Thyroid function in patients with chronic hepatitis C virus infection under interferon therapy

Mohammad E Abdel-Kader1, Mohamed K Azmy, Mahmoud A Hassan

  • 1Department of Internal Medicine, Faculty of Medicine, Al Azhar University, Cairo, Egypt.

The study examined 60 HCV patients with normal baseline levels of TSH. The patients received subcutaneous pegylated interferon a-2b weekly in addition to oral ribavirin. Before the start of the interferon therapy, serum TSH, thyroglobulin-Ab (TG-Ab) and antiperoxidase antibodies (TPO-Ab) were measured. Three months after interferon therapy serum levels of TSH were measured to all patients; patients with abnormal TSH were subjected to the measurements of FT3, FT4, TPO-Ab, TG-Ab, and thyroid stimulating immunoglobulin levels (TSI). After 3 months of therapy, 48 patients (80%) had normal TSH, and 12 patients (20%) had abnormal TSH. Of 12 patients with abnormal TSH 10 (16.6%) had high levels of TSH (hypothyroidism), while the other two (3.4%) had low levels of TSH (Hyperthyroidism). Of 10 patients with hypothyroidisms, 6 patients (10%) had overt hypothyroidism and 4 patients (6.6%) had subclinical hypothyroidism. All patients with abnormal TSH had significant higher levels of TG-Ab, TPO-Ab and TSI (in cases with hyperthyroidism only) than the patients with normal levels of TSH (p < 0.001), the levels of TPO-Ab only of the most patients with abnormal TSH were above the normal reference range before the start of interferon therapy. Patients with hyperthyroidism, one was presented by clinical picture of overt hyperthyroidism, and the second by subclinical hyperthyroidism. All patients with overt hypo and hyperthyroidism received medical treatment, with normalization of levels of TSH and improvement of clinical symptoms and completed their course of interferon therapy Forty patients (66.6%) responded to interferon (-ve PCR for HCV), while 20 (33.3%) did not respond, 5 had TSH abnormalities that were significantly higher than those in patient with normal TSH {5/12 (41.6%).versus 15/48 (31%); p < 0.01}.

Related Concept Videos

Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test01:22

Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test

In clinical practice, the direct measurement of hepatic blood flow to evaluate liver function presents significant challenges due to the intricate and specialized nature of the necessary techniques. Consequently, healthcare professionals often rely on empirical estimates derived from thorough patient examinations and liver function tests to gauge liver health. Among the tools at their disposal, the Child–Pugh and MELD scoring systems stand out for their ability to categorize and assess the...
Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow01:26

Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow

Chronic liver disease significantly impacts drug metabolism due to alterations in hepatic blood flow and enzyme accessibility. This disruption affects the body's pharmacokinetics—the movement and processing of drugs within the system. Key enzymes crucial for metabolizing medications become less accessible, changing how drugs are processed and utilized. Furthermore, liver disease influences the synthesis of plasma proteins, such as albumin and globulins, which play critical roles in drug binding...
Hepatitis01:25

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...