Skip to main content

Drug-Induced Ototoxicity!

 DRUG-INDUCED OTOTOXICITY

What is drug Induced Ototoxicity?

  • Drug-Induced ototoxicity can affect hearing (auditory or cochlear function0, balance (vestibular function) depending on the drug.
  • Drugs of almost every class have been reported to produce tinnitus (sounds in ear), as have placebos.

The following agents are associated with measurable changes in hearing or vestibular defect when administered systemically.



1. AMINOGLYCOSIDES:

  • Aminoglycosides antibiotics can cause cochlear or vestibular toxicities.
  • Cochlear toxicity: occurs as progressive hear loss, starting with highest tones and advancing to lower tones. Thus, considerable damage can occur before the patient recognizes it.
  • Symptoms of Vestibular damage: include;

  1.  Dizziness
  2. Vertigo
  3. Ataxia

  • Both forms of ototoxicity are bilateral and potentially reversible, but permanent damage is common and can progress even after discontinuation of aminoglycosides.
  • Clinically detectable ototoxicity in as many as 5% patients.
  • Most aminoglycosides-induced ototoxicity is associated with parenteral therapy but has also been associated with topical oral and irrigation use of these of these drugs, especially Neomycin.
  • Possible predisposing factors: 

  1. Decreased renal function.
  2. Long duration of therapy
  3. Large total damage
  4. Plasma level above therapeutic range
  5. Concurrent use of ototoxic drugs
  6. Dehydration
  7. Old age
  8. Genetic susceptibility to aminoglycoside-induced ototoxicity


2. HETEROCYCLIC ANTIDEPRESSANTS:

  • The presence of Tricyclic Antidepressants-associated tinnitus is associated to be 1%
  • Tinnitus can subside (occur) despite continuous therapy.


3.CHLORQUINE:

  • Nerve deafness is rare but consistent feature of chloroquine therapy.
  • Its onset is usually delayed and is thought of as irreversible. A partly reversible case and a case resulting from 1g have also been reported.


4.DIURETICS (LOOP DIURETICS):

  • Rapid onset hearing loss occurs at high dose, IV administration of Furosemide.
  • Gradual onset is with Ethacrynic acid.
  • Renal failure is usually the predisposing factor, but only renal failure patients are likely to receive large IV dose.
  • Co-administration of Aminoglycoside antibiotics often result in increased ototoxicity.
  • Permanent hearing loss has been reported with Ethacrynic acid and Furosemide.
  • Bumetanide or Torsemide produce less ototoxicity than Ethacrynic acid and Furosemide.


5.NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDs):

  • Although not as common as Salicylates, NSAIDs have been associated with hearing impairment and deafness, including some cases of permanent damage.
  • Tinnitus and vestibular dysfunction are also reported.


Labels:

Comments

Post a Comment

Popular posts from this blog

Diabetes Mellitus: Types!

TYPES OF DIABETES MELLITUS 1. TYPE1 DM Type 1 DM is usually diagnosed before age 30 years, but it can develop at any age. T1DM is an autoimmune disease in which insulin producing B-cells are destroyed. The presence of Human Leucocyte Antigens (HLAs ) is associated with the development of T1DM. In addition, these individuals often develop Islet cell antibodies , Insulin Autoantibodies or Glutamic Acid decarboxylase autoantibodies . At the time of development of diagnosis of T1DM, it is usually believed that most of the patients have 80-90%loss of beta cells. The remaining beta cells function at the diagnosis creates a " HONEYMOON PERIOD" during which the blood glucose levels are easier to control, and smaller amounts of insulin are required. after this, the remaining beta cells function is completely lost, and the patients become completely deficient of insulin and hence require exogenous insulin.  2. TYPE1.5 DM:  Also referred as Latent autoimmune diabetes in Adults (LAD) ...
Post a Comment
Read more

Diabetes Mellitus: Pharmacotherapy- Gliptins and a-Glycoside Inhibitors!

  PHARMACOTHERAPY:  Medications classifications include:  Sulfonyl Urea's Nonsylfonylurea Secretagogues (a-Glinides) Biguanides Thiazolidinediones a-Glucosidase Inhibitors Dipeptidyl Peptidase-4 Inhibitors (Gliptins) Sodium-glucose co-transporter (SGLT) Inhibitors  Central-Acting Dopamine Agonists Bile Acid Sequestrants Insulin therapy 5. a-GLUCOSIDASE INHIBITORS Acarbose and Miglitol are a-glucosidase inhibitors currently approved in the United States. Mechanism of Action: An enzyme that is along the brush border of the intestine cells called a-glucosidase; breaks down the complex carbohydrates into simple sugars, resulting in absorption. The a-glucosidase inhibitors work by delaying the absorption of carbohydrates from the intestinal tract, which reduces the rise in postprandial glucose levels. Therapy: As a monotherapy , a-glucosidase inhibitors primarily reduce post-prandial glucose excursions.  Clinical Use: FPG concentrations have been decreased by 40-5...
Post a Comment
Read more

Drug-Induced Nephrotoxicity!

 DRUG-INDUCED NEPHROTOXICITY Drug-Induced Nephrotoxicity is increasingly recognized as a significant contributor to kidney disease including Acute Kidney Injury (KI) and chronic kidney disease (CKD). Nephrotoxicity has a wide spectrum, reflecting damage to different nephron segments based upon individual drug-mechanisms. 1. ACE-INHIBITORS: ACE-Inhibitors are frequently associated with Proteinuria and Renal Insufficiency. The prevalence of Proteinuria in Captopril treated patient is estimated to be 1%. The risk of Renal Insufficiency is greater with long-acting ACE Inhibitors such as Lisinopril or Enalapril than with Captopril. Immune complex glomerulopathy is a major contribute to ACE Inhibitor nephrotoxicity. Predisposing factors include: Hyponatremia Diuretic therapy Pre-existing renal impairment Congestive Heart Failure (CHF) Diabetes Mellitus Recovery of renal function usually follows ACE-Inhibitor discontinuation. 2. CEPHLOSPORIN: The cephalosporin antibiotics are capable of...
Post a Comment
Read more