Author: FA Manian MD, MPH

Should I treat my patient with community-acquired pneumonia (CAP) with adjunctive corticosteroids?

FA Manian MD, MPH, , , , , , , , , , , , , , , , , Leave a comment

It depends! You should consider ACs in immunocompetent patients with severe bacterial CAP in the absence of concurrent influenza, particularly in patients with a very high inflammatory response (eg, serum C-reactive protein [CRP] >150-200 mg/L). 1-13 In contrast, ACs is NOT recommended for patients with non-severe CAP.

Depending on the study, ACs in severe CAP has been associated with improvement in various patient outcomes, including reduced mortality, need for vasopressor or invasive mechanical ventilation, decrease in ICU stay and decrease in hospital length of stay.1-13 Significantly higher risk of hyperglycemia has been reported in the ACs group without demonstrable increase in the risk of upper GI bleed or hospital-acquired infections.2  

Which definition of severe CAP should we use when considering ACs? Unfortunately, it varies but a commonly cited definition is that proposed by the American Thoracic Society/Infectious Diseases Society of America (ATS/IDSA).9  When determining which patients may benefit from ACs, I favor a broader definition of severe CAP through modification of the ATS/IDSA criteria to include several other criteria used in major trials such as the seminal Community-Acquired Pneumonia Evaluation Corticosteroids (CAPE COD) study criteria and the Pneumonia Severity Index. 1-4   According to this “modified ATS/IDSA criteria”, severe CAP is likely in the presence of either one major criterion OR ≥3 minor criteria as detailed below.

Major criteria (1 needed):1. Septic shock with need for vasopressor; 2. Respiratory failure requiring invasive, non-invasive mechanical ventilation or high-flow nasal cannula; OR 3. Pneumonia severity index class IV or V.  Note: high-flow nasal cannula and PSI IV or V have been added to ATS/IDSA criteria

Minor criteria (3 needed):1. Respiratory rate ≥30/min; 2. Pa02/Fi02 ratio ≤250; 3. Multilobar infiltrates; 4. Confusion/disorientation; 5. BUN≥20 mg/dL; 6. Leukopenia (WBC<4,000/uL); 7. Thrombocytopenia (platelet count < 100,000/uL; 8. Hypothermia (core temp <96.8 ⁰ F, 36 ⁰ C); 9. Hypotension requiring aggressive fluid resuscitation.

In addition, a high inflammatory response based on CRP greater than 150-200 mg/L significantly increases the odds of a favorable outcome (eg, reduced mortality) in CAP when ACs is used.2,3,8 In fact, in a meta-analysis involving data-driven analysis of randomized trials, a significant reduction in mortality with ACs was observed only in those with CRP>204 mg/dL (6.1% vs 13%).8  In a subgroup analysis of CAPE COD study, mortality was significantly reduced only in patients with CRP>150 mg/L (risk difference -7.3 %).2  A 2015 study involving only patients with CRP>150 mg/L and meeting ATS/IDSA criteria for severe CAP or PSI class V, treatment failure (composite deterioration/invasive mechanical ventilation and death within 72 h) was significantly lower in the ACs group (13% vs 31%).3   

Collectively, in the absence of any contraindication to corticosteroids or concurrent influenza, the weight of the evidence supports ACs in select patients with severe CAP, particularly when associated with CRP>150 mg/L.  In contrast, for patients with non-severe CAP and presumed lower level of inflammation, the benefit of ACs may not outweigh its risks and is not recommended, unless there are other indications for their use (eg, COPD exacerbation).  For all other patients, including those without severe CAP but with high CRP levels as above or severe CAP with lower CRP levels, ACs should be considered on a case-by-case basis.

When indicated for severe CAP, based on the inclusion criteria used by various clinical trials, ACs should be started as soon as severe CAP is diagnosed, preferably within 24 h.2,13 As for the choice of ACs regimen, no study has proven the superiority of one particular regime vs others.1  The CAPE COD study used IV hydrocortisone 200 mg/day continuous infusion for 4-8 days with taper over total of 8-14 days.2 Some have suggested methylprednisolone 0.5 mg/kg IV q 12 h or “typical doses” of 40-80 mg/day IV methylprednisolone equivalent for 5-7 days.1,3 Yet others have suggested that hydrocortisone 100 mg IV or methylprednisolone 40 mg IV be given in the emergency department as an initial dose when severe CAP is diagnosed. 11 If IV hydrocortisone is selected, a pragmatic approach using 50 mg every 6 hours, similar to that suggested in the management of septic shock by the 2026 Guidelines by the Surviving Sepsis Campaign14 may also be reasonable.

 

Bonus Pearls:

  1. Did you know that despite ready availability of antibiotics, mortality from CAP in hospitalized patients remains high with nearly 50,000 people dying each year in the U.S. alone? top-pneumonia-facts.pdf
  2. Did you know that in addition to their immune modulating action, experimental studies have shown that corticosteroids may decrease global bacterial burden in lung tissue and lead to less extensive pneumonia in piglets15 and significant reduction in intracellular bacterial survival in human monocytes?16 Who would have guessed?  

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References

  1. Chaudhuri D, Nei AM, Rochwerg B, et al. 2024 Focused update: Guidelines on use of corticosteroids in sepsis, acute respiratory distress syndrome, and community-acquired pneumonia. Crit Care Med 2024;52:e129-33. 2024 Focused Update: Guidelines on Use of… : Critical Care Medicine 
  2. Dequin P.-F, Meziani J.-P, Quenot T, et al. Hydrocortisone in severe community-acquire pneumonia. N Engl J Med 2023; 388: 1931-41. Hydrocortisone in Severe Community-Acquired Pneumonia | New England Journal of Medicine 
  3. Torres A, Sibila O, Ferrer M, et al. Effect of corticosteroids on treatment failure among hospitalized patients with severe community-acquired pneumonia and high inflammatory response: A randomized clinical trial. JAMA 2015;313:677-86 .Effect of corticosteroids on treatment failure among hospitalized patients with severe community-acquired pneumonia and high inflammatory response: a randomized clinical trial – PubMed
  4. Metlay JP, Waterer GW. Time to treat severe community-acquired pneumonia with steroids? N Engl J Med 2023; 388:2001-2. Time to Treat Severe Community-Acquired Pneumonia with Steroids? | New England Journal of Medicine
  5. Pitre Ty, Pauley E, Chaudhuri D, et al. Corticosteroids for adult patients hospitalized with non-viral community-acquired pneumonia: a systematic review and meta-analysis. Intensive Care Medicine 2025; 51:917-29. Corticosteroids for adult patients hospitalised with non-viral community-acquired pneumonia: a systematic review and meta-analysis | Intensive Care Medicine | Springer Nature Link
  6. Soumare A, Kapfer T, Botrel T, et al. Systemic corticosteroids, mortality, and infections in pneumonia and acute respiratory distress syndrome. Ann Intern Med 2026; 179L67-80. Systemic Corticosteroids, Mortality, and Infections in Pneumonia and Acute Respiratory Distress Syndrome : A Systematic Review and Meta-analysis – PubMed
  7. Keisham B, Duhan S, Bajaj D, et al. Steroid therapy in community-acquired pneumonia: an updated systematic review and meta-analysis. Heart & Lung 2026;79:102839. Steroid Therapy in Community-Acquired Pneumonia: An Updated Systematic Review and Meta-Analysis – PubMed
  8. Smit JM, Van Der Zee PA, Stoff SCM, et al. Predicting benefit from adjuvant therapy with corticosteroids in community-acquired pneumonia: a data-driven analysis of randomized trials. Lancet Resp Med 2025;13:221-33. Predicting benefit from adjuvant therapy with corticosteroids in community-acquired pneumonia: a data-driven analysis of randomised trials – The Lancet Respiratory Medicine. 
  9. Jones BE, Ramirez JA, Oren E, et al. Diagnosis and management of community-acquired pneumonia. Am J Resp Crit Care 2026;212:24. Jones BE, Ramirez JA, Oren E, et al. Diagnosis and management of community-acquired pneumonia. Am J Resp Crit Care 2026;212:24. – Search
  10. Reyes LF, Morris AC, Serrano-Mayorga C, et al. Community-acquired pneumonia. Lancet 2025;406:2371-88. Community-acquired pneumonia – The Lancet
  11. Long B, Gottlieb M. 2025 guideline updates for community-acquired pneumonia diagnosis and management. Am J Emerg Med 2026;107:16-20. 2025 guideline updates for community-acquired pneumonia diagnosis and management – EM consulte
  12. Confalonleri M, Urbino R, Potena A, et al. Hydrocortisone infusion for severe community-acquired pneumonia: A preliminary randomized study. Am J Respir Crit Care Med 2005;171:242-8. Hydrocortisone Infusion for Severe Community-acquired Pneumonia | American Journal of Respiratory and Critical Care Medicine | Oxford Academic
  13. Pirracchio R, Venkatesh B, Legrand M. Low-dose corticosteroids for critically ill adults with severe pulmonary infections: A review. JAMA 2024;332:318-328.jama_pirracchio_2024_rv_240011_1721328820.09305 give steroids.pdf
  14. Prescott HC, Antonelli M, Alhazzani W, et al. Surviving Sepsis Campaign: International guidelines for management of sepsis and septic shock 2026. Crit Care Med 2026;54:725-812. Surviving Sepsis Campaign: International… : Critical Care Medicine
  15. Sibila O, Luna CM, Agusti C, et al. Effects of glucocorticoids in ventilated piglets with severe pneumonia. Eur Respir J 2008;32:1037-46. Effects of glucocorticoids in ventilated piglets with severe pneumonia | European Respiratory Society
  16. Meduri GU, Kananagat S, Bronze M, et al. Effects of methylprednisolone on intracellular bacterial growth. Clin Diag Lab Immunol 2001;8:1156-63.Effects of Methylprednisolone on Intracellular Bacterial Growth – PMC

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Should I treat my patient with community-acquired pneumonia (CAP) with adjunctive corticosteroids?

Can an oral temperature of 37.4°C (99.4°F) in my 91-year-old patient be considered a fever?

FA Manian MD, MPH, , , , , , , , , , Leave a comment

Yes! The often-cited “normal body temperature” traces back to Carl Wunderlich’s seminal 1868 study, which measured axillary temperatures in thousands of hospitalized patients and reported an average temperature of 98.6°F (37°C), with an upper limit of 100.4°F (38°C).1 However, recent evidence suggests a decline in body temperature of about 0.05°F (0.03°C) per decade over the past 150 years2, prompting us to redefine “normal” temperature.

More specifically, a 2023 study of outpatients (mean age 52.7 years) found a mean oral temperature of 97.95°F (36.6°C) (95% range 96.7°F-99.2°F).3 The study also found that normal oral temperature declines with age, is lower in men than in women, and peaks in the late afternoon. 

Similarly, among non-infected hospitalized patients (mean age 61 years), a 2021 study reported a mean oral temperature of 98.0°F (36.7°C) (99% range 95.8°F-99.9°F),4 and a 2025 study in hospitalized adults concluded that the oral temperature threshold for fever should be 98.4°F (36.9°C) for those ≥85 years old.5

Additionally, the Infectious Diseases Society of America (IDSA) has recommended that for older adults in long-term care facilities, an oral temperature of 99°F (37.2°C) may indicate fever when observed across multiple measurements. 6 It also suggested that the most accurate method for establishing fever in older adults is a temperature elevation of >2°F (>1.1°C) above baseline, though this requires knowledge of the patient’s baseline temperature.6

Potential explanations for the decline in our body temperature—which reflects our basal metabolic rate— over the past 150 years include decreased prevalence of chronic infections (e.g., tuberculosis), improved sanitation, widespread use of anti-inflammatory medications, and even decreased physical activity! 3, 7

So, we should “personalize” the definition of fever and lower its threshold by 0.5°F, or as much as 2.0°F, depending on patient demographics and clinical settings. When repeated and confirmed, an oral temperature of 99.4°F (37.4°C) in our 91-year-old patient should not be automatically dismissed as “normal.” 

 Bonus pearl: Did you know that for his study, Carl Wunderlich measured axillary temperatures— a method now known to be less accurate than oral or rectal measurements— by utilizing a foot-long thermometer that required 20 minutes to register? 8

 

Contributed by Khaled Said, 4th year Medical Student, Ponce Health Sciences University School of Medicine, St. Louis, Missouri 

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References

  1. Mackowiak PA. Concepts of Fever. Arch Intern Med.1998;158(17):1870–1881.
  2. Myroslava P, Catherine L, Joanna L, Trevor H, Julie P. Decreasing human body temperature in the United States since the Industrial Revolution. ELife. 2020; 9:e49555
  3. Ley C, Heath F, Hastie T, Gao Z, Protsiv M, Parsonnet J. Defining Usual Oral Temperature Ranges in Outpatients Using an Unsupervised Learning Algorithm. JAMA Intern Med. 2023;183(10):1128–1135.
  4. Speaker SL, Pfoh ER, Pappas MA, Hu B, Rothberg MB. Oral Temperature of Noninfected Hospitalized Patients. 2021;325(18):1899–1901.
  5. Émond JP, Cheung VW, Brial A, Nguyen QD. Age-Adjusted Oral Temperature Thresholds for Rectal Fever Diagnosis in Hospitalized Older Adults. J Am Med Dir Assoc. 2026;27(2):106044.
  6. Rowe TA, Jump RLP, Andersen BM, et al. Reliability of nonlocalizing signs and symptoms as indicators of the presence of infection in nursing-home residents. Infection Control & Hospital Epidemiology. 2022;43(4):417-426.
  7. Yegian AK, Heymsfield SB, Lieberman DE. Historical body temperature records as a population-level ‘thermometer’ of physical activity in the United States. Curr Biol. 2021;31(20):R1375-R1376.
  8. Haidar G, Singh N. Fever of unknown origin. N Engl J Med. 2022;386(5):463-477.

 

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Can an oral temperature of 37.4°C (99.4°F) in my 91-year-old patient be considered a fever?

How should I interpret serum ferritin and transferrin saturation in my patient with anemia?

FA Manian MD, MPH, , , , , Leave a comment

Let’s start with serum ferritin, an iron containing protein that’s considered the most sensitive and specific noninvasive diagnostic test for evaluating total body iron stores (vs. the gold standard—but invasive— iron staining of bone marrow). 1

Although the optimal ferritin threshold to diagnose iron deficiency (ID) varies, compared to bone marrow iron reserves, levels below 15 ug/L are considered 98% specific and 78% sensitive.2 At a higher cut off of less than 45 ug/L, its sensitivity is 85% with a specificity of 92%.3 So if your patient’s ferritin level is less than 45 ug/L—especially less than 15 ug/L—you can be quite confident that they have ID.  

Argument is often made that ferritin levels may be misleadingly high even in the presence of ID because it is an acute phase reactant and its synthesis is expected to increase in a variety of infectious and non-infectious inflammatory conditions. But this argument can only be taken so far, because ferritin synthesis still depends on the presence of cellular iron, such that even in the presence of inflammation, its levels are unlikely to be more 100 ug/L in patients with low iron stores or “absolute ID”.

Absolute ID should be distinguished from “functional” ID which is associated with adequate iron stores but inadequate iron availability to tissues due to cytokine-mediated hepcidin production and macrophage sequestration of iron. 4

This brings us to another key protein, serum transferrin which transports iron to vital tissues, including the bone marrow.  Transferrin saturation (TSat) is not only low (≤20%) in absolute ID but also in functional ID. 1 This is where a combination of serum ferritin and TSat is helpful. A low TSat combined with a normal or high serum ferritin suggests functional ID with the previously discussed caveat that serum ferritin levels may be normal or elevated—but usually less than 100 ug/L)— in patients with absolute ID and concurrent inflammation.

So in your patient with anemia, after reviewing their serum ferritin and TSat, you should have a good idea of whether they have ID and, if so, whether it’s related to an absolute or functional ID. In another post, I will discuss guidelines on the diagnosis and treatment of functional ID.

Bonus Pearl: Did you know that the commonly-cited difference in the threshold for anemia in males vs females (<13.0 g/dL and <12 g/dL, respectively) by WHO may at least in part be related to unrecognized and untreated ID in the female population studies over 50 years ago? 1

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References

  1. Martens KL, DeLoughery TG. Iron deficiency anemia. Ann Intern Med 2026; 179:1-16. Iron Deficiency Anemia | Annals of Internal Medicine
  2. Hallberg L, Bengtsson C, Lapidus L, et al. Screening for iron deficiency: an analysis based on bone marrow examinations and serum ferritin determinations in a population sample of women. Br. J Haematol 199385:787-798. Screening for iron deficiency: an analysis based on bone-marrow examinations and serum ferritin determinations in a population sample of women. – Abstract – Europe PMC
  3. Rockey DC, Altayar O, Falck-Ytter Y, et al. AGA technical review on gastrointestinal evaluation of iron deficiency. Gastroenterology 2020;159:1097-1119. AGA Technical Review on Gastrointestinal Evaluation of Iron Deficiency Anemia – Gastroenterology
  4. Camaschella C, Girelli D. The changing landscape of iron deficiency. Mol Aspects Med 2020;75:100861. The changing landscape of iron deficiency – PubMed

 

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

 

How should I interpret serum ferritin and transferrin saturation in my patient with anemia?

My hospitalized patient with acute kidney injury and type 2 diabetes is persistently hypoglycemic, likely related to sulfonylurea use. Is there a role for octreotide?

FA Manian MD, MPH, , , , , , , , , , , , , , Leave a comment

Yes, octreotide is indicated in the treatment of sulfonylurea-induced hypoglycemia1.

Sulfonylureas are widely used in the treatment of type 2 diabetes mellitus. Hypoglycemia is a known potential adverse effect which may be prolonged and recurrent, and last for days after ingestion.1,2 The risk is higher in elderly patients, renal or hepatic dysfunction, alcohol use, and polypharmacy, as observed with certain antibiotics.3,4

The mode of action of sulfonylureas is through binding to SUR1 receptors on the pancreatic β-cell membrane which leads to an inhibition of ATP-dependent potassium efflux channels. This results in membrane depolarization, opening voltage-gated calcium channels which in turn triggers insulin release.1 Sulfonylureas are metabolized in the liver and are renally cleared, thus hepatorenal dysfunction can increase the magnitude and duration their action.2  Octreotide binds to somatostatin receptors on pancreatic β-cells, which closes the voltage-gated calcium channels, preventing insulin release.1

Treatment for sulfonylurea-induced hypoglycemia begins with carbohydrate administration, with oral glucose or IV dextrose boluses and infusion.1 Octreotide should be used in acute overdose as well in refractory hypoglycemia.5 In fact, the administration of carbohydrates can cause a transient hyperglycemia which potentiates further insulin release, leading to recurrent rebound hypoglycemia.1

Octreotide can be given subcutaneously or IV with equivalent bioavailability. The typical dose is 50-100 micrograms every 6-12 hours, with 12-72 hours of therapy usually considered adequate. Serum glucose should be closely monitored during treatment and at least for 16-24 hours afterwards. The good news is that octreotide is generally well tolerated, and, in most cases, adverse effects are mild including hyperglycemia, injection site pain, and GI upset.1,2,5

Bonus Pearl:

Did you know that sulfonylureas are also widely used as herbicides? Herbicidal sulfonylureas disrupt the synthesis of branched chain amino acids via inhibition of AHAS, an enzyme present in plants, bacteria, and fungi. There is low toxicity to humans and animals as our bodies lack this enzyme.6

Contributed by Tony Hiran, MD, Mercy Hospital, St. Louis, MO

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References

  1. Dougherty PP, Klein-Schwartz W. Octreotide’s role in the management of sulfonylurea-induced hypoglycemia. J Med Toxicol 2010;6:199-206. doi: 10.1007/s13181-010-0064-z. PMID: 20352540; PMCID: PMC3550273.
  2. Gonzalez RR, Zweig S, Rao J, Block R, Greene LW. Octreotide therapy for recurrent refractory hypoglycemia due to sulfonylurea in diabetes-related kidney failure. Endocr Pract 2007;13:417-23. doi: 10.4158/EP.13.4.417. PMID: 17669721.
  3. Harrigan RA, Nathan MS, Beattie P. Oral agents for the treatment of type 2 diabetes mellitus: pharmacology, toxicity, and treatment. Ann Emerg Med 2001; 38:68-78. doi: 10.1067/mem.2001.114314. PMID: 11423816.
  4. Pearls4Peers. My patient is being treated for a urinary tract infection with trimethoprim-sulfamethoxazole (TMP-SMX) and has developed hypoglycemia — can it be related? Pearls4Peers. 2016 Jul 27. Available from: https://pearls4peers.com/2016/07/27/my-patient-is-being-treated-for-a-urinary-tract-infection-with-trimethoprim-sulfamethoxazole-tmp-smx-and-has-developed-hypoglycemia-can-it-be-related/ [Accessed 1st January 2026].
  5. Glatstein M, Scolnik D, Bentur Y. Octreotide for the treatment of sulfonylurea poisoning. Clin Toxicol (Phila) 2012;50:795-804. doi: 10.3109/15563650.2012.734626. Epub 2012 Oct 10. PMID: 23046209.
  6. Lonhienne T, Garcia MD, Pierens G, Mobli M, Nouwens A, Guddat LW. Structural insights into the mechanism of inhibition of AHAS by herbicides. Proc Natl Acad Sci U S A. 2018;115:E1945-E1954. doi: 10.1073/pnas.1714392115. Epub 2018 Feb 13. PMID: 29440497; PMCID: PMC5834681.

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

My hospitalized patient with acute kidney injury and type 2 diabetes is persistently hypoglycemic, likely related to sulfonylurea use. Is there a role for octreotide?

My patient has painful pustules and nodules in her axillae.  How can I distinguish hidradenitis suppurativa (HS) from folliculitis or recurrent skin abscesses?

FA Manian MD, MPH, , , , , , , , , , , , , , , Leave a comment

A key differentiating factor between hidradenitis suppurativa (HS) and more common conditions such as folliculitis or recurrent abscesses is the location and recurrence pattern of the lesions. HS is clinically diagnosed based on the following typical lesion characteristics:

  • Morphology: open comedones, pustules, painful nodules, abscesses, sinus tracks and scarring; 
  • Distribution: intertriginous or apocrine gland-rich areas, such as the axillae, inframammary folds, lower abdomen/waist, gluteal cleft, groin and inner thighs; and
  • Frequency: recurrent lesions in the same locations, with at least two or more episodes in six months1,2

In contrast, folliculitis involves inflammation of the hair follicle and may present with pustules or boils; however, lesions are superficial, occur anywhere hair is present, and are not complicated by deep nodules, sinus tracks or scarring.2

Although recurrent abscesses may mimic HS, they are typically unilateral or asymmetric, fluctuant and caused by bacterial infection with positive wound cultures. In contrast, HS is frequently a symmetric, sterile inflammatory condition unless secondarily infected. Additionally, abscesses generally respond to incision and drainage and antibiotics and do not result in sinus tracks or scarring.2

Once you suspect HS, your management may be guided by its severity using the following disease stages (Hurley staging).

  • Mild disease (Hurley stage I): localized lesions without sinus tracks or scarring. Treat with antimicrobial washes (chlorhexidine) and topical antibiotics (clindamycin).3
  • Moderate disease (Hurley stage II): typical lesions in multiple locations with or without sinus tracks and scarring. Treat with antimicrobial washes, topical antibiotics, and systemic antibiotics (tetracyclines or clindamycin). Consider adding rifampin, metronidazole, or moxifloxacin in refractory cases.3
  • Severe disease (Hurley stage III): diffuse painful lesions with extensive sinus tracks and scarring. Requires dermatology referral for consideration of biologics (eg, adalimumab), laser, parenteral antibiotics and/or surgical interventions.3

Across all stages of severity, patients should be counseled on smoking cessation, weight loss, diet modification and appropriate pain management.4 Acute flares may be treated with warm compresses, tetracyclines, and intralesional steroids.3 Incision and drainage is reserved for severe, painful lesions as routine drainage could worsen tunneling.5

Bonus Pearl: Did you know the average diagnosis delay for HS is up to 10 years?2 Primary care physicians have a unique position in early recognition and treatment of this debilitating disease.

Contributed by Taylor Lynch, MD, Mercy Hospital-St. Louis, St. Louis, Missouri

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References:

  1. Wieczorek M, and Walecka I. Hidradenitis suppurativa – known and unknown disease. Reumatologia 2016: 56: 337-339. doi:10.5114/reum.2018.80709. https://pubmed.ncbi.nlm.nih.gov/30647478/.
  2. Snyder, CL, Chen XL, Porter ML. Obstacles to early diagnosis and treatment of hidradenitis suppurativa: Current Perspectives on Improving Clinical Management. Clin Cosm Invest Derm 2023;16:1833-1841. doi:10.2147/CCID.S301794. https://pmc.ncbi.nlm.nih.gov/articles/PMC10361090/.
  3. Alikhan A, Sayed C, Alavi A, et al. North American clinical management guidelines for hidradenitis suppurativa: A publication from the United States and Canadian Hidradenitis Suppurativa Foundations: Part II: Topical, intralesional, and systemic medical management. J Am Acad Derm 2019;81:91-101. doi:10.1016/j.jaad.2019.02.068. https://pubmed.ncbi.nlm.nih.gov/30872149/.
  4. Hermak S, and Lev-Tov H. Integrative approaches in the management of hidradenitis suppurativa. J Am Acad Derm 2024;91: S42-S45. doi:10.1016/j.jaad.2024.09.016. https://pubmed.ncbi.nlm.nih.gov/39626999/.
  5. Chawla S, Toale C, Morris M, et al. Surgical management of hidradenitis suppurativa: A narrative review. J Clin Aesth Derm 2022;15: 35-41. https://pubmed.ncbi.nlm.nih.gov/35309275/.

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

My patient has painful pustules and nodules in her axillae.  How can I distinguish hidradenitis suppurativa (HS) from folliculitis or recurrent skin abscesses?

My patient with long standing hypertension and obesity with significant weight loss while on a glucagon-like peptide-1 receptor agonist (GLP-1RA), now has a “borderline” blood pressure. Should I consider adjusting his antihypertensive medication(s)?

FA Manian MD, MPH, , , , , , , , , , , , , , , , Leave a comment

Yes, you may very well need to adjust antihypertensive regimen of patients who have experienced significant weight loss while on GLP-1RAs.1,2  

In the STEP-1 trial evaluating the impact of semaglutide on cardiometabolic risk factors in adults who were overweight or obese, 34.3% of the group receiving semaglutide had either reduction in the dose or cessation of antihypertensive medications, compared to 15.6% in the placebo group.2  In SURMOUNT-1 trial examining the impact of tirzepatide on blood pressure reduction, a significant net reduction of 6.8 mm Hg systolic and 4.2 mm Hg diastolic blood pressure compared to placebo over 72 weeks was found; weight loss accounted for ~70% of systolic or diastolic blood pressure reduction. 2

The need to lower the dose of or discontinue antihypertensive medications in the setting of significant weight loss should not come as a surprise since this phenomenon predates the widespread use of GLP-1RA in obesity. 1,3 However, in addition to their impact on blood pressure through weight loss, GLP-1RAs may  lower blood pressure through alternative  mechanisms, including natriuresis, direct vasodilation and reduction in sympathetic nervous system activity.4  It’s also important to remember that GLP-1RAs may reduce both systolic and diastolic blood pressures in patients with hypertension even before significant weight loss is observed! 5

But it’s not just about antihypertensive medications!  The use of GLP-1RAs with its attendant weight loss may also require dosage adjustment or discontinuation of several other commonly prescribed medications (eg, insulin, levothyroxine, and anticonvulsants, phenytoin, warfarin, lithium carbonate, and digoxin).2 So don’t forget to regularly review the medication list of patients who have experienced recent weight loss on GLP-1RAs!

Bonus Pearl:  Did you know that the concept of incretin effect was first proposed in the 1970s based on observations that insulin secretion was 2-3 times higher after oral glucose intake than that after intravenous glucose administration? 5

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References

  1. Manian FA. Antihypertensive medications in patients with weight loss. JAMA Intern Med 2025;185:475. Antihypertensive Medications in Patients With Weight Loss | JAMA Internal Medicine | JAMA Network
  2. Karakus KE, Shah VN, Akturk HK. Tirzepatide-induced rapid weight loss-related thyrotoxicosis. JAMA Intern Med 2024;184:1246-1247. Tirzepatide-Induced Rapid Weight Loss–Related Thyrotoxicosis | Lifestyle Behaviors | JAMA Internal Medicine | JAMA Network
  3. Shantha GPS, Kumar AA, Kahan S, et al. intentional weight loss and dose reductions of antihypertensive medications: a retrospective cohort study. Cardiorenal Med 2013;3:17-25. Intentional weight loss and dose reductions of antihypertensive medications: a retrospective cohort study – PubMed
  4. Lingway I, Mosenzon O, Brown K, et al. Systolic blood pressure reduction with tirzepatide in patients with type 2 diabetes: insights from SURPASS clinical program. Cardiovasc Diabetol 2023;22:66. Systolic blood pressure reduction with tirzepatide in patients with type 2 diabetes: insights from SURPASS clinical program – PubMed
  5. Liu QK. Mechanisms of action and therapeutic applications of GLP-1 and dual GIP/GLP-1 receptor agonists. Front Endocrinol 2024; 15:1431292. Frontiers | Mechanisms of action and therapeutic applications of GLP-1 and dual GIP/GLP-1 receptor agonists

Disclosures/Disclaimers: Reference 1 was written by this contributor. The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

My patient with long standing hypertension and obesity with significant weight loss while on a glucagon-like peptide-1 receptor agonist (GLP-1RA), now has a “borderline” blood pressure. Should I consider adjusting his antihypertensive medication(s)?

“My patient with severe hypothyroidism developed a large pericardial effusion. What is the pathophysiology underlying this process?”

FA Manian MD, MPH, , , , , , , , , , , , , Leave a comment

Pericardial effusion in hypothyroidism—responsible for up to 14% of all pericardial effusions¹⁻²—is thought to be related to an increase in permeability of the pericardial capillaries to serum proteins (eg, albumin) resulting in an exudative effusion.³   Increased capillary permeability may in turn be due to the release of histamine by mastocytes or a direct effect of thyroid hormone deficiency on vascular endothelial integrity. ¹⁻³ In addition, hypothyroidism can be associated with pulmonary hypertension and a decrease in catecholamines, both of which can impair lymphatic drainage and further exacerbate the effusion.¹

Of note, myxedema — the accumulation of acid mucopolysaccharides causing fluid retention –– by itself does not explain the accumulation of pericardial fluid, as there is a lack of acid mucopolysaccharide buildup in the pericardial space.¹⁻² Autoimmune processes also do not appear to play a role in this context as pericardial disease can occur in both autoimmune (eg, Hashimoto thyroiditis) and non-autoimmune hypothyroidism.¹ Thus, the pericardial effusion in hypothyroidism seems to be a direct consequence of the metabolic effects of thyroid hormone deficiency itself. 

Occasionally, pericardial effusion in hypothyroidism is not so “benign” and can be complicated by tamponade.¹ In addition to timely percutaneous or surgical drainage of the effusion, thyroid hormone supplementation should be initiated without delay. ¹⁻² Although most pericardial effusions resolve over several months with adequate thyroid supplementation, they may recur in severe or chronically untreated hypothyroidism due to persistent alterations in the pericardial vascular permeability and impaired lymphatic drainage. ¹⁻³ This is another reason to remind patients to not go off their thyroid supplementation!

Bonus pearl: Did you know that the attendant increase in metabolic demands, plasma volume and higher levels of thyroxine-binding globulin in pregnancy necessitates routine upward titration of levothyroxine in pregnant patients with hypothyroidism? ⁵

Contributed by: Sarah de la Serna, Ponce Health Sciences University, St. Louis, MO and Tony Hiran, MD, Mercy Hospital, St. Louis, MO

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References

  1. Chahine J, Ala CK, Gentry JL, Pantalone KM, Klein AL. Pericardial diseases in patients with hypothyroidism. Heart. 2019 Jul;105(13):1027-1033. doi: 10.1136/heartjnl-2018-314528. Epub 2019 Apr 4. PMID: 30948517. Pericardial diseases in patients with hypothyroidism – PubMed
  2. Chaker L, Papaleontiou M. Hypothyroidism: A Review. JAMA. Published online September 03, 2025. doi:10.1001/jama.2025.13559. Hypothyroidism: A Review | Endocrinology | JAMA | JAMA Network
  3. González Vílchez F, Castillo L, Pi J, Ruiz E. Manifestaciones cardíacas del hipotiroidismo primario. Factores determinantes y respuesta al tratamiento [Cardiac manifestations of primary hypothyroidism. Determinant factors and treatment response]. Rev Esp Cardiol. 1998 Nov;51(11):893-900. Spanish. PMID: 9859712. [Cardiac manifestations of primary hypothyroidism. Determinant factors and treatment response] – PubMed
  4. Kerber RE, Sherman B. Echocardiographic evaluation of pericardial effusion in myxedema. Incidence and biochemical and clinical correlations. Circulation. 1975 Nov;52(5):823-7. doi: 10.1161/01.cir.52.5.823. PMID: 126121. Echocardiographic evaluation of pericardial effusion in myxedema. Incidence and biochemical and clinical correlations – PubMed
  5. Alexander EK, Pearce EN, Brent GA, et al. 2017 Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and the Postpartum. Thyroid : Official Journal of the American Thyroid Association. 2017;27(3):315-389. doi:10.1089/thy.2016.0457. 2017 Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and the Postpartum – PubMed

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

“My patient with severe hypothyroidism developed a large pericardial effusion. What is the pathophysiology underlying this process?”

In my patient with iron deficiency anemia (IDA), should I prescribe daily or every other day oral iron supplementation?    

FA Manian MD, MPH, , , , , , , , Leave a comment

Oral iron supplementation dosed every 48 hours is preferred over a daily regimen for at least 2 reasons: higher absorption and better tolerability. Improved absorption is due to an increase in hepcidin after oral intake of iron that lasts up to 48 hours which, paradoxically, also results in blocking further iron absorption during that period. In fact, a study comparing consecutive-day versus alternate-day dosing of oral iron supplementation found the fractional iron absorption to be 40-50% higher in alternate-day dosing.1

As for tolerability, the most frequent side effect of oral iron is gastrointestinal in nature, including nausea, vomiting, diarrhea, and constipation which are related to: 1. Excess amounts of unabsorbed iron leading to inflammation in the gut; and 2. An increase in the production of free radicals and peroxidation in the gut.2 Not surprisingly, alternate-day dosing has been shown to result in less side effects due to higher fractional iron absorption – leading to reduced levels of unabsorbed iron in the gut.3

Understanding the importance of optimal dosing regimen for oral iron supplementation is more than an academic exercise. Iron deficiency is the number one nutritional deficiency globally, affecting 30% of the world’s population.4 The most common causes are gastrointestinal blood loss and menstrual cycle blood loss, followed by a decrease in dietary fiber intake and decreased iron absorption. Undoubtedly, many providers will encounter patients with iron deficiency in need of oral supplementation. To increase both efficacy and compliance of oral iron supplementation, providers should consider every other day (every 48 h) dosing of oral iron in preference to daily dosing. 

Bonus Pearl:  Did you know that heme sources of iron from animals (eg, red meat, liver or kidney) are usually more bioavailable than their non-heme counterparts (eg, from green leafy vegetables) except for blackstrap molasses which has high iron content as well as exceptionally high bioavailability?5,6 

Contributed by Morgan Walters, DO, Internal Medicine Resident, Mercy Hospital-St. Louis, St. Louis, Missouri 

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References: 

  1. Stoffel N, Zeder C, Brittenham G, et al. Iron absorption from supplements is greater with alternate day than with consecutive day dosing in iron-deficient anemic women. Haematologica. 2020 May;105(5):1232-1239. doi: 10.3324/haematol.2019.220830.  Epub 2019 Aug 14. https://pubmed.ncbi.nlm.nih.gov/32650997/
  2. DeLoughery T, Jackson C, Ko C, et al. AGA Clinical Practice Update on management of Iron Deficiency Anemia: Expert Review. Clinical Gastroenterology and Hepatology 2024;22:1575–1583. Doi:0.1016/j.cgh.2024.03.046.  https://pubmed.ncbi.nlm.nih.gov/38864796/
  3. Stoffel N, Zeder C, Brittenham G, et al. Iron absorption from supplements is greater with alternate day than with consecutive day dosing in iron-deficient anemic women Haematologica. 2020 May;105(5):1232-1239. doi: 10.3324/haematol.2019.220830.  Epub 2019 Aug 14. https://pubmed.ncbi.nlm.nih.gov/32650997/
  4. Kumar A, Sharma E, Marley A, et al. Iron deficiency anaemia: pathophysiology, assessment, practical management. BMJ Open Gastro 2022;9:e000759. doi:10.1136/bmjgast-2021-000759. https://pubmed.ncbi.nlm.nih.gov/34996762/
  5. Brittany Lubeck, MS. “Is Molasses Healthy? What to Know about This Sweetener.” Verywell Health, May 10, 2024. https://www.verywellhealth.com/molasses-8640108.
  6. Hamlett, C. (2024, March 22). Meet Blackstrap Molasses: The “best source” of plant-based Iron. Plant Based News. https://plantbasednews.org/lifestyle/health/blackstrap-molasses-is-an-iron-rich-nutritional-powerhouse/ 

 

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

In my patient with iron deficiency anemia (IDA), should I prescribe daily or every other day oral iron supplementation?    

“My patient with severe Crohn’s disease is found to have an elevated serum lipase without other supportive evidence of pancreatitis. What other sources of elevated lipase should I consider?” 

FA Manian MD, MPH, , , , , , , , , , , , , , , , , , , Leave a comment

Over 20 different conditions have been linked to elevated serum lipase levels or hyperlipasemia associated with conditions other than pancreatitis. The most common causes are sepsis and acute kidney injury, but less common causes include gastrointestinal bleeding, liver disease, and type 2 diabetes mellitus, and inflammatory bowel disease.1   More specifically, up to 9% of patients with Crohn’s disease may have hyperlipasemia, often associated with a more extensive and active disease.2  

Recall that hyperlipasemia is one of the hallmarks of acute pancreatitis (serum lipase greater than 3-5x the upper limit of normal) but, as noted above, it is not 100% specific for this condition.  Although pancreatic tissue has a 50-to-100-fold greater lipase activity than other organs in the gastrointestinal tract,3 serum amylase may also be elevated in diseases involving salivary glands, stomach, heart, skeletal muscle, white and brown adipose tissue, and even the brain.1 This finding should come as no surprise since, as an enzyme, lipase metabolizes triglycerides into glycerol and free fatty acids and plays a key role in the metabolism and transport of lipids into peripheral tissues. 4   

Last, despite potential extra-pancreatic sources, serum lipase is still preferred over amylase in diagnosing pancreatitis due to its higher specificity and sensitivity. 5  

Bonus Pearl: Did you know that increased intracranial pressure, including intracerebral hemorrhage, edema, and tumors may also be associated with elevated serum lipase levels? 6 

Contributed by Charles Hurth, D.O., Mercy Hospital, St. Louis, Missouri

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References: 

  1. Feher KE, Tornai D, Vitalis Z, Davida L, Sipeki N, Papp M. Non-pancreatic hyperlipasemia: A puzzling clinical entity. World J Gastroenterol. 2024 May 21;30(19):2538-2552. doi: 10.3748/v30.i19.2538. PMID: 38817657; PMCID: PMC11135416. https://pmc.ncbi.nlm.nih.gov/articles/PMC11135416/#B33  
  2. Heikius B, Niemelä S, Lehtola J, Karttunen TJ. Elevated pancreatic enzymes in inflammatory bowel disease are associated with extensive disease. Am J Gastroenterol. 1999 Apr;94(4):1062-9. doi: 10.1111/j.1572-0241.1999.x. PMID: 10201484. https://pubmed.ncbi.nlm.nih.gov/10201484/ 
  3. Tetrault GA. Lipase activity in serum measured with Ektachem is often increased in nonpancreatic disorders. Clin Chem. 1991 Mar;37(3):447-51. PMID: 1706233. https://pubmed.ncbi.nlm.nih.gov/1706233/
  4. Wang H, Eckel RH. Lipoprotein lipase in the brain and nervous system. Annu Rev Nutr. 2012 Aug 21;32:147-60. doi: 10.1146/annurev-nutr-071811-150703. Epub 2012 Apr 23. PMID: 22540257; PMCID: PMC4065112. https://pmc.ncbi.nlm.nih.gov/articles/PMC4065112/
  5. Tenner S, Vege SS, Sheth SG, Sauer B, Yang A, Conwell DL, Yadlapati RH, Gardner TB. American College of Gastroenterology Guidelines: Management of Acute Pancreatitis. Am J Gastroenterol. 2024 Mar 1;119(3):419-437. doi: 10.14309/ajg.0000000000002645. Epub 2023 Nov 7. PMID: 38857482. https://pubmed.ncbi.nlm.nih.gov/38857482/
  6. Larson GM, Koch S, O’Dorisio TM, Osadchey B, McGraw P, Richardson JD. Gastric response to severe head injury. Am J Surg. 1984 Jan;147(1):97-105. doi: 10.1016/0002-9610(84)90041-2. PMID: 6691557. https://pubmed.ncbi.nlm.nih.gov/6691557/

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

“My patient with severe Crohn’s disease is found to have an elevated serum lipase without other supportive evidence of pancreatitis. What other sources of elevated lipase should I consider?” 

What is the role of measuring serum uric acid level in my patient with hyponatremia suspected of having syndrome of inappropriate antidiuretic hormone secretion (SIADH)?

FA Manian MD, MPH, , , , , , , , , , , Leave a comment

The utility of checking serum uric acid (SUA) in hyponatremia primarily stems from the fact that it helps distinguish SIADH from volume contraction as the cause of hyponatremia.1 Whereas hyperuricemia commonly accompanies volume contraction, hypouricemia is found in the majority (70%) of patients with SIADH.2 This finding is caused by increased urinary excretion of SUA in patients with SIADH.3

There are several potential mechanisms for the association of SIADH with hypouricemia. First, the expanded vascular volume in these patients enhances UA clearance by decreasing its reabsorption, as supported by improved UA serum levels in SIADH patients on fluid restriction.4 Of note, UA normalization with fluid restriction is more pronounced in chronic SIADH patients compared to healthy individuals acutely volume overloaded via treatment with synthetic ADH (i.e. desmopressin).5 This may be due to the fact that, unlike endogenous ADH, desmopressin is a selective agonist of vasopressin 2 receptors (V2R), promoting water reabsorption in the collecting duct without binding to vasopressin 1 receptors (V1R), which promotes UA secretion and inhibits UA reabsorption in the proximal tubule.5,6  To make things worse, there is also evidence that chronic hyponatremia induced by SIADH can directly promote UA excretion!7

Last, keep in mind that salt-wasting disease, a less common cause of hyponatremia, may also be associated with hypouricemia. However, in contrast to patients with SIADH, UA excretion remains high and serum UA levels remain low in these patients even after their hyponatremia is corrected. 8

Bonus Pearl: Did you know that tolvaptan, a selective ADH (V2R) antagonist, has been shown to be effective in raising serum sodium and UA levels in SIADH patients with the caveat that its chronic use may also cause hyperuricemia? 9,10

Contributed by Stella Hoft, PhD, Medical Student, St. Louis University Medical School, St. Louis, Missouri

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References

  1. Liamis G, Christidis D, Alexandridis G, Bairaktari E, Madias NE, Elisaf M. Uric acid homeostasis in the evaluation of diuretic-induced hyponatremia. J Investig Med. 2007 Jan;55(1):36-44. doi: 10.2310/6650.2007.06027. PMID: 17441410. https://journals.sagepub.com/doi/10.2310/6650.2007.06027?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed
  2. Decaux G, Musch W. Clinical laboratory evaluation of the syndrome of inappropriate secretion of antidiuretic hormone. Clin J Am Soc Nephrol. 2008 Jul;3(4):1175-84. doi: 10.2215/CJN.04431007. Epub 2008 Apr 23. PMID: 18434618. https://journals.lww.com/cjasn/abstract/2008/07000/clinical_laboratory_evaluation_of_the_syndrome_of.38.aspx
  3. Li R, Wu B, Han M, Li M, Yang X, Zhang J, Zhang Y, Liu Y. Uric Acid Metabolic Disorders in Pituitary-Target Gland Axis. Diabetes Metab Syndr Obes. 2024 Feb 7;17:661-673. doi: 10.2147/DMSO.S448547. PMID: 38343584; PMCID: PMC10859102. https://www.dovepress.com/uric-acid-metabolic-disorders-in-pituitary-target-gland-axis-peer-reviewed-fulltext-article-DMSO
  4. Beck LH. Hypouricemia in the syndrome of inappropriate secretion of antidiuretic hormone. N Engl J Med. 1979 Sep 6;301(10):528-30. doi: 10.1056/NEJM197909063011005. PMID: 460306. https://www.nejm.org/doi/abs/10.1056/NEJM197909063011005
  5. Decaux G, Namias B, Gulbis B, Soupart A. Evidence in hyponatremia related to inappropriate secretion of ADH that V1 receptor stimulation contributes to the increase in renal uric acid clearance. J Am Soc Nephrol. 1996 May;7(5):805-10. doi: 10.1681/ASN.V75805. PMID: 8738818. https://journals.lww.com/jasn/abstract/1996/05000/evidence_in_hyponatremia_related_to_inappropriate.23.aspx
  6. Taniguchi K, Tamura Y, Kumagai T, Shibata S, Uchida S. Stimulation of V1a receptor increases renal uric acid clearance via urate transporters: insight into pathogenesis of hypouricemia in SIADH. Clin Exp Nephrol. 2016 Dec;20(6):845-852. doi: 10.1007/s10157-016-1248-x. Epub 2016 Mar 2. PMID: 26935049. https://link.springer.com/article/10.1007/s10157-016-1248-x
  7. Decaux G, Prospert F, Soupart A, Musch W. Evidence that chronicity of hyponatremia contributes to the high urate clearance observed in the syndrome of inappropriate antidiuretic hormone secretion. Am J Kidney Dis. 2000 Oct;36(4):745-51. doi: 10.1053/ajkd.2000.17623. PMID: 11007676. https://www.ajkd.org/article/S0272-6386(00)08495-X/ppt
  8. Momi J, Tang CM, Abcar AC, Kujubu DA, Sim JJ. Hyponatremia-what is cerebral salt wasting? Perm J. 2010 Summer;14(2):62-5. doi: 10.7812/TPP/08-066. PMID: 20740122; PMCID: PMC2912080. https://www.thepermanentejournal.org/doi/10.7812/TPP/08-066
  9. Nagamine T. Uric acid levels with tolvaptan treatment for syndrome of inappropriate antidiuretic hormone secretion. Endocrine. 2024 Mar;83(3):826-827. doi: 10.1007/s12020-023-03612-3. Epub 2023 Nov 20. PMID: 37982946. https://link.springer.com/article/10.1007/s12020-023-03612-3
  10. Bondanelli M, Aliberti L, Gagliardi I, Ambrosio MR, Zatelli MC. Long-term low-dose tolvaptan efficacy and safety in SIADH. Endocrine. 2023 Nov;82(2):390-398. doi: 10.1007/s12020-023-03457-w. Epub 2023 Jul 28. PMID: 37507553; PMCID: PMC10543144. https://link.springer.com/article/10.1007/s12020-023-03457-w

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

What is the role of measuring serum uric acid level in my patient with hyponatremia suspected of having syndrome of inappropriate antidiuretic hormone secretion (SIADH)?