© 2017 by Richard Matthews DC DACNB. Proudly created with Wix.com

To Schedule An Appointment

Call 888-516-1533​

September 13, 2017

September 5, 2017

Please reload

Recent Posts

I'm busy working on my blog posts. Watch this space!

Please reload

Featured Posts

All About Prednisone!

September 5, 2017

Prednisone: For a friend in need but a foe indeed

 

Prednisone, a synthetic corticosteroid drug, is perhaps the best example of a mixed blessing at best. It is an immunosuppressant commonly prescribed for many conditions, ranging from migraines to some cancers. It is also used after traumatic injuries, organ transplant surgery, to treat some ear problems and many gut problems. The most common uses for Prednisone are inflammatory and autoimmune conditions, both situations where the immune system is too active.

 

One aspect of intestinal function that defines inflammation during inflammatory or autoimmune disease is intestinal permeability. Our intestinal membranes are highly evolved to regulate the passage of some molecules and not others. Specific molecules form what are called “tight junctions” between the cells of the intestinal wall, and some molecules such as Zonulin specifically regulate permeability. If intestinal permeability increases and molecules of food are absorbed before digestion, the immune system may generate an antibody response, resulting in a food sensitivity that can cause ongoing inflammation if consumption is repeated. Prednisone is often used to treat conditions such as Crohn's disease, because the drug can inhibit the inflammatory cascade, specifically cytokines such as Tumor Necrosis Factor Alpha (or TNF-α) and others. Researchers have shown that while Prednisone can reduce intestinal permeability and bring some relief (Wild), using probiotics instead will also restore tight junction proteins such as Zonulin and Occludin (White). This makes the improvement both less risky and longer-lasting, as the probiotics improved the intestinal gut bacteria as well and these symbiont organisms help tame the immune system.

 

While Prednisone seems to provide relief or improvement with perhaps the widest range of problems of any class of drug, this improvement often is short-lived as side effects more severe than the initial problems can occur quite frequently. Many people on long-term Prednisone therapy find that it is quite challenging to reverse its adverse effects.

 

To understand the issues with Prednisone, it is important to first understand what glucocorticoids are and how they work. Naturally occurring glucocorticoids in the body activate receptors on cells, altering their glucose use and balance. This is part of how the autonomic nervous system addresses the needs of each cell in response to “fight or flight” stimuli, or simply to adjust for changes in activity and energy needs. In addition to regulating the glucose metabolism of virtually every cell in the body, glucocorticoids regulate immune function and some aspects of .

 

Cortisol is one example of a naturally occurring glucocorticoid, and is critical to the regulation of cell metabolism, immune function, circulation, and overall health. This natural glucocorticoid is also produced in response to stressful stimuli, by the adrenal glands located on the kidneys. If a person is stressed for too long a time, then adrenal fatigue and autonomic dysfunction can occur. Since cortisol is important for so many aspects of function and homeostasis, it is easy to see why stress is quite harmful to overall health!

 

Because Prenisone activates the same systems, its effects are quite profound. This is also why the side effects of Prednisone extend from bone loss to diabetes. Bone is constantly being “remodeled” according to physical forces such as gravity and muscle exertion. Cells called osteoblasts are tasked with laying down more bone mineralization, while osteoclasts remove minerals from bone where it isn't needed as much. This remodeling is called “Wolff's Law” after Dr. Julius Wolff, who observed the pattern of mineralization in the 19th century. Even low-dose Prednisone causes osteoporosis (Ton, Shah) and osteoporosis is a common side effect (Mitra, Shah) often resulting in bone fractures (Curtis). It is estimated that 20% of osteoporosis cases are secondary to glucocorticoid exposure (Mitra).

 

A process similar to Wolff's Law occurs with cartilage, as chrondrocytes grow more cartilage and physical processes of wear and tear reduce the cartilage. There exists a balance in healty individuals such that chondrocytes replace the cartilage that was used/eroded, and joints remain healthy. Prednisone alters this balance by altering how cartilage is formed, with different types of collagen that mimic aging cartilage forming (Dearden). The result is weaker cartilage that is more prone to injury. Prednisone eventually results in death (apoptosis) of chondrocytes, making the joint unable to repair the damage that results from normal “wear and tear”, with early joint degeneration being the outcome (Liu). A similar problem occurs with tendons, sometimes resulting in tendon rupture (deWolf).

 

The brain is also the site of Prednisone's unwelcome side effects, including reduced memory (Keenan, Fietta), mania, depression and suicidality (Fietta), psychosis, panic and delirium (Judd, Stojan). While these effects appear to often be reversible, they can also lead to more prescription medications to treat the symptoms, moving the patient further from a normal condition of homeostasis.

 

Another aspect of bone health that is affected by synthetic glucocorticoids such as Prednisone include osteonecrosis, or literally translated “bone death.” This condition occurs when a portion of bone no longer receives its blood supply—a side effect that makes sense when one considers that natural glucocorticoids normally help regulate blood supply to different body parts. Osteonecrosis is also called Avascular Necrosis, with the term “avascular” meaning “without blood circulation. Steroids, such as Prednisone are the most common cause of osteonecrosis (El Gamal). This can even occur with short-term low dose treatments (Kennedy).

 

Continued use of Prednisone or other synthetic glucocorticoids can also result in problems such as dependence, cataracts, and Cushingoid syndrome (a syndrome characterized by weight gain, fluid retention, central/abdominal weight gain, redness in the face and a full palette of additional symptoms. Medication is the most common cause, followed by tumors that produce hormones (https://en.wikipedia.org/wiki/Cushing%27s_syndrome)

 

Prednisone has been found to increase the risk of intestinal/digestive tract ulceration or perforation, particularly in some circumstances. This constitutes a potentially life-threatening complication, as a perforation allows gastrointestinal contents to enter the abdominal space, where sepsis or peritonitis can occur. For example, patients taking NSAID medication and also taking Prednisone have a seven-fold increased risk of gastrointestinal bleeding (ACG). There is also a strong association with perforated peptic ulcers in children being treated with Prednisone (Bickler). In a similar fashion, steroids increase the risk of upper gastrointestinal complications in adults, particularly when used with NSAIDS (Hernandez-Diaz). A common medical strategy to reduce the chances of a perforated ulcer is to block stomach acid production with an antacid (Boland). While this does reduce the chances of perforation, stomach acidity is needed for protein digestion (Berg). In addition, adding a proton pump inhibitor (acid blocker) results in dysbiosis of the small intestine and small intestinal bacterial overgrowth, itself a chronic debilitating condition (Fujimori).

 

Often discounted by physicians but critical for patients are the very common side effects of prednisone which include alteration to immune function, facial rounding, hirsutism (unwanted excess hair growth), lower carbohydrate tolerance, insomnia, restlessness, weakness, brain fog, acne, increased skin pigmentation and abdominal distress (Bollet).

 

In summary, Prednisone and other glucocorticoids are some of the most predictably dangerous drugs we have, and they should be used with extreme discretion and only if no safer alternative approaches are available. Natural alternatives should be used first in all but the most acute and critical of circumstances.

 

References:

ACG: “Ulcers and Gastrointestinal Bleeding: Protecting your Health” from American College of Gastroenterology http://s3.gi.org/patients/pdfs/ulcerprotect.pdf

 

Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition. New York: W H Freeman; 2002. Section 23.1, Proteins Are Degraded to Amino Acids. Available from: https://www.ncbi.nlm.nih.gov/books/NBK22600/

 

The risk benefit ratio of glucocorticoids in SLE: have things changed over the past 40 years?

Stojan G, Petri M.

Curr Treatm Opt Rheumatol. 2017 Sep;3(3):164-172. doi: 10.1007/s40674-017-0069-8. Epub 2017 Jul 27.

 

Randomized, controlled trial evaluating the effect of multi-strain probiotic on the mucosal microbiota in canine idiopathic inflammatory bowel disease.

White R, Atherly T, Guard B, Rossi G, Wang C, Mosher C, Webb C, Hill S, Ackermann M, Sciabarra P, Allenspach K, Suchodolski J, Jergens AE.

Gut Microbes. 2017 Jul 5:1-16. doi: 10.1080/19490976.2017.1334754. [Epub ahead of print]

 

Rate of Adverse Effects of Medium- to High-Dose Glucocorticoid Therapy in Systemic Lupus Erythematosus: A Systematic Review of Randomized Control Trials.

Sciascia S, Mompean E, Radin M, Roccatello D, Cuadrado MJ.

Clin Drug Investig. 2017 Jun;37(6):519-524. doi: 10.1007/s40261-017-0518-z. Review.

 

Bilateral Osteonecrosis of the Femoral and Humeral Heads after Short Term Corticosteroid Therapy. A Case Study.

El Gamal TA, El-Bakoury A, Hawkins A, Ed AlTayeb Mussa M, Er Ahmed Sweed T, Eh Samir Ansara S.

Ortop Traumatol Rehabil. 2016 Mar 23;18(2):187-190. doi: 10.5604/15093492.1205026.

 

Avascular necrosis after oral corticosteroids in otolaryngology: Case report and review of the literature.

Kennedy P, Bassiouni A, Psaltis A, Antisdel J, Brunworth J.

Allergy Rhinol (Providence). 2016 Jan;7(1):50-4. doi: 10.2500/ar.2016.7.0142.

Free PMC Article

 

What are the effects of proton pump inhibitors on the small intestine?

Fujimori S.

World J Gastroenterol. 2015 Jun 14;21(22):6817-9. doi: 10.3748/wjg.v21.i22.6817. Review.

Free PMC Article

 

Adverse consequences of glucocorticoid medication: psychological, cognitive, and behavioral effects.

Judd LL, Schettler PJ, Brown ES, Wolkowitz OM, Sternberg EM, Bender BG, Bulloch K, Cidlowski JA, de Kloet ER, Fardet L, Joëls M, Leung DY, McEwen BS, Roozendaal B, Van Rossum EF, Ahn J, Brown DW, Plitt A, Singh G.

Am J Psychiatry. 2014 Oct;171(10):1045-51. doi: 10.1176/appi.ajp.2014.13091264. Erratum in: Am J Psychiatry. 2014 Nov 1;171(11):1224.

 

Autophagy in human articular chondrocytes is cytoprotective following glucocorticoid stimulation.

Liu N, Wang W, Zhao Z, Zhang T, Song Y.

Mol Med Rep. 2014 Jun;9(6):2166-72. doi: 10.3892/mmr.2014.2102. Epub 2014 Apr 1.

Free PMC Article

 

Adverse effects of corticosteroids on bone metabolism: a review.

Mitra R.

PM R. 2011 May;3(5):466-71; quiz 471. doi: 10.1016/j.pmrj.2011.02.017. Review.

 

Distal humeral fracture with associated triceps tendon avulsion in a renal transplant recipient.

Gupta RR, Murthi AM.

Orthopedics. 2010 Mar;33(3). doi: 10.3928/01477447-20100129-26. Epub 2010 Mar 10.

 

Central nervous system effects of natural and synthetic glucocorticoids.

Fietta P, Fietta P, Delsante G.

Psychiatry Clin Neurosci. 2009 Oct;63(5):613-22. doi: 10.1111/j.1440-1819.2009.02005.x. Review.

Free Article

 

Prednisone-induced osteoporosis: an overlooked and undertreated adverse effect.

Shah SK, Gecys GT.

J Am Osteopath Assoc. 2006 Nov;106(11):653-7.

 

[Spontaneous bilateral rupture of the Achilles tendon in an elderly woman undergoing prednisone pulse therapy with a history of polymyalgia rheumatica].

de Wolf MM, van der Krans A, Frijns CJ.

Ned Tijdschr Geneeskd. 2006 Sep 30;150(39):2155-8. Dutch.

 

Population-based assessment of adverse events associated with long-term glucocorticoid use.

Curtis JR, Westfall AO, Allison J, Bijlsma JW, Freeman A, George V, Kovac SH, Spettell CM, Saag KG.

Arthritis Rheum. 2006 Jun 15;55(3):420-6.

Free Article

 

Effects of low-dose prednisone on bone metabolism.

Ton FN, Gunawardene SC, Lee H, Neer RM.

J Bone Miner Res. 2005 Mar;20(3):464-70. Epub 2004 Nov 29.

Free Article

 

The mechanisms of prednisone inhibition of inflammation in Crohn's disease involve changes in intestinal permeability, mucosal TNFalpha production and nuclear factor kappa B expression.

Wild GE, Waschke KA, Bitton A, Thomson AB.

Aliment Pharmacol Ther. 2003 Aug 1;18(3):309-17.

Free Article

 

Steroids and risk of upper gastrointestinal complications.

Hernández-Díaz S, Rodríguez LA.

Am J Epidemiol. 2001 Jun 1;153(11):1089-93.

 

The effect on memory of chronic prednisone treatment in patients with systemic disease.

Keenan PA, Jacobson MW, Soleymani RM, Mayes MD, Stress ME, Yaldoo DT.

Neurology. 1996 Dec;47(6):1396-402.

 

Perforated peptic ulcer disease in children: association of corticosteroid therapy.

Bickler SW, Harrison MW, Campbell JR.

J Pediatr Surg. 1993 Jun;28(6):785-7.

 

The effect of prolonged prednisone treatment on human costal cartilage.

Dearden LC, Mosier HD Jr.

Am J Pathol. 1975 Nov;81(2):267-82.

Free PMC Article

 

Effectiveness of antacids in reducing digestive disturbances in patients treated with prednisone and prednisolone.

BOLAND EW.

Calif Med. 1958 Oct;89(4):262-6.

Free PMC Article

 

Major undesirable side-effects resulting from prednisolone and prednisone.

BOLLET AJ, BLACK R, BUNIM JJ.

J Am Med Assoc. 1955 Jun 11;158(6):459-63. No abstract available.

 

Share on Facebook
Share on Twitter
Please reload

Follow Us

I'm busy working on my blog posts. Watch this space!

Please reload

Search By Tags
Please reload

Archive
  • Facebook Basic Square
  • Twitter Basic Square
  • Google+ Basic Square