DRUGS THAT SUPPRESS TSH OR CAUSE CENTRAL HYPOTHYROIDISM

TTP/HUS, in some cases resulting in death, has occurred in patients with advanced HIV-1 disease and also in allogeneic bone marrow transplant and renal transplant recipients participating in clinical trials of VALTREX at doses of 8 grams per day. Treatment with VALTREX should be stopped immediately if clinical signs, symptoms, and laboratory abnormalities consistent with TTP/HUS occur. The recommended dosage of VALTREX for treatment of recurrent genital herpes is 500 mg twice daily for 3 days. The recommended dosage of VALTREX for treatment of cold sores is 2 grams twice daily for 1 day taken 12 hours apart. Therapy should be initiated at the earliest symptom of a cold sore (e.g., tingling, itching, or burning). Valacyclovir is converted to acyclovir and L-valine by first-pass intestinal and/or hepatic metabolism.

• Patients should be instructed that treatment for cold sores should not exceed 1 day (2 doses) and that their doses should be taken about 12 hours apart.
• The recommended dosage of VALTREX for treatment of chickenpox in immunocompetent pediatric patients aged 2 to less than 18 years is 20 mg/kg administered 3 times daily for 5 days.
• About one-third of acyclovir in the body is removed by dialysis during a 4-hour hemodialysis session.

Drug and food interactions

Most of these drugs act at the level of the thyroid in patients with normal thyroid function, or at the level of thyroid hormone absorption or metabolism in patients requiring exogenous levothyroxine. A small subset of medications including glucocorticoids, dopamine agonists, somatostatin analogs and rexinoids affect thyroid function through suppression of TSH in the thyrotrope or hypothalamus. Fortunately, most of these medications do not cause clinically evident central hypothyroidism. A newer class of nuclear hormone receptors agonists, called rexinoids, cause clinically significant central hypothyroidism in most patients and dopamine agonists may exacerbate ‘hypothyroidism’ in patients with nonthyroidal illness. In this review, we explore mechanisms governing TSH suppression of these drugs and the clinical relevance of these effects. The recommended dosage of VALTREX for treatment of chickenpox in immunocompetent pediatric patients aged 2 to less than 18 years is 20 mg/kg administered 3 times daily for 5 days.

Elderly patients are also more likely to have renal or CNS adverse events see DOSAGE AND ADMINISTRATION, WARNINGS AND PRECAUTIONS, CLINICAL PHARMACOLOGY. The recommended dosage of VALTREX for treatment of initial genital herpes is 1 gram twice daily synthroid kinetics for 10 days. Therapy was most effective when administered within 48 hours of the onset of signs and symptoms. Dopamine exerts its effect on the hypothalamic-pituitary-thyroid axis through the activation of dopamine D2 receptors (D2R), but appears to have opposite effects on the hypothalamus and the pituitary thyrotrope. Dopamine infusions in healthy volunteers reduces TSH pulse amplitude without significantly altering TSH pulse frequency (12;13).

Side Effects for Valtrex

• Fortunately, the widely used glucocorticoids and the somatostatin analogs do not induce clinically evident central hypothyroidism even after prolonged high dose use.
• The pharmacokinetic disposition of acyclovir delivered by valacyclovir is consistent with previous experience from intravenous and oral acyclovir.
• There is no information specific to administration of VALTREX in patients receiving peritoneal dialysis.
• TTP/HUS, in some cases resulting in death, has occurred in patients with advanced HIV-1 disease and also in allogeneic bone marrow transplant and renal transplant recipients participating in clinical trials of VALTREX at doses of 8 grams per day.

Subjects self-initiated therapy within 24 hours of the first sign or symptom of a recurrent genital herpes episode. After single-dose administration of 1 gram of VALTREX in healthy geriatric subjects, the half-life of acyclovir was 3.11 ± 0.51 hours compared with 2.91 ± 0.63 hours in healthy younger adult subjects. The pharmacokinetics of acyclovir following single- and multiple-dose oral administration of VALTREX in geriatric subjects varied with renal function.

Valtrex showed no effects on the fetus in animal studies; however, there has been no adequate evaluation of Valtrex or (acyclovir) in pregnant women. Valtrex should only be used during pregnancy when the benefits to the mother outweigh risks to the fetus. The safety of Valtrex in breastfeeding infants has not been established. Methods other than breastfeeding should be considered if Valtrex must be taken while nursing. Add your drug list to My Med List to view medical information in a simple, easy-to-read, personalized format.

• Therefore, patients should be counseled to use safer sex practices in combination with suppressive therapy with VALTREX.
• Valtrex may interact with, lithium, methotrexate, pain or arthritis medicines, medicines used to treat ulcerative colitis, medicines used to prevent organ transplant rejection, IV antibiotics, antiviral medicines, or cancer medicines.
• In summary, glucocorticoids can lower serum TSH levels and decrease TSH secretion through direct effects on TRH in the hypothalamus.
• Valacyclovir hydrochloride is rapidly converted to acyclovir, which has demonstrated antiviral activity against HSV types 1 (HSV-1) and 2 (HSV-2) and VZV both in cell culture and in vivo.

The EC50 values for acyclovir against most laboratory strains and clinical isolates of VZV range from 0.53 to 48 microM (0.12 to 10.8 mcg/mL). Acyclovir also demonstrates activity against the Oka vaccine strain of VZV with a mean EC50 value of 6 microM (1.35 mcg/mL). The plasma elimination half-life of acyclovir typically averaged 2.5 to 3.3 hours in all trials of VALTREX in subjects with normal renal function. There is no accumulation of acyclovir after the administration of valacyclovir at the recommended dosage regimens in adults with normal renal function. Valacyclovir was noncarcinogenic in lifetime carcinogenicity bioassays at single daily doses (gavage) of valacyclovir giving plasma acyclovir concentrations equivalent to human levels in the mouse bioassay and 1.4 to 2.3 times human levels in the rat bioassay.

Drugs that suppress serum TSH levels

In addition, absorption of levothyroxine may be decreased and/or delayed by foods such as soybean flour, cotton seed meal, walnuts, dietary fiber, calcium, calcium fortified juices and grapefruit or grapefruit juice. These foods should be avoided within several hours of dosing if possible. It is important to tell your doctor about all other medications you use, including vitamins and herbs.

There are no data on the safety or effectiveness of chronic suppressive therapy of more than 6 months’ duration in HIV-1-infected patients. Zovirax treats viral infections caused by genital herpes, cold sores, shingles, and chicken pox … Dopamine used in critical illness and the dopamine agonist bromocryptine used for disorders like hyperprolactinemia can suppress serum TSH.

Bromocryptine appears to have the same effect on TSH pulse amplitude and is likely occurring through the same D2R mechanism (14). Prolonged treatment with bromocryptine does not appear to cause central hypothyroidism since many patients treated with bromocryptine for macroprolactinomas actually have resolution of central hypothyroidism caused by the adenoma (16). Studies using dopamine infusions in critically ill adults and neonates with the nonthyroidal illness (NTI) syndrome suggest that dopamine and NTI have and additive effect of HPT axis suppression. This may lead to iatrogenic central hypothyroidism in these patients (17;18). It is not clear whether treatment with levothyroxine is indicated in patients with NTI who are receiving dopamine infusions.

Bexarotene rapidly and significantly suppressed serum TSH, but had no effect on prolactin or cortisol levels, suggesting this was a specific effect on thyrotropes. Our group and others have also shown that rexinoids likely affect thyroid hormone metabolism as well through deiodination, sulfation and possibly glucuronidation (39). Figure 1 is a summary of the proposed mechanisms by which rexinoids cause clinically significant central hypothyroidism.