Related Experiment Video

Updated: Aug 18, 2026

Preparation of Washed Human Platelets for Quantitative Metabolic Flux Studies
07:06

Preparation of Washed Human Platelets for Quantitative Metabolic Flux Studies

Published on: January 10, 2025

Aspirin sensitivity of platelet aggregation in diabetes mellitus

Stewart G Albert1, Bibi I Hasnain, Detlef G Ritter

  • 1Department of Internal Medicine, Division of Endocrinology, Diabetes and Metabolism, Saint Louis University School of Medicine, 1402 South Grand Blvd., St. Louis, MO 63104, USA. albertsg@slu.edu

Diabetes Research and Clinical Practice
|May 17, 2005
PubMed

Insights

Patients with poorly controlled diabetes show normal aspirin sensitivity in platelet aggregation and prostaglandin suppression. However, aspirin resistance is noted with ADP-mediated platelet aggregation, suggesting other factors may affect aspirin

Area of Science:

  • Cardiovascular Medicine
  • Endocrinology
  • Pharmacology

Background:

  • Aspirin is cardioprotective in high-risk individuals.
  • Many patients with diabetes mellitus (DM) do not experience aspirin's cardioprotective benefits.
  • Poorly controlled diabetes may influence aspirin responsiveness.

Purpose of the Study:

  • To investigate aspirin sensitivity in platelet function in individuals with poorly controlled diabetes mellitus.
  • To determine if cardiovascular unresponsiveness to aspirin in diabetes is linked to in vitro platelet function.

Main Methods:

  • Assessed aspirin sensitivity via platelet aggregation assays and urinary prostaglandin metabolite levels (2,3 dinor thromboxane B2 and 2,3 dinor 6-keto PGF1alpha).
  • Compared 10 individuals with poorly controlled diabetes (glycohemoglobin 11.9+/-2.2%) to 10 age- and sex-matched controls.
  • All participants received 81 mg aspirin daily after a 2-week washout period.

Main Results:

  • Individuals with poorly controlled diabetes and controls demonstrated similar aspirin sensitivity to platelet aggregation induced by arachidonic acid and collagen.
  • Aspirin sensitivity to ADP-mediated platelet aggregation was observed in half of the participants with diabetes and half of the controls.
  • Urinary prostaglandin metabolites (TxB2 and PGF1alpha) were suppressed in both groups, with no significant differences between those with and without diabetes.

Conclusions:

  • Poorly controlled diabetes does not appear to cause differential lack of aspirin sensitivity in platelet aggregation or prostaglandin suppression.
  • Aspirin resistance was most evident in ADP-mediated platelet aggregation, irrespective of diabetes status.
  • The lack of aspirin's cardioprotective effect in diabetes may stem from undefined platelet function aspects beyond the tested parameters.

More Related Videos

Microfluidics in Assessing Platelet Function06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Dynamic Multiparameter Platelet Function Assessment Using a Capacitive Biosensor06:32

Dynamic Multiparameter Platelet Function Assessment Using a Capacitive Biosensor

Published on: May 2, 2025

Related Concept Videos

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Drug toxicity: Drug–Drug Interaction01:30

Drug toxicity: Drug–Drug Interaction

Drug–drug interactions can precipitate toxicity through multiple mechanisms. Absorption interactions alter how drugs enter the body, exemplified when ranitidine increases the absorption of basic drugs, while cholestyramine decreases the levels of propranolol. Protein binding interactions occur when drugs share the same binding sites on plasma proteins. Drugs like aspirin and warfarin, when bound in excess, can lead to increased free drug concentrations, enhancing the potential for...
Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood glucose levels...
Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
Acarbose and miglitol are typically...
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...
Type II Diabetes Mellitus III: Clinical Manifestations and Diagnosis01:25

Type II Diabetes Mellitus III: Clinical Manifestations and Diagnosis

Type 2 diabetes mellitus develops gradually and is often asymptomatic in early stages.Clinical ManifestationsWhen symptoms appear, they include fatigue, blurred vision, pruritus, delayed wound healing, and recurrent infections, particularly candidal infections. Peripheral neuropathy may present as numbness or tingling in the extremities. Classic hyperglycemia symptoms—polyuria, polydipsia, and polyphagia—are less common. Most patients are overweight and frequently have associated hypertension...