Related Experiment Video
Updated: May 10, 2026
04:36
An Assay to Detect Protection of the Retinal Vasculature from Diabetes-Related Death in Mice
Published on: January 12, 2024
[Association between pioglitazone and diabetic macular edema]
Yuko Hoshikawa1, Kishiko Ohkoshi
1Department of Ophthalmology, St. Luke's International Hospital, 9-1 Akashi-cho, Chuo-ku, Tokyo 104-8560, Japan. hoshiyu@luke.or.jp
Nippon Ganka Gakkai Zasshi
|June 18, 2013
Summary
Pioglitazone use showed a very low incidence of new diabetic macular edema (DME). However, patients with pre-existing DME should be monitored closely as the condition can worsen with pioglitazone therapy.
Area of Science:
- Ophthalmology
- Endocrinology
- Pharmacology
Background:
- Diabetic macular edema (DME) is a significant cause of vision loss in diabetic patients.
- Pioglitazone is a thiazolidinedione antidiabetic medication.
- Understanding the ocular side effects of pioglitazone is crucial for patient management.
Purpose of the Study:
- To evaluate the early association between pioglitazone initiation and the development or worsening of diabetic macular edema (DME).
Main Methods:
- A retrospective study included 304 eyes from 285 patients initiating pioglitazone therapy.
- Patients were categorized into those without pre-existing DME and those with pre-existing DME.
- Macular status was assessed via slit-lamp biomicroscopy or optical coherence tomography within three months of starting pioglitazone.
Main Results:
- In eyes without pre-existing DME, the incidence of new DME was very low (0.34%).
- In eyes with pre-existing DME, 28.6% showed an increase in macular edema.
- This suggests a potential risk of DME exacerbation in patients with prior macular edema.
Conclusions:
- Pioglitazone appears to have a low risk of causing new-onset DME.
- Caution is advised for patients with pre-existing DME, requiring close ophthalmologic monitoring.
- Collaborative management between ophthalmologists and physicians is recommended for patients on pioglitazone therapy.
Related Concept Videos
01:27Diabetic Retinopathy
DefinitionDiabetic retinopathy is a microvascular complication of diabetes affecting the retinal blood vessels.Risk FactorsDiabetic retinopathy is present in almost all individuals with type 1 diabetes and more than 60% of those with type 2 diabetes after two decades of disease.The risk increases with poor glycemic control, hypertension, dyslipidemia, smoking, pregnancy, and puberty.Although cataracts and glaucoma are also more frequent in people with diabetes, retinopathy remains the leading...
01:26Oral 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...
01:23Dipeptidyl 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...
01:06Oral Hypoglycemic Agents: Glinides
Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively manages...
01:24Type II Diabetes II: Pathophysiology
PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
01:19Type I Diabetes III: Clinical Manifestations
Type 1 diabetes mellitus typically presents with rapid-onset symptoms due to the body’s inability to utilize glucose in the absence of insulin. Since insulin is required for glucose uptake into cells, its deficiency leads to hyperglycemia and cellular energy deprivation, resulting in characteristic clinical features.Polyuria and PolydipsiaOne of the earliest, most prominent symptoms is polyuria (excessive urination). When blood glucose concentrations rise above the renal threshold, the kidneys...