Author: FA Manian MD, MPH

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)?

Why should I check serum magnesium level in my patient with hypokalemia in need of potassium replacement?

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

Short answer: Potassium and magnesium are highly intertwined in their physiological roles and magnesium is critical for renal retention of potassium.

Hypomagnesemia increases the release of renin from the kidney, leading to elevated levels of angiotensin II, which stimulates the adrenal cortex to secrete aldosterone. 1,2 The resulting secondary hyperaldosteronism contributes to refractory hypokalemia through increased sodium reabsorption via epithelial sodium channels (ENaC) in the distal nephron.  Increased sodium reabsorption in turn increases the expression and activity of the renal outer medullary potassium (ROMK) channels, which increases potassium secretion into the tubular lumen.1,3 Interestingly, magnesium also directly inhibits ROMK channels which, in the setting of hypomagnesemia, further leads to potassium loss.1,4

Parenthetically, most patients with mild to moderate hypomagnesemia are asymptomatic or have non-specific symptoms such as lethargy, muscle weakness or cramps. So don’t rely on symptoms to decide who should have their serum magnesium checked in the setting of hypokalemia. 5

Last, hypomagnesemia is not uncommon. It is found in 3-10% of general population, 10-30% of patients with type 2 diabetes, 10-60% of hospitalized patients and over 65% of those in the intensive care unit.5   What’s more concerning is that hypomagnesemia is also associated with an elevated risk of death from any cause and death from cardiovascular diseases.5

So, don’t forget to check serum magnesium level in your patient with hypokalemia in need of potassium replacement!

Bonus Pearls: Did you know that many drugs such as proton pump inhibitors (PPIs), thiazide and loop diuretics, aminoglycosides and chemotherapeutic agents are associated with magnesium wasting and hypomagnesemia, while sodium-glucose cotransporter-2 (SGLT2) inhibitors may be associated with increased renal magnesium reabsorption? 5

Contributed by Andy Wu, PhD, Medical Student, St. Louis University Medical School, St. Louis, Missouri

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References

  1. Huang CL, Kuo E. Mechanism of hypokalemia in magnesium deficiency. J Am Soc Nephrol. 2007 Oct;18(10):2649-52. doi: 10.1681/ASN.2007070792. Epub 2007 Sep 5. PMID: 17804670. https://pubmed.ncbi.nlm.nih.gov/17804670/
  2. AlShanableh Z, Ray EC. Magnesium in hypertension: mechanisms and clinical implications. Front Physiol. 2024 Apr 10;15:1363975. doi: 10.3389/fphys.2024.1363975. PMID: 38665599; PMCID: PMC11044701. https://pubmed.ncbi.nlm.nih.gov/38665599/
  3. Valinsky WC, Touyz RM, Shrier A. Aldosterone, SGK1, and ion channels in the kidney. Clin Sci (Lond). 2018 Jan 19;132(2):173-183. doi: 10.1042/CS20171525. PMID: 29352074; PMCID: PMC5817097. https://pubmed.ncbi.nlm.nih.gov/29352074/
  4. Rodan AR, Cheng CJ, Huang CL. Recent advances in distal tubular potassium handling. Am J Physiol Renal Physiol. 2011 Apr;300(4):F821-7. doi: 10.1152/ajprenal.00742.2010. Epub 2011 Jan 26. PMID: 21270092; PMCID: PMC3074996. https://pubmed.ncbi.nlm.nih.gov/21270092/
  5. Touyz RM, de Baaij JHF, Hoenderop JGJ. Magnesium Disorders. N Engl J Med. 2024 Jun 6;390(21):1998-2009. doi: 10.1056/NEJMra1510603. PMID: 38838313. https://pubmed.ncbi.nlm.nih.gov/38838313/

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!

Why should I check serum magnesium level in my patient with hypokalemia in need of potassium replacement?

Should I discontinue the glucagon-like peptide-1 receptor agonist (GLP-1RA) perioperatively in my patient with an upcoming elective surgery?

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

Despite initial concerns, GLP-1RAs need not be categorically discontinued in patients undergoing surgery and, in fact, may be continued safely in most patients.

A December 2024 clinical practice “guidance”—not “guidelines” due to lack of firm evidence—involving several professional societies, including the American Society of Anesthesiologists (ASA) and the American Gastroenterological Association suggests that GLP-1RA therapy may be continued perioperatively in the absence of the following high risk factors: escalation phase of GLP-1RA (vs maintenance phase),1 higher dose, weekly dosing, presence of GI symptoms suggestive of delayed gastric emptying (eg, nausea, vomiting, abdominal pain, dyspepsia, constipation) and medical conditions associated with delayed gastric emptying (eg, gastroparesis, Parkinson’s disease).2

In the presence of one or more of the above risk factors that may contribute to delayed gastric and aspiration perioperatively, withholding GLP-1RAs should be considered.  When balancing the risks and benefits of withholding these drugs, shared decision making involving the patient and members of the care team including the procedural, anesthesia and prescribing providers is prudent.  For example, with discontinuation of GLP-1RAs, one should also consider the possibility of hyperglycemia in patients with diabetes with its potential adverse effects on surgical outcome .1

As far as the timing of discontinuation of GLP1-RAs, ASA recommends holding such drugs on the day of surgery for daily formulations and a week prior to surgery for weekly formulations while maintaining glycemic control. The above “guidance” also recommends assessment for symptoms of delayed gastric emptying on the day of surgery with use of point of care ultrasound (POCUS), if available, to assess degree of delayed gastric emptying.1

It’s worth noting that despite early case reports of pulmonary aspiration of gastric contents in patients on GLP-1RAs undergoing procedural sedation and/or general anesthesia, (3,4) recent larger studies have not substantiated such claims. Interestingly, a 2024 retrospective observational cohort of over 13,000 adults with diabetes found a lower risk of perioperative and postoperative delayed gastric emptying and antiemetic use among patients treated with GLP1-RA compared to non-users; aspiration/pneumonitis and ileus risks within 7 days were not significantly different between the 2 groups. 5

Bonus Pearl: Did you know that scintigraphy via ingestion of a radio-labelled meal is the gold standard for diagnosis of gastroparesis with the 13 C breath test using a solid meal as an acceptable alternative?6

Contributed by Shirley Joo, MD, Internal Medicine Associate Program Director, Mercy Hospital, St. Louis, Missouri

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References

  1. van Zuylen ML, Siegelaar SE, Plummer MP, et al. Perioperative management of long-acting glucagon-like peptide-1 (GLP-1) receptor agonists: concerns for delayed gastric emptying and pulmonary aspiration. Br J Anaesth. 2024;132:644-648. Perioperative management of long-acting glucagon-like peptide-1 (GLP-1) receptor agonists: concerns for delayed gastric emptying and pulmonary aspiration – PubMed
  2. Kindell TL, Wang AY, Wadhwa A, et al. Multisociety clinical practice guidance for the safe use of glucagon-like peptide-1 receptor agonists in the perioperative period. Surgery for Obesity and Related Diseases 2024;20:1183-1186. Multisociety clinical practice guidance for the safe use of glucagon-like peptide-1 receptor agonists in the perioperative period
  3. Klein SR, Hobai    Semaglutide, delayed gastric emptying, and intraoperative pulmonary aspiration: a case report.   Can J Anaesth. 2023;70(8):1394-1396.  Semaglutide, delayed gastric emptying, and intraoperative pulmonary aspiration: a case report – PubMed
  4. Silveira SQ, da Silva  LM, de Campos Vieira Abib  A,  et al.  Relationship between perioperative semaglutide use and residual gastric content: a retrospective analysis of patients undergoing elective upper endoscopy.   J Clin Anesth. 2023;87:111091.  Relationship between perioperative semaglutide use and residual gastric content: A retrospective analysis of patients undergoing elective upper endoscopy – PubMed
  5. Klonoff DC, Kim SH, Galindo RJ, et al. Risks of peri- and postoperative complications with glucagon-like peptide-1 receptor agonists. Diabetes Obes Metab 2024; 26:3128-3138. Risks of peri- and postoperative complications with glucagon-like peptide-1 receptor agonists – PubMed
  6. Ghazanfar H, Allena N, Javed N, Ponnachan D, Narasimhadevara S, Komadur T, et al. Diagnostic Modalities Used in Diagnosing Gastroparesis: A Clinical Review. Cureus. 2022 Oct 21;14(10):e30540. https://pmc.ncbi.nlm.nih.gov/articles/PMC9675943/ 

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 discontinue the glucagon-like peptide-1 receptor agonist (GLP-1RA) perioperatively in my patient with an upcoming elective surgery?

Is it just my imagination or are Covid-19 cases going down as influenza cases are surging out of control during this flu season?

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

No, you are not imagining! Although during respiratory tract infection (RTI) season several viruses such as rhinovirus, respiratory syncytial virus (RSV) and coronavirus may cocirculate, influenza virus frequently outcompetes many RTI viruses, likely through a phenomenon called “viral interference.” 1-4

A negative viral interference is observed when a virus that has already infected a host makes that host resistant to infection by the second virus (isn’t that fascinating?). Although there a lot of virus, host and environmental variables that affect infection risk, potential mechanisms for this interference include a rapid and robust innate immune response to the first virus such as through upregulation of interferon (IFN) production which can protect against unrelated viruses, thereby creating a temporary “antiviral state.” 1-4

A negative viral interference has been shown between influenza-A virus (IAV) and SARS-CoV-2 by a cool 2024 study using the air-liquid interface culture model of the differentiated human airway epithelium. 4 Replicating IAV induced a robust interferon response and suppressed SARS-CoV-2 replication in both sequential and simultaneous infections. In contrast, SARS-CoV-2 did not demonstrate significant viral interference with IAV.  The researchers took their experiment a step further and found that oseltamivir (Tamiflu), an anti-IAV agent, restored SARS-CoV-2 replication with IAV coinfection by reducing induction of IFN!

One explanation for the inability of SARS-CoV-2 to interfere with the production of influenza virus is its slower induction of IFN stimulating genes likely due to its more effective mechanisms of antagonizing the IFN response with infected cells.4 Another explanation is that SARS-CoV-2 has a slower growth rate than IAV, making it more susceptible to being “outgunned” by faster growing viruses. Some strains of IAV may also cause more damage to the epithelial cells than SARS-CoV-2 thus reducing the number of host cells available for SARs-CoV-2 infection.2 Last, secreted IFNs (eg, IFN λ) can also bind to receptors present at the surface of infected and neighboring state blocking the second virus from infecting the host.1

So, it looks like competition among living forms in this world also applies to the world of viruses!

Bonus Pearl: Did you know that the concept of viral interference was first described in the 1960s following observation that oral administration of live enterovirus vaccines decreased detection of several unrelated respiratory viruses such as influenza virus, RSV and human adenovirus?1

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References

  1. Piret J, Bolvin G. Viral interference between respiratory viruses. Emerg Infect Dis 2022;28:273-280. Viral Interference between Respiratory Viruses – PubMed
  2. Gilbert-Girard S, Piret J, Carbonneau J, et al. Viral interference between severe acute respiratory syndrome coronavirus 2 and influenza A viruses. PLOS Pathogens 2024;20(7):e1012017. Viral interference between severe acute respiratory syndrome coronavirus 2 and influenza A viruses – PubMed
  3. Kaaijk P, Swaans N, Nicolaie AM, et al. Contribution of influenza viruses, other respiratory viruses and viral co-infections to influenza-like illness in older adults. Viruses 2022;14, 797. Contribution of Influenza Viruses, Other Respiratory Viruses and Viral Co-Infections to Influenza-like Illness in Older Adults – PubMed
  4. Cheemarla NR, Watkins TA, Mihaylova VT, et al. Viral interference during influenza A-SARS-CoV-2 coinfection of the human airway epithelium and reversal by oseltamivir. J Infect Dis 2024;229:1430-4. Viral Interference During Influenza A-SARS-CoV-2 Coinfection of the Human Airway Epithelium and Reversal by Oseltamivir – 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!

 

 

Is it just my imagination or are Covid-19 cases going down as influenza cases are surging out of control during this flu season?