30-60 min spray-eat interval
Glargine 1-2 h – 20-26 h ICT 30-60 min spray-eat interval
Detemir 1-2 h 6-8 h up to 24 h
Degludec 30-90 min – > 42 h
Glargine U 300 1-2 h – up to 36 h
Combination insulins
Depending on the exact compositionof normal and delayed-release insulin. CT < 30 min spray-eat interval

* Synonyms: Basal insulin, basic insulin, depot insulin, intermediate insulin, long-acting insulin

Important facts about insulin

  • Daily insulin requirement approximately 0.5-1.0 I.U./kg/die (average ≈ 40 I.U./d for insulin deficiency).
  • 1 bread unit (BE) ≡ amount of food containing 12 g of carbohydrate; 1 BE ≡ 2 I:E: insulin: 1 IU at noon and 1.5 IU in the eveningCalculation of the amount of insulin needed = amount of bread units per meal multiplied by the so-called BE factor; BE factor ≡ amount of insulin needed by the patient to break down a bread unit without a rise in blood glucose.
  • 1 I.U. normal insulin lowers blood glucose (Bz) by ≈ 30 mg %, slightly less in low BZ, slightly more in ketoacidotic derailment.
  • Dose adjustment insulin amount: (current Bz minus target (120 mg%)) divided by 30, the result multiplied times (quotient: daily insulin requirement divided by 40).
  • Caveat: 1 ml of normal insulin ≡ 40 I.E:/ml; insulin for the pen: 100 I.I./ml!

Insulin therapy regimens

  • Basal-assisted oral therapy (BOT).
  • Supplemental insulin therapy with preprandial (“after meals”) injections without basal insulin (SIT).
    • If necessary, maintain oral antidiabetic agents
  • Conventional insulin therapy (CT)
    • Rigid injection regimen: administration of insulin mixture (usually 1/3 normal insulin, 2/3 intermediate insulin).
    • 2 x daily (morning, evening) ≈ 2/3 of total, 30 min before breakfast,≈ 1/3, 30 min before dinner
      • Morning: normal insulin (covering breakfast), intermediate insulin (for baseline needs + lunch).
      • Evening: normal insulin (covering dinner), intermediate insulin (basic needs).
    • No flexibility
    • Indications: elderly and dependent patients (due topoor compliance).
  • Intensified conventional insulin therapy (ICT), first-line therapy.
    • Basal insulin level: coverage of basal requirement via long-acting insulin/intermediate insulin (dose is determined individually; administration late in the evening, possibly additionally early in the morning).
    • Meal-related insulin requirement: meal-adapted injection of alteinsulin (depending on appetite, blood glucose, time, physical exertion) by well-trained patient.
  • Intensified insulin therapy:
    • At least 3 insulin injections per day.
    • Substitution as follows:
      • Basal insulin level: basal insulin requirement with long-acting basal insulin/delayed-release insulin (1 x /d).
      • Meal-related insulin requirement: prandial (meal-related) insulin requirement with short-acting “bolus insulin”
    • Implementation with: Insulin syringe, insulin pens or insulin pumps.
    • Flexible insulin doses depending on the situation.
  • Insulin pump therapy (PT)
    • Basal insulin level: delivery of a continuous amount of alte insulin s.c. as basal requirement.
    • Meal-related insulin requirement: bolus altinsulin at meals; adjust dose to current blood glucose level and energy content of food
    • Indications: frequent hypoglycemia (low blood glucose), highly fluctuating blood glucose levels, poorly adjustable diabetes mellitus during pregnancy (gestational diabetes), planned pregnancy in type 1 diabetic women.

Patient recommendation

  • Regularly changing the injection site avoids lipodystrophy (fat distribution disorder; fat shrinkage).

Insulin allergy

  • In 95% of cases with suspected insulin allergy, no allergic component is the cause of symptoms
  • Measures to be taken in cases of insulin allergy (modified from Jaquier et al. 2013).
    • Severity: mild
      • Investigations: Rule out defective needles; confirm response to insulin.
      • Measures: replace needles and/or insulin preparation if necessary; antihistamine if needed.
    • Severity: moderate
    • Severity: severe or persistent.
      • Investigations (in addition to above):
        • Prick or intradermal skin test.
        • C1 inhibitor
        • Complement factors
        • Exclude viral and bacterial infections as a cause of urticaria (hepatitis B, CMV, EBV).
        • If necessary, dermatologist / rheumatologist / immunologist / consult.
      • Measures:
        • H1 and H2 antihistamines (loratadine + ranitidine).
        • Type 2 diabetes: discontinue insulin
        • If necessary, insulin i.v. briefly
        • Insulin pump therapy with or without hydrocortisone.
        • Hyposensitization
        • Systemic steroids; leukotriene receptor antagonist; omalizumab (anti-IgE monoclonal antibody); systemic immunosuppression.
        • Pancreas transplantation

Therapy of type 2 diabetes in the hospital

Treatment goals during hospitalization are:

  • Adjustment of blood glucose levels to moderate target levels.
  • Strict avoidance of hypoglycemia (low blood glucose).
  • Initiation of long-term diabetes therapy or optimization of an existing therapy.

In critically ill patients, the American Diabetes Association (ADA) recommends: initiation of insulin therapy at BG levels > 180 mg/dL (BG target: 140-180 mg/dL).In clinically stable patients: < 140 mg/dL preprandial and < 180 mg/dL postprandial. Individually, even in the absence of hypoglycemic risk, lower target values can be aimed for. Key recommendations for therapy of diabetes mellitus in the hospital setting:

  • Passage insulin therapy is recommended for hospitalized patients
  • Metformin should be discontinued at least 24 h, preferably 48 h, before the planned procedure or before administration of iodine-containing contrast media
  • In patients with coronary artery disease (CAD; coronary artery disease), moderate lowering of blood glucose and avoidance of hypoglycemia should be aimed for
  • When taking oral antidiabetic drugs, the restrictions on use in reduced renal function must be observed (see the HWZ below in each case).
  • Basic bolus therapy is preferable to simple correction regimens with regard to the quality of blood glucose control

Agents (main indication) for the treatment of hyperkalemia (excess potassium).

Agents (main indication) for the treatment of hypertension (high blood pressure)

  • First-line therapy using RAAS blockers.
  • Calcium channel blocker and/or thiazide diuretic therapy.
  • See hypertension/drug therapy for details.

Specific therapeutic measures for diabetic sequelae

See under the topics of the same name: