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About gutsandgrowth

I am a pediatric gastroenterologist at GI Care for Kids (previously called CCDHC) in Atlanta, Georgia. The goal of my blog is to share some of my reading in my field more broadly. In addition, I wanted to provide my voice to a wide range of topics that often have inaccurate or incomplete information. Before starting this blog in 2011, I would tear out articles from journals and/or keep notes in a palm pilot. This blog helps provide an updated source of information that is easy to access and search, along with links to useful multimedia sources. I was born and raised in Chattanooga. After graduating from the University of Virginia, I attended Baylor College of Medicine. I completed residency and fellowship training at the University of Cincinnati at the Children’s Hospital Medical Center. I received funding from the National Institutes of Health for molecular biology research of the gastrointestinal tract. During my fellowship, I had the opportunity to work with some of the most amazing pediatric gastroenterologists and mentors. Some of these individuals included Mitchell Cohen, William Balistreri, James Heubi, Jorge Bezerra, Colin Rudolph, John Bucuvalas, and Michael Farrell. I am grateful for their teaching and their friendship. During my training with their help, I received a nationwide award for the best research by a GI fellow. I have authored numerous publications/presentations including original research, case reports, review articles, and textbook chapters on various pediatric gastrointestinal problems. In addition, I have been recognized by Atlanta Magazine as a "Top Doctor" in my field multiple times. Currently, I am the vice chair of the section of nutrition for the Georgia Chapter of the American Academy of Pediatrics. In addition, I am an adjunct Associate Clinical Professor of Pediatrics at Emory University School of Medicine. Other society memberships have included the North American Society for Pediatric Gastroenterology Hepatology and Nutrition (NASPGHAN), American Academy of Pediatrics, the Food Allergy Network, the American Gastroenterology Association, the American Association for the Study of Liver Diseases, and the Crohn’s and Colitis Foundation. As part of a national pediatric GI organization called NASPGHAN (and its affiliated website GIKids), I have helped develop educational materials on a wide-range of gastrointestinal and liver diseases which are used across the country. Also, I have been an invited speaker for national campaigns to improve the evaluation and treatment of gastroesophageal reflux disease, celiac disease, eosinophilic esophagitis, hepatitis C, and inflammatory bowel disease (IBD). Some information on these topics has been posted at my work website, www.gicareforkids.com, which has links to multiple other useful resources. I am fortunate to work at GI Care For Kids. Our group has 17 terrific physicians with a wide range of subspecialization, including liver diseases, feeding disorders, eosinophilic diseases, inflammatory bowel disease, cystic fibrosis, DiGeorge/22q, celiac disease, and motility disorders. Many of our physicians are recognized nationally for their achievements. Our group of physicians have worked closely together for many years. None of the physicians in our group have ever left to join other groups. I have also worked with the same nurse (Bernadette) since I moved to Atlanta in 1997. For many families, more practical matters about our office include the following: – 14 office/satellite locations – physicians who speak Spanish – cutting edge research – on-site nutritionists – on-site psychology support for abdominal pain and feeding disorders – participation in ImproveCareNow to better the outcomes for children with inflammatory bowel disease – office endoscopy suite (lower costs and easier scheduling) – office infusion center (lower costs and easier for families) – easy access to nursing advice (each physician has at least one nurse) I am married and have two sons (both adults). I like to read, walk/hike, bike, swim, and play tennis with my free time. I do not have any financial relationships with pharmaceutical companies or other financial relationships to disclose. I have helped enroll patients in industry-sponsored research studies.

Avoid ranitidine (acid suppression) in neonates

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More evidence that ranitidine may contribute to necrotizing enterocolitis and fatal outcomes has been published (Pediatrics 2012; 129: e40-45).

In this study (which was reviewed in The Journal of Pediatrics 2012; 161: 168-69), four neonatal intensive care units in Italy performed a multicenter prospective observational study of very low birth weight (VLBW) inants.  There were 274 neonates with gestational ages ranging from 24-32 weeks and birth weights ranging from 401-1500 grams.  The patients receiving ranitidine were similar to the unexposed group in terms of risk factors for infection/NEC, birth weight, gestational age, sex, APGAR scores, PDA, intubation duration, and central vascular access duration.

  • 34 of 91 (37%) exposed to ranitidine developed infections compared with 9.8% of the group not exposed to ranitidine (OR 5.5)
  • Risk of necrotizing enterocolitis (NEC) was 6.6-fold higher among ranitidine-treated neonates
  • Mortality was 9.9% for ranitidine-treated patients compared with 1.6% of control patients
Since gastric acid acts as a defense against ingested pathogens, theoretically inhibition of acid production allows proliferation of these pathogens with subsequent infections and development of necrotizing enterocolitis.  These potential risks and the general lack of benefit of acid suppression in neonates should help guide clinician decision-making.
Another concern with ranitidine has been among acute appendicitis patients (see references below) where it has been associated with an increased likelihood of developing an abscess.

Additional references/previous related blog entries:

Helicobacter pylori –useful advice

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Helicobacter pylori (H pylori) infections remain an important cause of gastritis, ulcers, and adenocarcinoma of the stomach.  One new approach in treatment has been the use of sequential therapy.  More data is now available on the effectiveness of this approach and choice of antibiotics (Gastroenterology 2012; 143: 55-61 & editorial 10-12).

In the study, a 10-day sequential regimen (SR) was compared with a 5-day concomitant regimen (CR).

  • CR group (n=90): esomeprazole 40 mg BID, amoxicillin 1 g BID, levofloxacin 500 mg BID, tinidazole 500 mg BID.  Eradication rate (intention-to-treat): 92%
  • SR group (n-90): esomeprazole 40 mg BID, amoxicillin 1 g BID for 5 days, then esomeprazole 40 mg BID, levofloxacin 500 mg BID, tinidazole 500 mg BID for 5 days. Eradication rate (intention-to-treat): 93%
  • Both groups had good results in part due to low resistance rates

Useful advice on this study from the editorial:

  • ‘We prefer concomitant therapy because it is not complex and it may retain its effectiveness at a slightly higher level of resistance compared with sequential therapy.”  Authors prefer 4-drug non-bismuth-containing concomitant treatment.
  • With bismuth therapy (eg. bismuth-metronidazole-tetracycline-PPI), authors prefer a 14 day course.  10-day treatment may be effective when metronidazole resistance is considered unlikely.
  • “Clarithromycin should be abandoned as an empiric regimen” due to resistance in U.S.
  • Fluoroquinolone resistance is increasing rapidly and “prior use virtually ensures resistance.”  Suggested use of fluoroquinolone therapy among adults would be as a rescue therapy (failed 2 different therapies), using dosing regimen as noted in cited study, and in patient without history of prior fluoroquinolone use (&/or proof on susceptibility testing)
What about treatment in kids?
In pediatrics, guidelines for treatment have been recently updated (JPGN 2011; 53: 230-43). (Benjamin Gold, MD -one of my partners is one of the authors and was the lead author of the first guidelines published in 2000.)  NASPGHAN guidelines. PDF of powerpoint slides: H. pylori infection in children: ESPGHAN/ NASPGHAN guidelines … & pdf of text: Evidence-based guidelines from ESPGHAN and NASPGHAN for …
Recommendations for first line treatment are a triple-based therapy with PPI and two antibiotics (eg. amoxicillin and metronidazole).  Alternatives, include bismuth plus two antibiotics, or sequential therapy.  Use of clarithromycin is recommended only after susceptibility testing.

Additional references:

  • -Gut 2010; 59: 1143-53.  Changing treatment recommendations for Helicobacter pylori in the face of resistance.
  • -Am J Gastroenterol 2007;  102: 1808-1825. American College of Gastroenterology Guideline on the Management of Helicobacter pylori Infection.  Doxycycline can be used in place of tetracycline
  • -Gastroenterol 2007; 133: 985. Review. Good article for resistant infections.
  • -Gastroenterol 2005; 129:1414-19.  Sequential Rx (amox + PPI x 5 days, then biaxin, tinidazole, PPI for 5 days) had 97% success.

Clues about constipation and more than 2.5 million views

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A recent article identifies some important factors contributing to constipation in Hong Kong children (JPGN 2012; 55: 56-61).

Using a territory-wide questionnaire in 2318, Hong Kong Chinese elementary school students, the authors identified several factors associated with constipation which was present in 12.2% of this cohort:

  • Refusal to pass bowel movements at school (OR 1.97).  In Hong Kong, students spend >8 hours per day at school.
  • Having dinner with one/both parents <50% of time (OR 1.52).  May indicate less time with parents and less parental prompting.
  • Nighttime sleep <7 hours (OR 1.87).  This is postulated to be related to increased homework and more stress which may affect gut motility.
  • Frequent fast food consumption (OR 1.14).  This may be associated with less fiber intake.

On a tangential note, one of my sons informed me of “bad lip reading” on YouTube; some of these clips are really funny.  Since there was one relevant to the subject at hand, with over 2.5 million views, I’ve provided a link:

“Everybody Poops” – a bad lip reading of the Black Eyed Peas …

Additional blog entries related to constipation:

Stimulants for constipation

Diagnostic tests hardly ever help patients poop

It’s worth the cost

Think twice about checking thyroid

Long-chain polyunsaturated fatty acids, breastmilk, and infant cognition

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A lot has been written about improving infant cognition and breastfeeding, even on this blog (More evidence that breastfeeding improves cognitive development).  Formula companies in their efforts to duplicate the nutritional value of breast milk have supplemented with a number of agents, including long-chain polyunsaturated fatty acids (LCPUFA).  But, does this work?

A meta-analysis of LCPUFA supplementation failed to show any significant effect on early infant cognition (Pediatrics 2012; 129: 1141-49).  Twelve trials with 1802 infants met inclusion criteria.  Included trials were randomized clinical studies that measured cognition with Bayley Scales of Infant Development.

LCPUFAs have been hypothesized to be a potential reason for improved cognition.  LCPUFAs are vital for cell membranes and play a critical role in development and growth.  The two main LCPUFAs are docosahexaenoic acid (DHA) and arachidonic acid (AHA). “An estimated 30-fold increase in the amount of DHA and AA in the infant forebrain occurs between the last trimester of pregnancy and the first 2 years of life.”

The authors note that while breastfed babies tend to have higher intelligence, confounding factors have made it difficult to determine whether actual nutritional differences in breast milk are the reason for this difference.  On average, breastfeeding mothers have higher intelligence, larger incomes, and spend more time with their infants.  Thus, bonding/social interactions as well as other breast milk properties (eg antimicrobial, antiinflammatory, and immunomodulatory) may be important factors.

On the same subject, a second article in the same issue (Pediatrics 2012; 129: 1134-40) also showed that breastfed infants had slightly improved cognitive development compared with formula-fed babies (both cow’s milk and soy formula).  This conclusion was based on Bayley Scales of Infant Development and the Preschool Language Scale-3.  In total, this study examined 391 infants at ages 3, 6, 9, and 12 months.  The authors state that “models were used while adjusting for socioeconomic status, mother’s age and IQ, gestational age, gender, birth weight, head circumference, race, age, and diet history”  –that’s a lot of variables to adjust!

More on breast milk from previous blog entries:

Breastfed babies less likely to develop fatty liver

Breastfeeding: protection from asthma

Looking better or feeling better in EoE?

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When seeing a new diagnosis of eosinophilic esophagitis (EoE), I often try to explain that there are two potential goals of treatment: clinical remission (improvement in symptoms) and histologic remission (improvement in appearance of esophagus with microscope).  Unfortunately, these two outcomes are not always synchronous; more proof of this comes from a recent study (Clin Gastroenterol Hepatol 2012; 10: 742-49, 750-52 [editorial]).

In this double-blind, randomized, placebo-controlled study of fluticasone in adult patients with a new diagnosis of EoE, 19 patients were treated with fluticasone (880 μg BID) and 15 patients were treated with placebo inhaler –for six weeks.  Initially, 21 patients were assigned to each group; 2 dropped out of treatment group and 6 dropped out of placebo group before completion of followup EGD.   The average age in the treatment group was 37 years versus 38 years in the placebo group.  A complete histologic response was defined as >90% reduction in mean eosinophil count; this occurred in 62% of fluticasone patients and in none of the placebo group, based on an intention-to-treat analysis.  Another measure of eosinophil activity, eosinophil-derived neurotoxin (EDN), was reduced by 81% on intracellular staining in the treatment group compared with 8% in the placebo group.  Figures 1 through 3 show this staining –it’s pretty cool!

Yet, the clinical response was not statistically different.  Dysphagia was reduced by 57% in the treated subjects compared to 33% in the placebo subjects in an intention-to-treat analysis.  Results were improved modestly in those who actually were treated: 63% (12 of 19) compared to 47% of placebo patients.  A complete response for dysphagia was noted in 42.9% of fluticasone group compared with 28.6% of control group based on an intention-to-treat analysis.  A fairly high rate of candidiasis was noted in treated patients 26%;  no placebo patients developed candida.

Another interesting finding was that among those who continued PPIs for heartburn symptoms the response to fluticasone was not improved.  40% of PPI users had a complete histologic response compared with 79% of non-PPI users.

So what are the reasons for the discrepancy between clinical and histologic response?

  • Established strictures and small-caliber esophagus may require dilation rather than medicines to relieve dysphagia
  • Esophageal fibrosis and subsequent esophageal compliance may not respond to topical therapy or take a lot longer to improve
  • Secondary candidiasis may reduce clinical response –though in this study, 5 of 6 patients with candida did in fact have symptom resolution
  • Compensatory behaviors may improve clinical symptoms –chewing food, cutting up food better, drinking more fluids, and avoiding some foods.  This may make it harder to detect important differences.

Patient information link: (Eosinophilic esophagitis – CCDHC Home)

Related posts:

Look of improvement on an EoE diet

Guidelines for Eosinophilic Esophagitis

Eosinophilic Esophagitis -Six Food Group Diet

The undiscovered country

MicroRNA signature for eosinophilic esophagitis

Pregnancy after Liver Transplantation

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As there are about 14,000 women of reproductive age in the U.S. who have undergone liver transplantation (LT), data about the outcomes of pregnancy are important for counseling.  A review and meta-analysis (Liver Transpl 2012; 18: 621-29) provides some information; going forward the National Transplantation Pregnancy Registry (NTPR) which was established in 1991 offers the promise of additional insight.

In the current review, Deshpande et al found 8 of 578 studies which met inclusion criteria; in total 450 pregnancies in 306 LT recipients were examined.  While healthy live births were the most common outcome, there were several pertinent risks identified.  The main concerns were development of preeclampsia, rejection/graft loss as well as the potential for birth defects.  While miscarriage rates were similar to the general population (15.6% compared with 17.1%), the following were much higher:

  • preeclampsia 21.9% vs. 3.8% in general population
  • cesarean section delivery 44.6% vs. 31.9% in general population
  • preterm birth 39.4% vs. 12.5% in general population

While rates of rejection and graft loss are not given for the entire cohort, specific study results were discussed.  In one study, rates of acute rejection ranged from 2% to 8% and loss of graft within two years of pregnancy occurred in 6-11%.

Similar to rejection data, the data for birth defects was not uniformly reported.  Specific study results were discussed and included several birth defects: 1 patient with total anomalous pulmonary venous return, 1 with pyloric stenosis, 2 with hypospadias, 1 with tracheoesophageal fistula, 1 with unilateral cystic kidney, and 2 with ventricular septal defects.

Take-home message:

Liver transplant recipients can have successful pregnancies but should be considered high risk.  Active reporting to established registries can give more accurate and up-to-date information.

Related post:

Alive and well? 10 years after liver transplantation

Advice on drug-induced liver injury (DILI)

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Practical information and advice on continuing or stopping drugs with associated hepatoxicity is available from a recent commentary (Gastroenterol Hepatol 2012; 8: 333-36).

Most drugs with a “bump” in aminotransferases do not need to be stopped.  Many drugs induce an “adaptive response” in which elevated LFTs will spontaneously resolve; this is most common in the first 12 weeks of drug usage.  This type of response must be distinguished from an immune reaction/hypersensitivity response which is much more likely to progress.  A hypersensitivity response could include rash, fever, and eosinophilia.

Recommended STOP RULES:

  • Drugs that cause symptomatic hepatitis: abdominal pain, jaundice, loss of appetite.
  • ALT values that exceed 8 times the ULN
  • ALT values >3 times the ULN and Bilirubin >2 times the ULN

Other caveats:

  • If the ALT value is >3 times the ULN but not associated with symptoms or rise in bilirubin, the drug can likely be continued with periodic monitoring.
  • ALT values >5 times the ULN require more intensive monitoring.
  • Hy’s law (named for Hyman Zimmerman): AST or ALT > 3 ULN AND   bili > 3 ULN indicate serious hepatotoxicity with >10% mortality rate.
  • Statins have similar rates of hepatotoxicity as the general population
  • Acetaminophen accounts for 40-50% of the 2000-2500 U.S. cases per year of acute liver failure (ALF).  Of the remaining cases of ALF, about 12% (250-300) are due to other cases of DILI.  Isoniazid is the 2nd most common cause of ALF due to DILI with about 50 cases.
  • Potential risk factors for DILI include alcohol usage, obesity, adult age group, and female gender.

Additional blog entries and references:

When death is on the line

Pediatric pharmaceutical poisoning

  • -J Pediatr 2011; 158: 802. Developing liver toxicity with valproic acid (VPA) is a contraindication to OLTx (even in the absence of documented mitochondrial dz). Rx with carnitine and d/c VPA. 82% of 17 children died w/in 1 yr of OLTx. POLG1 mutations are associated with Alpers syndrome. (Ann Neurol 2004; 55: 706.)
  • -NEJM 2009; 360: 1575. propylthiouracil assoc c liver failure in ~1 in 2000
  • -JPGN 2008; 47: 395-405. Drug-related hepatotoxicity and acute liver failure.
  • -NEJM 2003; 349: 474. (review)
  • PDF] What Do We Mean by Looking?  FDA powerpoint with related information

Regurgitation harder to treat than heartburn, especially for NERDs

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While all pediatric gastroenterologists know that the title of this blog entry is right, it is helpful to have data.

A recent study (Clin Gastroenterol Hepatol 2012; 10: 612-19) used a reflux questionnaire to evaluate responsiveness of regurgitation from 2 randomized controlled trials.  The trials compared a newer acid blocker (AZD0865 dosed at 25-75 mg/day)) to esomeprazole (20-40 mg/day).  Patients had either non-erosive reflux disease (NERD , n=1460),  or reflux esophagitis, (RE, n=1314).  Inclusion criteria included the presence of substernal burning for ≥4 days/week.

Regurgitation-taste (RT), defined as an “acid taste in the mouth,” or regurgitation-movement (RM), defined as an “unpleasant movement of material upwards from the stomach” were analyzed.  Among NERD patients, either or both symptoms were present in 53% at baseline compared with 54% among the RE group.  In both NERD and RE patients, the presence of these regurgitation symptoms was associated with a poorer response to therapy.

  • Complete response of NERD patients with regurgitation symptoms:  RT 34%, RM 26%; in comparison to heartburn response of NERD patients which was 49%
  • Complete response of RE patients with regurgitation symptoms:  RT 44%, RM 33%; in comparison to heartburn response of NERD patients which was 55%

Additional references/blog entries:

Diet or drugs for cyclic vomiting syndrome

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Dietary modifications are frequently recommended for migraines.  Given the overlapping features between migraines and cyclic vomiting syndrome (CVS), dietary treatments for CVS have aimed at eliminating trigger foods.  Investigators from the UK describe a single center cohort of 21 children (2-16 years) were placed on a low-amine diet with instruction from a dietician (JPGN 2012; 54: 698-99).  16 (76%) of the children had a strong family history of migraines.  The diet was implemented for a ‘minimum of 6 to 8 weeks.’ 13 had a complete resolution of vomiting and 18 (86%) had at least a partial response.

Specific foods that were avoided included cheese, chocolate, citrus fruits, pork, peas, broad beans, shellfish, yeast extract, beef extract, gravies, caffeine, and alcohol.

This small study does not prove that a low-amine diet is effective.  In fact, most of the information on a low-amine diet is derived from alternative medicine sources (eg .  Low Amine Diet | www.integrative-medicine.com.au).  Nevertheless, it is likely that a subset of patients will benefit from avoidance of trigger foods.  How to identify potential culprits is unclear.

NASPGHAN Guidelines for CVS (JPGN 2008; 47: 379):

  • Diagnostic criteria: (90% will have idiopathic CVS)

1. at least 5 attacks or 3 over 6-month interval
2. episodic, last 1 hour to 10 days & at least a week apart
3. stereotypical pattern for individual patient
4. vomiting >4 times/hr for at least 1 hour
5. healthy in between & no other attributable problem

  • PROPHYLACTIC Measures:

Avoid triggers:
fasting, excessive excitement (eg. downplay big events), sleep deprivation
foods that trigger symptoms (?chocolate, cheese, caffeine, MSG)
excessive fatigue

Assure adequate carbohydrates
-provide sugar-containing drinks & extra snacks before exertion & bedtime

  • PROPHYLACTIC TREATMENT:

Less than 5 years:
1. cyproheptadine (0.25-0.5mg/kg/day divided bid)
2. propranolol 0.25-1/kg/day –often 10mg bid or tid
contraindications: asthma, diabetes, heart disease, depression
keep resting heart rate >60

5 years & older
1. amitriptyline (or nortriptyline -liquid formulation) start at 0.25mg/kg qhs and increase ’til 1mg/kg/dose
check EKG before and 10 days after peak dose
2. propranolol 0.25-1/kg/day –often 10 mg bid or tid
contraindications: asthma, diabetes, heart disease, depression
keep resting heart rate >60

Alternative prophylactic treatments:
1. phenobarbital 2mg/kg qhs
2. anticonvulsants: topiramate, valproid acid, gabapentin, levetiracetam -?consult neurology

Supplements:
L-carnitne 50-100mg/kg/day divided bid (max 1gm tid)
Co-enzyme Q10 10mg/kg/day divided bid (max 100mg tid)

  • SUPPORTIVE/ABORTIVE CARE

Fluids: D10NS w KCL @ 1.5 maintenance (or possibly D10 0.45NS -some children prone to hyponatremia); add TPN if no enteral intake for 3-5 days
Antiemetics:
1. ondansetron 0.3-0.4mg/kg/dose q4hours (max 20mg); alternative granisetron
Sedatives:
Benadryl 1mg/kg/dose q6hours
Ativan 0.05-0.1mg/kg/dose q6hours
Thorazine (chlorpromazine) 0.5-1mg/kg/dose q6hrs (with benadryl)
Analgesics:
Toradol 0.4-1mg/kg/dose q6hrs (max 30mg)
Narcotics (morphine)

May need to treat hyponatremia, hypertension, hematemesis (H2RAs & PPIs)

Also, can try Sumatriptan 20mg intranasally at onset of episode as potential abortive measure or other triptan

  • TYPICAL EVALUATION:

1. CMP, Amylase/lipase, UGI on all patients
2. If pain/hematemesis, check U/S of abd/pelvis, and EGD
3. If abnormal neuro features: (motor asymmetry, gait abnormality, severe altered mental status)
ammonia
lactate, serum amino acids, urine organic acids, plasma carnitine/acylcarnitine profiles, urine ketones
MRI brain
4. If precipitated by fasting/high protein meals, or intercurrent illness= neuro w/u w/o brain MRI.

  • ALARM symptoms:

1. pain & bilious emesis
2. attacks precipitated by intercurrent illness, fasting or high protein meals
3. progressive/worsening/chronic pattern
4. abnormalities on neuro exam

**Note to blog readers –I recommend that all drug dosing be reviewed for individual patients.  The recommended doses are based on my reading of the referenced material & transcription errors are possible.

Additional references:

  • -Clin Gastro & Hep 2007; 5: 44. Use of zonisamide or levetiracetam (used at Sz dosing in 20 adults); 75% response & 20% remission.
  • -J Pediatr 2002; 141: 724. Suggests initial treatment along with UGI as most cost-effective strategy. Extensive w/u in those with persistent sx.
  • -Am J Gastro 1999; 94: 2855. response to TCAs.
  • -J Pediatr 1999; 134: 567. 82% migraine-assoc or FHx. Better response to Rx
  • NASPGHAN 2003:  postgraduate course (B Li):80% response to elavil if fhx migraines.
    “There are no controlled randomized, double-blinded trials, only open label ones. In these studies, beta-blockade (Pfau Pediatrics 97:364,1996), cyproheptadine (Anderson Pediatrics 100:977, 1997), amitriptyline (Anderson), phenobarbital (Gokhale JPGN 25:64, 1997) and erythromycin (Vanderhoof JPGN 17:387, 1993) all have approximately 70% efficacy as prophylactic agents. In Dave Fleisher’s work, he has demonstrated a 70% effect of consultation alone without pharmacologic therapy. In other words, there appears to be a striking placebo effect in this disorder that should temper any interpretation of results. In addition, I believe CVS is a heterogeneous disorder that has multiple etiologies that could allow it to respond to multiple classes of agents.”

DDx:
Infection, IBD, addison’s, diabetes, renal dysfxn, metabolic errors/urea cycle d/o, FAO d/o, porphyria, CDG (glycosylation), pregnancy, ipecac/munchausen, PUDz, Giardia, pancreatitis, UPJ, malrotation/duplication, increased ICP/CNS Dz, Migraine-equivalent

Workup:

1. CBC, ESR, amylase, ammonia,UA, stool heme, chem 20, HCG
2. UGI
3. giardia ag, abd U/S & DPTA, EGD, urine organic acids, plasma amino acids, carnitine, lactate, pyruvate, sinus films, head CT/MRI, toxicology, delta-aminolevulic acid/ porphobilinogen (urine), beta-HCG, serum transferrin isoelectric focusing

Fish intake may reduce liver cancer

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In a large Japanese adult population (n=90,296), the consumption of n-3 fatty acids and fish was associated with reduced risk for hepatocellular cancer (HCC) (Gastroenterology 2012; 142: 1468-75 and editorial 1411-12).

HCC ranks fifth among cancer incidence and third for mortality worldwide.  Many factors contributing to HCC cannot be modified.  The main factors subject to modification include diet and avoidance of viral hepatitis.  Dietary studies are methodologically-challenging due to difficulties assessing diet and due to the complex nature of diets.  Without going into any significant detail, this study shows an inverse relationship between fish intake and incidence of HCC.  The hazard ratio for the highest quintiles compared to the lowest were 0.56-0.64 depending on the specific dietary agent.  The specific n-3 polyunsaturated fatty acids (PUFA) examined included eicosapentaenoic acid (EPA), docosapentaenoic adic (DPA), and docosahexaenoic acid (DHA).

HCC Established Risk Factors:

Age, males, family history of HCC, HCV/HBV infection, alcohol, cirrhosis, tobacco, aflatoxin exposure, Hereditary Hemochromatosis, α-1 antitrypsin deficiency, primary biliary cirrhosis

Likely Risk Factors:

Diabetes, obesity, NAFLD

Possible Risk Factors:

Red meat, saturated fat, fructose, oral contraceptives

Possible Protective Factors:

Coffee, micronutrients (vitamin D, vitamin E, selenium), white meat (fish, poultry), and n-3 fatty acids

Related blog posts:

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