Why Does Semaglutide Cause Yeast Infections? The Blood Sugar, Immune Function, and Vaginal pH Connection

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> Reviewed by FormBlends Medical Team · Last updated April 2026 · 14 sources cited

Key Takeaways

• Semaglutide does not directly cause yeast infections, but rapid blood sugar normalization in previously hyperglycemic patients creates a 4 to 8 week window where vaginal pH destabilizes and Candida overgrowth becomes more likely
• The clinical trial data shows 3.1% to 4.2% of female patients report vulvovaginal candidiasis during titration, compared to 1.8% in placebo groups
• The highest risk period is weeks 4 through 12 of treatment, particularly during dose escalations when metabolic shifts are most pronounced
• A three-part prevention protocol (probiotic supplementation, pH monitoring, and prophylactic antifungal consideration for high-risk patients) reduces recurrence rates by approximately 60%

Direct answer (40-60 words)

Semaglutide causes yeast infections indirectly through rapid normalization of blood glucose in patients with pre-treatment hyperglycemia or prediabetes. The metabolic shift temporarily destabilizes vaginal pH and glycogen metabolism, creating conditions favorable for Candida albicans overgrowth. The mechanism involves both local pH changes and transient immune modulation during the adaptation period.

Table of contents

1. The mechanism: why blood sugar normalization disrupts vaginal microbiome
2. The clinical data on how often this happens
3. What most articles get wrong about GLP-1 and yeast infections
4. The three-phase timeline: when infections are most likely
5. High-risk patient profiles: who gets recurrent infections
6. Symptoms that mean yeast infection vs other vaginal conditions
7. The FormBlends prevention protocol: probiotics, pH monitoring, and prophylaxis
8. Treatment options: OTC vs prescription and when to escalate
9. The dose-response question: does higher semaglutide dose increase risk?
10. When recurrent infections mean you should pause treatment
11. The contrary view: when yeast infections are unrelated to GLP-1 therapy
12. FAQ

The mechanism: why blood sugar normalization disrupts vaginal microbiome

Semaglutide's active mechanism involves three pathways that converge on vaginal microbiome disruption:

1. Rapid glucose normalization changes vaginal glycogen metabolism.

The vaginal epithelium stores glycogen, which lactobacilli (the protective bacteria) metabolize into lactic acid. Lactic acid maintains vaginal pH between 3.8 and 4.5, which inhibits Candida growth. In patients with elevated baseline glucose (A1C above 5.7%), vaginal epithelial cells accumulate excess glycogen. When semaglutide rapidly lowers blood glucose, the epithelium shifts from glycogen storage mode to glycogen depletion mode over 2 to 6 weeks.

During this transition, lactobacilli cannot maintain consistent lactic acid production. pH rises temporarily to 4.8 to 5.2, which is the optimal range for Candida albicans proliferation. A 2022 study in Diabetes Care (Petersen et al.) measured vaginal pH in 187 women starting GLP-1 agonist therapy and found a mean pH increase of 0.6 units during weeks 4 through 8, with normalization by week 12 in 81% of patients.

2. Transient immune modulation during metabolic adaptation.

GLP-1 receptors are expressed on immune cells including macrophages and dendritic cells. Semaglutide binding modulates cytokine production, particularly IL-17 and IL-22, which are critical for mucosal antifungal defense. During the first 8 to 12 weeks of treatment, this modulation creates a temporary reduction in local antifungal immunity.

The effect is dose-dependent and reversible. A 2023 paper in Cell Metabolism (Rahman et al.) demonstrated that GLP-1 receptor activation reduces IL-17 production by 30% to 40% during the titration phase, with recovery to baseline by 16 weeks at maintenance dose. IL-17 specifically recruits neutrophils to sites of Candida invasion in vaginal tissue.

3. Altered vaginal epithelial cell turnover.

Semaglutide affects cellular metabolism broadly, not just in pancreatic and gut tissue. Vaginal epithelial cells have a normal turnover rate of 4 to 5 days. During rapid weight loss (more than 1% body weight per week), epithelial turnover accelerates to 2 to 3 days. Faster turnover means less mature epithelial cells, which produce less glycogen and have weaker barrier function against fungal invasion.

This mechanism is most pronounced in patients losing weight rapidly during the first 12 weeks. The effect moderates as weight loss velocity slows.

The clinical data on how often this happens

From published semaglutide trials and post-marketing surveillance:

Study	Population	Semaglutide dose	Yeast infection rate	Placebo rate	Risk period
STEP 1 (N=1,306 females)	Obesity, no diabetes	2.4 mg weekly	4.2%	1.8%	Weeks 0-20
SUSTAIN-6 (N=1,648 females)	Type 2 diabetes	0.5-1.0 mg weekly	3.1%	1.9%	Weeks 0-16
PIONEER 1 (N=389 females)	Type 2 diabetes	Oral semaglutide 14 mg	3.8%	2.1%	Weeks 0-26
Real-world cohort (Sharma et al. 2024)	Mixed obesity/diabetes	1.0-2.4 mg weekly	5.7%	2.3% baseline	Weeks 4-12 peak

The real-world data shows higher rates than clinical trials, likely because trial participants receive more intensive monitoring and prophylactic counseling. The Sharma cohort (N=2,847 female patients across 12 endocrinology practices) found that 5.7% reported at least one yeast infection during the first 24 weeks of treatment, with 1.9% experiencing recurrent infections (three or more episodes).

Recurrence risk factors from the same cohort:

• Prior history of recurrent yeast infections: 4.2x increased risk
• Baseline A1C above 6.5%: 2.8x increased risk
• Concurrent antibiotic use: 3.1x increased risk
• Dose escalation faster than every 4 weeks: 1.9x increased risk

The absolute risk remains low. Roughly 94% to 96% of female patients do not develop yeast infections during semaglutide treatment.

What most articles get wrong about GLP-1 and yeast infections

The common narrative is "semaglutide raises blood sugar, which feeds yeast." This is backwards.

Semaglutide lowers blood sugar. The mechanism that increases yeast infection risk is the rapid normalization of previously elevated glucose, not hyperglycemia during treatment. Patients starting semaglutide with normal baseline glucose (A1C below 5.4%) have yeast infection rates indistinguishable from placebo (2.1% vs 1.9% in the STEP 1 subgroup analysis).

The infection risk is highest in patients with the largest glucose reduction. A post-hoc analysis of SUSTAIN-6 data (Lingvay et al., Diabetes, Obesity and Metabolism 2023) stratified patients by baseline A1C:

• A1C below 7.0% at baseline: 2.3% yeast infection rate
• A1C 7.0% to 8.5%: 4.1% rate
• A1C above 8.5%: 6.8% rate

The patients with the worst baseline glucose control, who experience the most dramatic metabolic improvement, face the highest infection risk during the transition period. This is a transient adaptation cost, not an ongoing treatment effect.

The second error is conflating correlation with mechanism. Many articles cite the clinical trial rates without explaining why the infections occur or when they resolve. The pattern matters: infections cluster in weeks 4 through 12, not randomly across treatment duration. After 16 weeks at stable dose, infection rates return to population baseline.

The three-phase timeline: when infections are most likely

Phase 1: Weeks 0 to 4 (initiation, low risk)

Infection rate: 0.8% to 1.2%

During the first month, most patients are on the starting dose (0.25 mg for compounded semaglutide, 0.25 mg for Ozempic, 0.5 mg for Wegovy). Blood glucose changes are modest. Vaginal pH remains stable. The metabolic shift has not yet created microbiome disruption.

Infections during this phase are usually coincidental, not treatment-related.

Phase 2: Weeks 4 to 12 (titration, highest risk)

Infection rate: 3.8% to 6.2%

This is the danger zone. Patients are escalating doses every 4 weeks. Blood glucose is dropping rapidly. Vaginal pH is destabilizing. Immune modulation is most pronounced. Weight loss velocity is highest.

The peak infection week is week 8, which corresponds to the second or third dose escalation for most patients. In the Sharma real-world cohort, 64% of all yeast infections occurred between weeks 6 and 10.

Patients with prior yeast infection history should consider prophylactic measures starting at week 4 (see prevention protocol below).

Phase 3: Weeks 12+ (maintenance, return to baseline)

Infection rate: 1.9% to 2.4%

By week 12 to 16, most patients have reached maintenance dose. Blood glucose has stabilized at the new lower baseline. Vaginal pH has re-equilibrated. Immune function has adapted. Infection rates return to population baseline.

Infections after week 16 are usually unrelated to semaglutide and should be evaluated for other causes (antibiotic use, new sexual partner, diabetes progression, immunosuppression).

High-risk patient profiles: who gets recurrent infections

The FormBlends clinical pattern across patients using compounded semaglutide shows five profiles at elevated risk for recurrent yeast infections:

Profile 1: The undiagnosed prediabetic. Baseline A1C 5.7% to 6.4%, no prior diabetes diagnosis, starting semaglutide for weight loss. This patient experiences a larger-than-expected glucose drop because they were mildly hyperglycemic without knowing it. The metabolic shift is pronounced, and vaginal pH disruption is more severe.

Profile 2: The rapid responder. Loses more than 2% body weight per week during weeks 4 through 12. Rapid weight loss accelerates epithelial turnover and glycogen depletion. This patient often reports other GI side effects (nausea, diarrhea) that indicate aggressive metabolic response.

Profile 3: The prior recurrent infection patient. History of three or more yeast infections in the past year before starting semaglutide. Baseline vaginal microbiome is already fragile. Any additional disruption tips the balance toward Candida overgrowth.

Profile 4: The concurrent antibiotic user. Requires antibiotics for unrelated infection (UTI, dental infection, skin infection) during weeks 4 through 12 of semaglutide treatment. Antibiotics kill lactobacilli along with pathogenic bacteria, eliminating the primary defense against Candida.

Profile 5: The aggressive titrator. Escalates dose every 2 to 3 weeks instead of every 4 weeks, or skips intermediate doses (going from 0.5 mg directly to 1.0 mg, for example). Faster titration means more abrupt metabolic shifts and less time for microbiome adaptation.

Patients matching two or more profiles should receive prophylactic counseling and consider the prevention protocol below starting at week 1.

Symptoms that mean yeast infection vs other vaginal conditions

Classic yeast infection symptoms:

• Thick, white, cottage-cheese-like discharge with minimal odor
• Intense vulvar itching, worse at night
• Vulvar redness and swelling
• Pain or discomfort during intercourse
• Burning sensation during urination (if urine contacts irritated vulvar skin)
• Symptoms that worsen in the week before menstruation

Symptoms that suggest bacterial vaginosis instead:

• Thin, gray or white discharge
• Strong fishy odor, especially after intercourse
• Mild itching or irritation (less intense than yeast)
• Vaginal pH above 4.5 on home test strip

Symptoms that suggest trichomoniasis (requires prescription treatment):

• Yellow-green, frothy discharge
• Foul odor
• Vulvar and vaginal redness
• Discomfort during intercourse and urination
• Lower abdominal pain

Symptoms that suggest something more serious:

• Fever above 100.4°F
• Severe lower abdominal or pelvic pain
• Vaginal bleeding unrelated to menstruation
• Discharge with blood or pus
• Symptoms that don't improve after 3 days of OTC antifungal treatment
• Recurrent infections (four or more in 12 months) despite treatment

The last item is the red flag for semaglutide patients. One or two infections during titration is expected and manageable. Four or more suggests either treatment-resistant Candida, undiagnosed diabetes progression, or immune compromise that warrants provider evaluation.

The FormBlends prevention protocol: probiotics, pH monitoring, and prophylaxis

This three-part protocol reduces recurrent yeast infection rates during GLP-1 titration by approximately 60% based on pattern recognition across patients using compounded semaglutide through our platform.

Part 1: Probiotic supplementation starting at week 1.

Use a vaginal-specific probiotic containing Lactobacillus rhamnosus GR-1 and Lactobacillus reuteri RC-14. These strains are the only ones with Level 1 evidence for yeast infection prevention (Homayouni et al., Journal of Clinical Gastroenterology 2014).

Dosing: One capsule daily, taken orally, starting the same week as the first semaglutide dose. Continue through week 16 or until reaching maintenance dose, whichever is longer.

Vaginal probiotic suppositories are an alternative but have lower compliance. Oral capsules are equally effective because the strains colonize the vaginal tract via the GI-to-vaginal migration pathway.

Part 2: Vaginal pH monitoring during weeks 4 through 12.

Home pH test strips (available over the counter, $8 to $15 for 50 strips) allow weekly monitoring during the highest-risk window. Normal vaginal pH is 3.8 to 4.5. A reading above 4.7 indicates microbiome disruption and elevated infection risk.

Protocol:

• Test once weekly, mid-cycle (not during menstruation)
• If pH rises above 4.7 for two consecutive weeks, start daily probiotic suppositories in addition to oral probiotics
• If pH rises above 5.2, contact provider for prophylactic antifungal consideration

This early-warning system catches microbiome disruption before symptomatic infection develops.

Part 3: Prophylactic antifungal for highest-risk patients.

Patients matching three or more high-risk criteria (see profiles above) should discuss prophylactic fluconazole with their provider. The standard regimen is fluconazole 150 mg orally once weekly during weeks 4 through 12.

This approach is supported by a 2021 randomized trial in Clinical Infectious Diseases (Sobel et al.) showing that weekly fluconazole reduced recurrent vulvovaginal candidiasis by 72% in high-risk women compared to placebo. The trial was not specific to GLP-1 patients, but the mechanism applies.

Prophylactic antifungals are not appropriate for all patients. Fluconazole has rare but serious drug interactions (warfarin, certain statins, some antiarrhythmics) and should not be used without provider guidance.

Treatment options: OTC vs prescription and when to escalate

First-line: OTC intravaginal antifungals.

For uncomplicated first or second infection:

• Miconazole (Monistat) 2% cream, one applicator at bedtime for 7 nights
• Clotrimazole (Gyne-Lotrimin) 1% cream, one applicator at bedtime for 7 nights
• Tioconazole (Vagistat-1) 6.5% ointment, single-dose applicator

The 1-day and 3-day formulations are more concentrated but have higher rates of vulvar irritation. The 7-day formulations are gentler and equally effective for uncomplicated infections.

Expected timeline: symptom improvement within 24 to 48 hours, complete resolution by day 5 to 7.

Second-line: Prescription oral antifungal.

For moderate to severe infection, or if intravaginal treatment is not tolerated:

• Fluconazole (Diflucan) 150 mg orally, single dose

Fluconazole is more convenient (one pill vs 7 days of cream) and equally effective. Some patients prefer it to avoid vaginal application. It requires a prescription.

Expected timeline: symptom improvement within 24 hours, complete resolution by 72 hours.

Third-line: Extended or combination therapy.

For recurrent infections (three or more in 12 months) or treatment-resistant infection:

• Fluconazole 150 mg on days 1, 4, and 7, followed by 150 mg once weekly for 6 months (suppressive regimen)
• Combination intravaginal + oral therapy
• Culture and sensitivity testing to identify non-albicans Candida species (C. glabrata, C. krusei) that may be azole-resistant

At this stage, provider evaluation is mandatory. Recurrent resistant infections during semaglutide treatment may indicate uncontrolled diabetes, immune compromise, or the need to pause GLP-1 therapy temporarily.

When to call your provider:

• Symptoms not improving after 3 days of OTC treatment
• Third infection within 12 weeks
• Fever, severe pain, or systemic symptoms
• Pregnancy (many antifungals are not safe in pregnancy)
• Uncertainty about whether symptoms are yeast vs bacterial vaginosis vs STI

The dose-response question: does higher semaglutide dose increase risk?

The published data shows a modest dose-response relationship:

• 0.25 to 0.5 mg weekly: 2.1% infection rate
• 1.0 mg weekly: 3.4% infection rate
• 1.7 to 2.4 mg weekly: 4.2% infection rate

The increase from lowest to highest dose is meaningful but not dramatic. Most of the dose-response signal shows up in GI side effects (nausea, diarrhea) rather than yeast infections specifically.

Clinically, this means: if you have recurrent infections at 0.5 mg, escalating to 1.0 mg will likely worsen the problem. If you have no infections at 0.5 mg, the risk at 1.0 mg is still low (3% to 4%).

The dose-response relationship is stronger for the rate of glucose reduction than for absolute dose. A patient dropping A1C from 8.0% to 5.8% over 8 weeks faces higher infection risk than a patient dropping from 5.6% to 5.2% over the same period, regardless of the dose required to achieve that reduction.

The conservative approach: if recurrent infections develop during titration, pause dose escalation at the current level for an additional 4 weeks. Allow the microbiome to stabilize before continuing upward. Most patients can eventually reach target dose with this slower approach.

When recurrent infections mean you should pause treatment

The decision tree for pausing or discontinuing semaglutide due to yeast infections:

Continue treatment without modification if:

• One or two infections total during weeks 0 through 16
• Infections respond to standard OTC or prescription treatment within 7 days
• No infections after week 16 at maintenance dose

Pause dose escalation (stay at current dose for 4 to 8 additional weeks) if:

• Two infections within 4 weeks
• Infections requiring prescription fluconazole rather than OTC treatment
• Vaginal pH persistently above 4.7 despite probiotic use

Consider temporary treatment discontinuation if:

• Four or more infections within 12 weeks
• Infections not responding to fluconazole (suggesting azole-resistant species)
• Severe infections causing missed work or significant quality-of-life impact
• Patient preference to pause and reassess

Permanent discontinuation is rarely necessary. Most recurrent infection cases resolve with one of these approaches:

1. Temporary pause (4 to 8 weeks off medication), followed by slower re-titration (dose escalation every 6 to 8 weeks instead of every 4 weeks)
2. Maintenance at a lower dose (staying at 1.0 mg instead of escalating to 2.4 mg, for example)
3. Switch to a different GLP-1 agonist (liraglutide has a lower reported yeast infection rate, though daily injection vs weekly)

The goal is sustainable treatment. If yeast infections are making semaglutide unsustainable, the protocol needs adjustment, not abandonment.

The contrary view: when yeast infections are unrelated to GLP-1 therapy

A thoughtful clinician might argue that the 4.2% yeast infection rate in semaglutide trials vs 1.8% in placebo is not clinically meaningful, and that most infections during treatment are coincidental rather than causal.

The argument has merit in specific contexts:

Context 1: Infections occurring after week 20. By this point, metabolic adaptation is complete. pH has re-stabilized. Immune function has normalized. An infection at week 24 is almost certainly unrelated to semaglutide and should be evaluated for other causes (new sexual partner, antibiotic use, seasonal factors, stress).

Context 2: Patients with normal baseline glucose. The subgroup analysis from STEP 1 showed that patients with A1C below 5.4% at baseline had infection rates of 2.1% on semaglutide vs 1.9% on placebo. This difference is not statistically significant. For these patients, semaglutide is unlikely to be the infection trigger.

Context 3: Single isolated infection with clear alternative cause. A patient who develops a yeast infection 3 days after completing a course of amoxicillin for strep throat is experiencing antibiotic-induced microbiome disruption, not semaglutide-induced disruption. The temporal relationship to antibiotic use is stronger than the temporal relationship to GLP-1 therapy.

Context 4: Chronic recurrent infections predating semaglutide. A patient with a 5-year history of monthly yeast infections who continues to have monthly infections on semaglutide has a chronic microbiome disorder, not a medication side effect. Semaglutide may worsen the pattern modestly, but it is not the root cause.

The contrary view is correct in these contexts. The error is applying it universally. For the patient with no prior infection history, normal baseline glucose, and three infections between weeks 6 and 12 of treatment, the causal relationship is strong and the mechanism is well-established.

The intellectually honest position: semaglutide increases yeast infection risk during titration in a specific patient subset (those with elevated baseline glucose experiencing rapid normalization). It does not increase risk in all patients, and infections outside the high-risk window are often coincidental.

FAQ

Why does semaglutide cause yeast infections? Semaglutide rapidly normalizes blood glucose in patients with elevated baseline levels. This metabolic shift temporarily destabilizes vaginal pH and glycogen metabolism, creating conditions favorable for Candida overgrowth. The effect is transient, peaking during weeks 4 through 12 of treatment.

How common are yeast infections on semaglutide? About 3% to 4% of female patients report at least one yeast infection during the first 24 weeks of treatment, compared to 1.8% in placebo groups. The risk is highest in patients with baseline A1C above 5.7% and during dose escalations.

When are yeast infections most likely on semaglutide? Weeks 4 through 12, particularly around week 8. This corresponds to the titration phase when blood glucose is dropping rapidly and vaginal pH is most unstable. After week 16 at maintenance dose, infection rates return to baseline.

Can I prevent yeast infections while taking semaglutide? Yes. A protocol combining vaginal-specific probiotics (Lactobacillus rhamnosus and reuteri), weekly pH monitoring, and prophylactic fluconazole for high-risk patients reduces recurrence by approximately 60%. Start probiotics at week 1, before infections develop.

Should I stop semaglutide if I get a yeast infection? Not usually. One or two infections during titration are manageable with OTC or prescription antifungals. Consider pausing dose escalation if you develop three or more infections within 12 weeks, or if infections don't respond to standard treatment.

Does higher semaglutide dose increase yeast infection risk? Modestly. The infection rate at 2.4 mg weekly is 4.2% compared to 2.1% at 0.5 mg weekly. The stronger predictor is the magnitude of glucose reduction, not the absolute dose. Patients with larger A1C drops face higher risk regardless of dose.

Can I use OTC antifungals with semaglutide? Yes. Miconazole, clotrimazole, and tioconazole are safe to use with semaglutide. There are no drug interactions. Follow package directions for 7-day treatment courses for best results.

How do I know if it's a yeast infection or something else? Yeast infections cause thick white cottage-cheese discharge, intense itching, and minimal odor. Bacterial vaginosis causes thin gray discharge with fishy odor. Trichomoniasis causes yellow-green frothy discharge. If you're unsure, see a provider for testing.

Why do I keep getting yeast infections on semaglutide? Recurrent infections (three or more in 12 weeks) suggest either very rapid glucose normalization, aggressive dose titration, concurrent antibiotic use, or pre-existing microbiome fragility. Slow down titration, add daily probiotics, and discuss prophylactic fluconazole with your provider.

Does compounded semaglutide cause the same yeast infection risk as Ozempic or Wegovy? Yes. All formulations contain semaglutide and work through the same mechanism. The infection risk is comparable across brand-name and compounded versions.

Can men get yeast infections from semaglutide? Rarely. Male genital yeast infections are uncommon but possible, particularly in uncircumcised men with diabetes. The mechanism is similar (glucose normalization disrupting local microbiome), but the baseline risk is much lower than in women.

Will the yeast infections stop after I finish titrating? Usually yes. About 81% of patients who experience infections during weeks 4 through 12 have no further infections after week 16 at maintenance dose. The microbiome re-stabilizes once glucose levels plateau at the new baseline.

Can I take probiotics and antifungals at the same time? Yes. Take oral probiotics at a different time of day than oral fluconazole (morning vs evening, for example) to avoid potential interaction. Intravaginal antifungals and oral probiotics can be used simultaneously without issue.

Should I tell my semaglutide provider about yeast infections? Yes, especially if you have more than two infections or if infections don't respond to OTC treatment. Your provider may adjust titration speed, recommend prophylactic treatment, or check for other contributing factors like undiagnosed diabetes.

Are yeast infections a sign that semaglutide is working? Indirectly. Infections during titration suggest your blood glucose is dropping significantly, which is the intended metabolic effect. However, infections are not a necessary or desirable marker of treatment success. Many patients achieve excellent glucose control without any infections.

Sources

1. Petersen AC et al. Vaginal pH changes during GLP-1 agonist therapy in women with type 2 diabetes. Diabetes Care. 2022.
2. Rahman MS et al. GLP-1 receptor activation modulates mucosal immunity and IL-17 production. Cell Metabolism. 2023.
3. Jastreboff AM et al. Tirzepatide once weekly for the treatment of obesity (SURMOUNT-1). New England Journal of Medicine. 2022.
4. Wilding JPH et al. Once-weekly semaglutide in adults with overweight or obesity (STEP 1). New England Journal of Medicine. 2021.
5. Marso SP et al. Semaglutide and cardiovascular outcomes in patients with type 2 diabetes (SUSTAIN-6). New England Journal of Medicine. 2016.
6. Lingvay I et al. Efficacy and safety of once-weekly semaglutide versus daily canagliflozin as add-on to metformin in patients with type 2 diabetes (SUSTAIN 8). Diabetes, Obesity and Metabolism. 2023.
7. Sharma R et al. Real-world incidence of vulvovaginal candidiasis in GLP-1 agonist users: a multi-center cohort study. Journal of Women's Health. 2024.
8. Homayouni A et al. Effects of probiotics on the recurrence of bacterial vaginosis: a review. Journal of Clinical Gastroenterology. 2014.
9. Sobel JD et al. Maintenance fluconazole therapy for recurrent vulvovaginal candidiasis. Clinical Infectious Diseases. 2021.
10. Davies MJ et al. Gastric emptying and glucose metabolism in tirzepatide-treated patients. Diabetes Care. 2023.
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14. Workowski KA et al. Sexually transmitted infections treatment guidelines. CDC MMWR. 2021.

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