Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease where the immune system mistakenly attacks healthy tissues and organs, causing widespread inflammation. While lupus is primarily known for affecting the skin, joints, and kidneys, its systemic nature means it can disrupt nearly any bodily function, including metabolic processes. Hypoglycemia, defined as an abnormally low blood glucose level, is not a direct or common symptom of lupus itself. However, the underlying autoimmune activity, the medications used for treatment, and resultant organ damage can all lead to episodes of low blood sugar. Understanding these indirect mechanisms is important for managing the condition and its potential complications.
Autoimmune Attacks on Glucose Regulation
Lupus can rarely generate specific autoantibodies that directly interfere with the body’s glucose-regulating machinery. This mechanism represents a direct link between the disease and low blood sugar, independent of organ damage or medication side effects. The most prominent example is the production of autoantibodies that target the insulin receptor on cells, a condition known as Type B insulin resistance syndrome (TBIRS).
In TBIRS, autoantibodies initially block insulin receptors, causing severe insulin resistance and high blood sugar. However, these antibodies can also act as agonists, mimicking insulin’s action and continuously stimulating receptors to pull glucose out of the bloodstream. This excessive signaling can lead to episodes of profound hypoglycemia. Although TBIRS is exceptionally rare, SLE is frequently the underlying autoimmune disease in reported cases, highlighting a direct pathway for blood sugar instability.
Another direct, though poorly understood, autoimmune mechanism involves antibodies targeting insulin itself, termed Insulin Autoimmune Syndrome (IAS) or Hirata’s disease. In this scenario, antibodies bind to circulating insulin and later release it suddenly and inappropriately into the bloodstream. This delayed release of active insulin triggers a rapid drop in blood glucose, typically several hours after a meal. While the relationship between IAS and SLE is not firmly established, the presence of autoantibodies against insulin or insulin receptors represents a significant, albeit rare, direct autoimmune cause of hypoglycemia in lupus patients.
Medication Influence on Blood Sugar
The pharmacological treatments used to control lupus activity are a more common indirect cause of blood sugar fluctuation, primarily involving glucocorticoids (steroids) like prednisone. While effective at suppressing the immune system and reducing inflammation, glucocorticoids are typically associated with high blood sugar (hyperglycemia) by increasing the liver’s glucose output and reducing cellular sensitivity to insulin. The risk for hypoglycemia occurs when these medications are withdrawn or rapidly tapered.
Chronic steroid use suppresses the hypothalamic-pituitary-adrenal (HPA) axis, which regulates the body’s natural stress hormones. This suppression can lead to iatrogenic adrenal insufficiency (AI), meaning the adrenal glands are temporarily unable to produce sufficient cortisol. Cortisol is a counter-regulatory hormone that raises blood glucose levels, particularly during fasting or stress.
When the external steroid dose is reduced too quickly, the body lacks both the synthetic hormone and its own natural cortisol due to the suppressed HPA axis. This sudden lack of cortisol impairs gluconeogenesis, the process of generating new glucose from non-carbohydrate sources. The resulting deficit in glucose production, combined with the normal action of insulin, can precipitate significant hypoglycemia until the HPA axis recovers.
Secondary Organ Damage and Endocrine Conditions
The most frequent pathway for lupus to cause low blood sugar is through chronic damage to major internal organs, especially the kidneys and liver, which play central roles in glucose metabolism. Lupus Nephritis, the inflammation and damage to the kidneys caused by SLE, can progress to severe chronic kidney disease or failure. Healthy kidneys clear about 20% of circulating insulin and contribute to glucose production through gluconeogenesis, especially when fasting.
When kidney function declines due to Lupus Nephritis, insulin clearance slows significantly, causing insulin to remain active in the bloodstream longer. This prolonged activity promotes excessive glucose uptake by cells, leading to hypoglycemia. Furthermore, the impaired ability of damaged kidneys to perform gluconeogenesis removes a crucial mechanism for maintaining blood sugar during fasting, exacerbating the risk of low blood sugar.
Similarly, severe liver involvement, often termed Lupus Hepatitis, can disrupt the liver’s function as the body’s primary glucose reservoir. The liver stores glucose as glycogen and releases it as needed, while also performing the majority of gluconeogenesis. Significant autoimmune damage impairs both processes, resulting in a failure to release glucose into the bloodstream to compensate for fasting or increased energy demands. This failure of hepatic glucose output is a direct cause of low blood sugar in the context of severe organ damage.
Beyond organ failure, lupus is frequently associated with other autoimmune endocrine disorders that independently affect blood sugar regulation. For instance, the co-occurrence of SLE with Addison’s disease, an autoimmune condition causing the destruction of the adrenal cortex, results in a severe deficiency of cortisol and other adrenal hormones. Hypoglycemia is a recognized feature of Addison’s disease due to the loss of cortisol’s counter-regulatory effects, demonstrating another indirect link between lupus and blood sugar issues.
Recognizing and Managing Low Blood Sugar
Recognizing the signs of hypoglycemia is important for anyone with lupus, given the potential for the disease and its treatments to disrupt glucose balance. Mild symptoms often include a rapid heartbeat, sweating, unexplained anxiety, and shakiness or tremors. If blood sugar continues to drop, individuals may experience more concerning neurological symptoms such as confusion, difficulty concentrating, slurred speech, or blurred vision.
If a person experiences these symptoms, they should immediately check their blood glucose level, if possible, to confirm the reading is below 70 milligrams per deciliter (mg/dL). For mild to moderate low blood sugar, the standard immediate treatment is the “Rule of 15.” This involves consuming 15 grams of a fast-acting carbohydrate, such as four ounces of fruit juice, a tablespoon of honey, or three to four glucose tablets.
After consuming the fast-acting carbohydrate, the individual should wait 15 minutes and recheck their blood sugar. If the level remains below 70 mg/dL, the 15-gram carbohydrate dose should be repeated until the blood sugar returns to a safe range. Once stabilized, eating a small snack that includes protein and a longer-acting carbohydrate helps prevent the blood sugar from dropping again. Anyone experiencing recurrent or severe episodes of low blood sugar must consult their rheumatologist or endocrinologist to investigate the underlying cause and adjust their treatment plan.