Introduction
Multiple endocrine glands in the body are impacted by autoimmune disease. The role of alleles in HLA (human leukocyte antigen) like molecules in tissue-specific targeting that results in organ-specific autoimmunity when tolerance is lost is highlighted in both animal models and human research. Disorders brought on by autoimmune-mediated tissue damage include type 1A diabetes, Grave's disease, Hashimoto's thyroiditis, Addison's disease, and many others. Each disorder can be broken down into stages, starting with genetic predisposition, environmental triggers, active autoimmunity, and then metabolic derangements with obvious clinical symptoms.
Autoimmunity brought on by drugs is a unique, non-immunoglobulin E immune-related drug reaction. Numerous medicines have been claimed to cause autoantibodies, but only a handful have a proven link to drug-induced autoimmune illness. Drug-induced lupus is the prototypical disease, and Minocycline is the conventional treatment for this condition. A number of mechanisms, including the suppression of central or peripheral tolerance, changes in the transcription of T and B cell genes, abnormal cytokine or cytokine receptor balance and function, chromatin structure modification, and antigen modification, result in the production of autoantibodies and the induction of symptoms in drug-induced lupus.
How Are Autoimmune Endocrine Disorders Induced by Drugs?
Each system and organ's homeostasis is maintained by the endocrine system's exact interactions with various mechanisms. The dynamic endocrine system's balance can be altered by a number of things, including pharmaceuticals and prescriptions, in the overwhelming polypharmacy period. This can result in endocrine and metabolic disorders.
Drugs can influence hormone synthesis directly, disrupt the feedback axis' control, and affect hormonal transport, binding, and signaling, as well as comparable modifications to counter-regulatory hormone systems. These are only a few of the different ways that drugs can induce endocrine disorders. Drugs can also interact with hormonal tests, resulting in inaccurate laboratory results that confuse clinicians about the proper diagnosis.
What Medications Cause Drug-Induced Lupus Erythematosus?
Drug-induced lupus erythematosus is comparable to systemic lupus erythematosus but not exactly the same (systemic lupus erythematosus). It is an autoimmune condition. This suggests that healthy tissue is being attacked by mistake by the body. It results from a drug reaction. Drug-induced cutaneous lupus and antineutrophil cytoplasmic antibodies vasculitis are related diseases.
The following drugs are the most frequently implicated in drug-induced lupus erythematosus:
-
Isoniazid.
-
Hydralazine.
-
Procainamide.
-
Morphogenic factor (tumor necrosis factor) alpha inhibitors (such as Etanercept, Infliximab, and Adalimumab).
-
Minocycline.
-
Quinidine.
Systemic lupus erythematosus may also be triggered by other, less prevalent medicines. These may consist of the following:
-
Anti-epileptic drugs.
-
Capoten.
-
Chlorpromazine.
-
Methyldopa.
-
Sulfasalazine.
-
Levamisole is frequently found in cocaine as a contaminant.
Pembrolizumab, a cancer immunotherapy medicine, and other autoimmune reactions, including drug-induced lupus, are all possible side effects.
Drug-induced lupus symptoms typically appear three to six months or more after starting the medication.
What Are the Symptoms Associated With SLE?
Some symptoms could be:
-
General unease (malaise).
-
Joint discomfort.
-
Joint swelling.
-
Reduced appetite.
-
Pleuritic chest discomfort.
-
Areas of exposed skin develop a rash.
What Are the Treatment Modalities Used to Treat SLE?
Typically, symptoms disappear within a few weeks of ceasing the medication that triggered the disease.
Treatment options include:
-
Medications known as nonsteroidal anti-inflammatory drugs (NSAIDs) are used to treat pleurisy and arthritis.
-
To treat skin rashes, use corticosteroid creams.
-
Skin and arthritis symptoms are treated with antimalarial medications (Hydroxychloroquine).
-
High doses of corticosteroids (Prednisone, Methylprednisolone) and immune system suppressants may be administered if the illness affects your heart, kidney, or nervous system (Azathioprine or Cyclophosphamide).
The patient should use protective clothing and sunglasses to prevent overexposure to the sun when the disease is active.
What Are the Drugs That Cause Diabetes Mellitus?
The anti-hypertensive vasodilator Diazoxide and large doses of corticosteroids, such as those used to treat brain tumors, are the only medications that frequently cause diabetes when used therapeutically. The lower doses now used are likely to only slightly increase the risk of developing diabetes because Thiazide diuretics have historically been used in larger doses than necessary to treat hypertension. Although there is some indication that Thiazides taken with beta-blockers may increase the chance of developing diabetes compared to either medicine alone, the risk from beta-blockers is also fairly low. In people with a family history of non-insulin-dependent diabetes, it is usually advisable to avoid the combination.
Only women who have experienced gestational diabetes are in danger from the low-estrogen combined oral contraceptive pill's effect, which appears to be minimal. Massive doses of anabolic androgens can lead to decreased glucose tolerance in bodybuilders. Theophylline, Aspirin, Isoniazid, and Nalidixic acid are among the medications that might temporarily elevate blood sugar levels when taken in excess. Still, only Streptozotocin, Alloxan, and the Rodenticide vacor are likely to result in long-term diabetes.
What Are the Drugs That Cause Hypothyroidism?
The list of medications that can interact with the thyroid axis becomes longer and longer every year. The most common result of thyroid malfunction caused by drugs is hypothyroidism. The primary immune mechanisms associated with the use of Interferon and other cytokines, the immune mechanisms related to the use of tyrosine kinase inhibitors, and the induction of thyroiditis associated with the use of drugs blocking the receptors for vascular endothelial growth factor are the main mechanisms involved in the development of primary hypothyroidism. Thyroid-stimulating hormone inhibition (by Bexarotene or corticosteroids) or immunological processes may cause central hypothyroidism.
Additionally, it is critical to identify medications that contribute to hypothyroidism throughout its therapy, either by lowering Levothyroxine absorption or by changing its transport and metabolism. Therefore, it is highly advised to assess thyroid function before prescribing drugs like Amiodarone, Lithium, or Interferon, as well as novel biological therapies that exhibit significant interactions with thyroid and endocrine function in general.
Conclusion
The dynamic and fragile endocrine system's delicate equilibrium can be readily upset by intervening pharmacological agents. The regulation of the feedback axis, changes in hormonal transport, binding, and signaling, as well as analogous modifications to counter-regulatory hormone systems, are some of the different mechanisms by which drugs can cause endocrine disorders. Additionally, medications may interact with hormonal assays, resulting in false laboratory results that confuse clinicians about the proper diagnosis.
