Category Archives: Uncategorized

Case report: Spondylodiscitis After Button Battery Ingestion

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Chris Fritzen and Erica Riedesel passed along a case report: a 16 mo presented to our hospital system with coughing, gagging and hematemesis after an unwitnessed FB ingestion; she was emergently taken to the OR where a button battery was noted to be densely adherent to the posterior wall of the upper thoracic esophagus and removed with a flexible endoscope. Postoperatively, she received 7 days of ampicillin/sulbactam. 14 days after presentation, an MRI revealed esophageal injury was evident at T3 level as well as an abnormal signal was seen within the esophagus spanning C7-T4. In addition, there was edema and enhancement of the intervertebral disc space at T1-T2 and T2-T3 consistent with spondylodiscitis. Prior reports (see below) have emphasized the need for antimicrobial coverage for Staphylococcus and upper respiratory pathogens. Children with spondylodiscitis may present with refusal to walk or limping, back or leg pain, and local stiffness of the neck/spine.

My take: Spondylodiscitis is another rare complication following button battery ingestion.

References:

  • NEO Grey et al. Pediatr Radiol 2021; 51:1856–1866. In this report, 1 of 23 children had spondylodiscitis. Other complications: esophageal perforation (n=11), tracheoesophageal fistula (n=3)
  • V Kieu et al. J Pediatr 2014; 164: 1500-1501. Highlights increased risk from unwitnessed button battery ingestions.
  • H Eshaghi et al. Pediatr Emer Care 2013;29: 368Y370. Spondylodiscitis: A Rare Complication of Button Battery Ingestion in a 10-Month-Old Boy

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Disclaimer: This blog, gutsandgrowth, assumes no responsibility for any use or operation of any method, product, instruction, concept or idea contained in the material herein or for any injury or damage to persons or property (whether products liability, negligence or otherwise) resulting from such use or operation. These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) should be confirmed by prescribing physician.  Because of rapid advances in the medical sciences, the gutsandgrowth blog cautions that independent verification should be made of diagnosis and drug dosages. The reader is solely responsible for the conduct of any suggested test or procedure.  This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

IQ and Pediatric Chronic Liver Disease

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DH Leung et al. JPGN: 2022 – Volume 74 – Issue 1 – p 96-103. Neurodevelopmental Outcomes in Children With Inherited Liver Disease and Native Liver

In this longitudinal study, the authors evaluated Full Scale Intelligence Quotient (FSIQ) in children with chronic liver disease (mean age 7.6 yrs). Key finding:

  • Patients with Alagille syndrome (ALGS) are at increased risk of lower FSIQ (with 29% <85), whereas our data suggest A1AT and PFIC are not

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Losartan: Not Effective for Pediatric NAFLD

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M Vos et al. Hepatology 2022; https://doi.org/10.1002/hep.32403. Open Access: Randomized placebo-controlled trial of losartan for pediatric NAFLD (Thanks to Jeff Schwimmer’s twitter feed for this link)

Rationale for study: “A number of studies suggest the utility of losartan in NAFLD.[11–17] In adults, two meta-analyses have found that angiotensin receptor blockers (ARBs) improve insulin sensitivity and reduce the incidence of type 2 diabetes.[18, 19] A large retrospective review of hypertensive patients treated with angiotensin-converting enzyme inhibitors and/or ARBs demonstrated a significant association of renin-angiotensin system (RAS) antagonists with reduced odds of advanced hepatic fibrosis on biopsy.[20] “

Design: 83 participants (81% male, 80% Hispanic) with histologically proven NAFLD were randomized to losartan (100 mg daily) (n = 43) or placebo (n = 40). ALT was chosen as a primary endpoint, because “reduction of elevated serum ALT … has been shown to significantly correlate with improvement in histology in children, including fibrosis”

Key findings:

  • The 24-week change in ALT did not differ significantly between losartan versus placebo groups (adjusted mean difference: 1.1 U/l; p = 0.95), although alkaline phosphatase decreased significantly in the losartan group (adjusted mean difference: −23.4 U/l; p = 0.01).
  • The authors “found no benefit of losartan on markers of insulin sensitivity, despite an improvement in systolic blood pressure”

My take: This study shows a very low likelihood that Losartan could be beneficial in NAFLD. I would recommend a book (a quick read) to my colleagues: “How I Killed Pluto and Why It Had It Coming.” In this book, the author, Michael Brown, describes years of seemingly-Sisyphean efforts to locate planetoids in our distant solar system; his work ultimately yielded important discoveries.

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Low Anti-TNF Levels or Antibodies Are Associated with Antibodies to Subsequent Anti-TNF Agent

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NV Castelle et al. Clin Gastroenterol Hepatol 2022; 20: 465-467. Open Access: Patients With Low Drug Levels or Antibodies to a Prior Anti-Tumor Necrosis Factor Are More Likely to Develop Antibodies to a Subsequent Anti-Tumor Necrosis Factor

Design: Retrospective case-control study in 5828 patients (2171 cases, 1445 controls). Subjects needed to have consecutively orders of 2 anti-TNF therapies (infliximab (IFX) prior to adalimumab (ADM) or vice versa).

Key findings:

  • Before switch from IFX to ADM, median (interquartile range) IFX serum concentrations were lower in cases versus control subjects (1.0 μg/mL [1.0–1.0] vs 11.7 μg/mL [4.2–27.1]; P < .0001).
  • As noted in figure below, prior antidrug antibodies ADAb) to anti-TNF agent was associated with development of ADAb with 2nd anti-TNF agent. This risk was >2-fold higher when switching from IFX to ADM (B in Figure) and even more when switching from ADM to IFX (D in Figure)
  • Increasing concentrations of ADAb to IFX were associated with higher proportions of patients developing ADAb to ADM (P < .0001). In contrast, increasing concentrations of ADAb to ADM did not result in a significantly higher proportion of patients developing ADAb to IFX.

My take:

  • In my experience, many patients with subtherapeutic anti-TNF levels, even those with ADAb, can remain on initial anti-TNF with more frequent dosing and often with combination therapy. So before jumping off the initial treatment, make sure it has been optimized.
  • In those who do start a 2nd anti-TNF agent, the authors recommend using combination therapy (with an immunomodulator) which “leads to lower rates of clinical failure and more favorable pharmacokinetics, compared with monotherapy.”
  • “Alternatively, a strategy with optimized monotherapy using proactive TDM may be effective as well, but remains to be assessed in a prospective manner.”
Kaplan-Meier curves representing proportion of patients who developed ADAb when (A) switched from infliximab to adalimumab and (C) switched from adalimumab to infliximab. Difference in rate of ADAb formation between cases (red) and control subjects (teal) for those patients who (B) switched from infliximab to adalimumab and (D) switched from adalimumab to infliximab.

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Disclaimer: This blog, gutsandgrowth, assumes no responsibility for any use or operation of any method, product, instruction, concept or idea contained in the material herein or for any injury or damage to persons or property (whether products liability, negligence or otherwise) resulting from such use or operation. These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) should be confirmed by prescribing physician.  Because of rapid advances in the medical sciences, the gutsandgrowth blog cautions that independent verification should be made of diagnosis and drug dosages. The reader is solely responsible for the conduct of any suggested test or procedure.  This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

Slinky for Short Bowel Syndrome?

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From GeneralSurgeryNews.com: Open Access: Novel Device Uses Mechanotransduction To Treat Small Bowel Syndrome

An excerpt:

“The basic concept is similar to distraction osteogenesis, which orthopedic surgeons have used for years, applying distraction force to broken bone that will grow up to a millimeter a day,” said Andre Bessette, the CEO and a co-founder of Eclipse Regenesis, Inc…

To regenerate small-bowel tissue, a surgeon inserts the device, which looks like a small, compressed coil, inside the small intestine and secures both ends with plication sutures applied to the outside of the intestine. Over two to three weeks, the device slowly expands to its uncompressed state, stimulating new tissue growth—ultimately two to three times the segment’s original length, about 4 cm...[thus]  they’ll need more than one device applied or more than one procedure.

Once this process is complete, the chromic sutures dissolve over about a month, allowing the device to pass through the body to be excreted...

[The researchers] expect to start these [human] trials in the first half of 2022, and they have identified two primary investigator sites: Boston Children’s Hospital and Cincinnati Children’s Hospital

Preclinical studies: Eclipse’s website at www.eclipseregenesis.com/ publications.

“Do Not Stop Anti-TNF Medications in Children with IBD When They Are Working”

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In 2014, one of the posts on this blog addressed stopping anti-TNF therapy: Marriage, Divorce and Separation with Anti-TNF Therapy. My take at that time was “most patients are better off staying married to their anti-TNF therapy.”

Despite changes in therapeutic options, a recent study and editorial come to the same conclusion in 2022:

In the retrospective study, 78 patients with CD and 56 patients with UC underwent endoscopic reassessment. Key findings:

  • Mucosal healing (MH) was achieved by 32 patients with CD (41%) and 30 patients with UC (53.6%); 26 patients with CD (33.3%) and 22 patients with UC (39.3%) achieved histologic healing (HH)
  • Among 45 patients (n=24 CD, n=21 UC) with both MH & HH, anti-TNF therapy was stopped & patients received either an immunomodulatory or mesalamine. 76% of patients with CD had clinical relapse within 3 years and 17% within 1 year. Importantly, objective markers of relapse, including calprotectin and endoscopy were NOT performed; thus, this is certainly an underestimation of relapse rate and time to relapse.

In the commentary, the authors note the high rate of relapse in other studies with anti-TNF withdrawal (eg. STORI trial) and high rate of surgery in patients with perianal CD who stopped therapy. In the STORI trial, “the best outcomes [for infliximab withdrawal] were those with subtherapeutic infliximab trough levels, ie, those for whom infliximab was not responsible for maintaining their remission.”

The data are less certain for UC. The editorial notes that 85% of the 21 patients in the Scarallo study had limited left-sided colitis and only 17 were followed for at least 1 year. In adult studies on anti-TNF discontinuation with UC (Kennedy et al. Aliment Pharm Ther 2016; 43: 910-23 and Molander et al. Inflamm Bowel Dis 2014; 20: 1021-28), 42% and 35% relapsed within 12 months, whereas another small study (Farkas et al. World J Gastroenterol 2014; 20: 2995-3001) found 100% of patients on combination therapy who stopped anti-TNF agent had to restart anti-TNF therapy.

My take (from editorial): “The totality of the currently available evidence suggests that discontinuing anti-TNF medications in children with IBD is associated with a greatly increased risk of disease exacerbation, especially if the anti-TNF trough level was therapeutic.”

Broadwalk; Hollywood, FL

How Effective are Stents for Anastomotic Esophageal Strictures in Patients with Esophageal Atresia

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O Baghdadi et al. JPGN 2022; 74: 221-226. Predictors and Outcomes of Fully Covered Stent Treatment for Anastomotic Esophageal Strictures in Esophageal Atresia

This retrospective review of 45 patients (n=92 stents) examine the effectiveness of esophageal stenting in patients with esophageal atresia (EA). All patients had multiple dilatations prior to stenting and/or had a stricture diameter that rapidly narrowed within 2 weeks of dilatation to a diameter that was the same or smaller to predilatation. Patients were observed in the hospital after stent placement and outpatient management was considered if oral nutrition was tolerated for at least 3 days.

Key findings:

  • According to the authors, the stents prevented surgical resection in 41% of patients
  • ΔD (change in diameter) of ≤4 mm (area under the curve = 0.790; 95% confidence interval: 0.655–0.924; P < 0.001) was the optimal cutoff point in differentiating stent success. If the change in diameter decreases by 4 mm or more after stent removal at endoscopic followup, it is likely that stricture contains significant scar tissue and is not amenable to dilatation/stenting.
  • Median stent duration was 11.5 days
  • The most common adverse events were erosions/ulcerations (29%), granulation tissue formation (27%), vomiting/retching (26%) and stent migration (9%). Three stents were complicated by an esophageal leak (treated medically).

My take: Complications were frequent; thus, stenting for refractory strictures requires highly-specialized technical expertise.

Related blog posts:

Azalea trail, near the Chattahoochee River (Atlanta)

Menetrier Disease in a Pediatric Patient

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During my training, we reported a case of Menetrier’s disease in a pediatric patient associated with CMV infection (Open Access PDF: Diagnosis of Cytomegalovirus Infection in Pediatric Menetrier’s Disease by In Situ Hybridization).

Recently, JPGN’s twitter feed shared the images below from a recent report (SJ Pathak et al. JPGN January 2022 – Volume 74 – Issue 1 – p e16doi: 10.1097/MPG.0000000000003276. Menetrier Disease in a Pediatric Patient With Ulcerative Colitis and Primary Sclerosing Cholangitis)

From JPGN Twitter Feed

Related blog post: Image Only: Pediatric Menetrier’s Disease

Vedolizumab for Refractory Microscopic Colitis, Plus, Vedolizumab and Serious Infections

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LC Shipley et al. Clin Gastroenterol Hepatol 2022; 20: 455-457. Vedolizumab Therapy in Refractory Microscopic Colitis: A Single Center Case Series

In this report, the authors describe nine patients with refractory microscopic colitis (median age 55 years) who were treated with vedolizumab.

Key findings:

  • Clinical response with induction in 9 (100%); time to >50% response ranged from 1 to 7 weeks with 5 patients responding within 2 weeks.
  • Sustained response with maintenance therapy in 6 (67%); duration of follow-up ranged from 1 month to 15 months. The three patients without response had symptom duration of 10 yrs, 12 yrs, and 25 yrs prior to institution of vedolizumab.
  • Only two patients had histologic follow-up. While both had clinical response, the patient with lymphocytic colitis had histologic resolution whereas a patient with collagenous colitis had histologic persistent.

My take: Given vedolizumab’s favorable safety profile, further studies (with endoscopic endpoints) of vedolizumab are needed to define its efficacy for microscopic colitis.

Another study with vedolizumab: J Kirchgesner et al. Clin Gastroenterol Hepatol 2022; 20: 314-324. Risk of Serious Infections With Vedolizumab Versus Tumor Necrosis Factor Antagonists in Patients With Inflammatory Bowel Disease

Key finding: The risk of serious infections was not different between vedolizumab and anti-TNF in the overall IBD cohort (HR, 0.95; 95% CI, 0·79-1.13), while the risk was decreased for vedolizumab users in patients with UC (HR, 0.68; 95% CI, 0.50-0.93), but not CD (HR, 1.10; 95% CI, 0.87-1.38)

Related blog post/related article:

Disclaimer: This blog, gutsandgrowth, assumes no responsibility for any use or operation of any method, product, instruction, concept or idea contained in the material herein or for any injury or damage to persons or property (whether products liability, negligence or otherwise) resulting from such use or operation. These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) should be confirmed by prescribing physician.  Because of rapid advances in the medical sciences, the gutsandgrowth blog cautions that independent verification should be made of diagnosis and drug dosages. The reader is solely responsible for the conduct of any suggested test or procedure.  This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

“Separating Fact from Fiction in the Diagnosis and Management of Food Allergy”

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This great article/commentary is available as open access: Separating Fact from Fiction in the Diagnosis and Management of Food Allergy EM Abrams et al. J Pediatr 2022; 241: 221-228.

Key points:

  • “The risk of fatal anaphylaxis is about 1 in 10 million (about equivalent to being struck by lightning)..and fatality on first ingestion of an allergen in infancy has never been described”
  • Food allergy causes considerable morbidity/worsens quality of life (QOL): bullying, meal preparation, stress, social activities, and school attendance (with 10% choosing home schooling because of a food allergy). Some of this detriment on QOL is due to fear “that accidental exposure could result in fatal anaphylaxis”
  • “The impact of peanut allergy on QoL has been noted to be significantly worse than the impact of other chronic childhood diseases such as rheumatologic disease and type 1 diabetes mellitus”
  • Uriticaria does not equal allergy. “Although urticaria is commonly equated with a food allergy, food allergy accounts for less than 10% of the causes of all acute urticaria and is not a cause of chronic urticaria.” Urticaria can be triggered by an acute infection (most common etiology)
  • “Food proteins are digested within several hours; therefore, urticaria associated with a food ingestion will occur within minutes to 2 hours of ingestion, but typically last no more than a few hours (and less with treatment)” (an exception is meat anaphylaxis owing to galactose-α-1,3-galactose allergy)
  • Other common symptoms that are often incorrectly attributed to food allergy include headaches, chronic behavioral symptoms, or chronic nonspecific abdominal pain
  • Allergy testing: “the presence of a food-specific IgE is not itself indicative of an allergy…Although both skin prick testing and food-specific IgE testing are highly sensitive (>90% for skin prick tests, 70%-90% for sIgE), the specificity and positive predictive values of testing are often very low. The rate of false-positive tests is up to 40%.” 
  • Broad “panel testing” (eg, to a panel of “common” foods), or any food allergy diagnostic testing in the absence of a convincing clinical history has high potential to overdiagnose food allergy and result in unnecessary food avoidances
  • Don’t do IgG testing. “There is no evidence that IgG testing marks food sensitivity; in fact, the presence of IgG is both expected and is a potential indicator of ongoing tolerance”
  • For first-line management anaphylaxis, (intramuscular) epinephrine is the “only life-saving intervention available.” Antihistamines are useful only in the treatment of cutaneous symptoms/urticaria.
  • “Although oral corticosteroids are often administered in the setting of anaphylaxis, there is no convincing evidence that their use prevents a biphasic reaction…their routine use is not recommended” (for anaphylaxis)

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Siesta Beach, FL (2021)