IBD, Celiac, Lactose Intolerance Flashcards
what is the etiology of IBD?
dysregulated mucosal immune response to host gut flora in genetically susceptible individuals
AUTOIMMUNE RESPONSE TO OWN GUT FLORA
what are the 2 types of IBD?
Ulcerative Colitis and Crohn’s Disease
in terms of where UC and Crohn’s affect the GIT, what are there differences?
UC is limited to colon and rectum
Crohn’s is entire GI tract (mouth to anus)
what type of lesions does Crohn’s have?
skip lesions
-areas of inflammation, then normal tissue, then area of inflammation, then normal tissue, etc.
what type of inflammation does UC have?
diffuse inflammation, friability, erosions, and bleeding of mucosa
what is Crohn’s disease associated with?
abscesses, fistulae, sinus tracts (incomplete fistulae ending in a cul-de-sac), strictures, and adhesions
what is the pathophysiology of IBD?
A COMBO OF FACTORS IN GUT:
- Damage to epithelial mucin proteins and tight junctions
- Breakdown of homeostatic balance b/w host’s mucosal immunity and enteric microflora (host immune response to own gut flora)
- Genetic polymorphisms in toll-like receptors (TLRs) - body can’t recognize itself
- Disrupted homeostatic balance b/w regulatory and effector T-cells (more attack T-cels vs regulatory T-cells)
IBD Global incidence
Developing more in industrialized countries -> means something to do with environment, diet, etc.
what has a higher incidence, UC or CD?
UC - more commonly seen in North America and Europe
UC epidemiology ages
Bimodal incidence pattern
-Onset at 15-30 years or 50-70 year olds
what people have high risk of UC?
Ashkenazi Jews have 3-5x higher risk
fam hx very important
smoking and UC
Smoking associated with paradoxically lower risk/incidence, milder disease
environmental factors and UC
Smoking has lower risk, milder disease
Hx of prior GI infections (ex: Shigella, Salmonella, Campylobacter) during adulthood double risk of developing UC - 2/2 change in gut flora triggering chronic inflammatory process
Weak associations b/w NSAIDs, OCPs and increased risk of UC
what are the common presenting sx’s of someone with UC?
Rectal bleeding
Diarrhea (HALLMARK BLOODY MUCOID DIARRHEA)
Abdominal pain in LLQ
what is the HALLMARK sx of UC?
Bloody mucoid diarrhea
where is the abdominal pain in UC located?
LLQ - b/c usually in sigmoid colon
mild to moderate UC disease presentation
- Gradual onset diarrhea (<4/day) and intermittent blood mucoid stool mild disease
- Moderate disease is 4-6 bloody stools/day and more abdominal pain
- Urgency and tenesmus
- No significant abdominal pain, but LLQ cramping normal and often relieved by BM
- Mild fever, anemia, hypoalbuminemia possible
severe UC disease presentation
> 6 bloody diarrhea stools/day
Severe anemia (anemia of chronic disease), hypovolemia (d/t diarrhea), hypoalbuminemia w/ nutritional deficit
Abd pain/tenderness
Fulminant colitis = subset of severe UC disease w/systemic sx’s
what is fulminant colitis?
subset of UC severe disease which is rapidly worsening sx’s with toxicity
SURGICAL EMERGENCY
Look septic - systemic six’s - fever, leukocytosis, tachycardia, severe and pain/diarrhea, may develop toxic megacolon
what manifestations are more common in UC than CD?
extraintestinal manifestations
what extraintestinal manifestations occur in UC?
- Aphthous oral ulcers
- Iritis/uveitis/episcleritis (present with extremely red/painful eye b/c inflammation of uveal tissue)
- Seronegative arthritis, ankylosing spondylitis, sacroilitis (have back pain, stiff joints; Need to watch for 20 y/o that has abd pain and also knee pain/swollen knee - may be UC)
- Erythema nodosum - Nodular, erythematous discrete lesions that are very painful – develop on lower extremities extensor surfaces anterior tibialis (anterior lesions)
- Pyoderma gangrenosum
- Autoimmune hemolytic anemias
- Primary sclerosing cholangitis - chronic long-term disease of your biliary tree
UC PE
LLQ abdominal tenderness; peritonitis
DRE = bright red blood and mucoid appearance to it
what extraintestinal manifestations of UC IMPROVE after colectomy?
Arthritis (20%)
- Knees, ankles, hips, shoulders
- Joints become inflamed and irritated when disease is flaring
Ankylosing spondylitis (3-5%) -HLA-B27+ or Fam Hx of AS
Erythema nodosum (10-15%) -Often in conjunction with arthropathy
Pyoderma gangrenosum (rare)
- Ulcerative cutaneous lesion, dx by biopsy
- PG is associated with IBD in 50% of cases
what extraintestinal manifestation is associated with IBD in 50% of cases?
Pyoderma gangrenosum
what extraintestinal manifestations DON’T improve after colectomy?
Primary Sclerosing Cholangitis
- in men <40 y/o
- colitis not as severe (vs pts that don’t have PSC colitis more severe)
- risk of colon cancer increased 5x compared to UC alone
- LIVER TRANSPLANT = CURE
Classification system of UC
Montreal classification
- used to categorize extent and severity of disease
- classified by severity and where in the colon it is
3 components of diagnosing UC
(1) Clinical sx’s and presentations
(2) Sigmoidoscopy/colonoscopy - six’s confirmed by their findings
(3) Biopsy results/Histologic examinations – have infiltration of lamina propia (basement layer) with WBCs and inflammatory cells
what must the initial work-up of UC do?
r/o infectious and non-infectious causes of the patients’ diarrhea
possible infectious and non-infectious causes of UC pts diarrhea that must be ruled out
Infectious colitis
- Fecal leukocytes (WBCs in stool)
- Stool cultures, Ova, & Parasites
- Campylobacter, Salmonella, Shigella, C. diff, Amebiasis, E. Coli - NEED TO RUN LABS FOR THESE
Radiation proctitis
Ischemic colitis (low blood flow to particular part of colon ischemia -> it bleeds) -Very common in elderly patients and patients that are dehydrated (ex: run a marathon)
CMV colitis (immunocompromised) - UNCOMMON
STI proctitis – DON’T MISS THIS!!!***
- Gonorrhea, chlamydia, herpes, syphilis all cause proctitis
- NEED TO DO SEXUAL HX – ASK ABOUT ANAL INTERCOURSE
what is something you should NOT miss when doing initial work-up for UC pt?
STI proctitis – DON’T MISS THIS!!!***
- Gonorrhea, chlamydia, herpes, syphilis all cause proctitis
- NEED TO DO SEXUAL HX – ASK ABOUT ANAL INTERCOURSE
UC lab values
ESR is high (inflammatory marker)
CRP is high (inflammatory marker)
H/H is low
Albumin is low d/t malnutrition
-These patients will have anemia of chronic disease, microcytic hypochromic type of anemia
UC radiography
Plain films not much value
CT abd/pelvis (shows colitis/wall thickening, bowel obstruction, perforation)
is imaging part of the core dx of UC or CD?
NO!!! b/c you need to see what the tissue actually looks like -> DO TISSUE BX
imaging won’t tell you what type of colitis it is
what is the cornerstone tx of UC mild disease?
Aminosalicylates (5-ASA) drugs
-NSAID for colon
Meds:
- Mesalazine PR suppository for mild proctitis
- Rectal (suppository) and oral 5-ASA (ex: PO sulfasalazine and PR mesalazine) for distal colon inflammation (COMMON TO GIVE BOTH ORAL AND SUPPOSITORY)
what medication is recommended for maintenance (after remission) for UC?
5-ASA - RECOMMENDED FOR ALL MAINTENANCE THERAPY
medications for UC mild-moderate disease/failure of 5-ASA
Budesonide PO - targets colon with minimal systemic effects (can use prednisone, but budesonide is preferred)
MUST TAPER OVER 60 DAYS ONCE GAIN CONTROL OF SX’S
***NOT FOR MAINTENANCE THERAPY -> SWITCH TO 5-ASA AFTER TAPER FOR MAINTENANCE!!!
is Budesonide for maintenance therapy of UC?
NO!!!! Must taper over 60 days once gain control of six’s and then put on 5-ASA for maintenance
medications for UC severe disease
Hospitalization and IV steroids w/IVF
-Methylprednisolone (if doesn’t work use TNF-alpha blockers)
TNF-alpha blockers (used if IV steroids don’t work) - infliximab, adalimumab, golimumab
VGEF blocker - use if TNF-alpha blockers fail
-Vedolizumab
what medication do you use for UC if 5-ASA failed?
Budesonide PO
what is a last resort medication for severe UC?
cyclosporine
if methylprednisolone (IV steroids) doesn’t work for severe UC, what do you use?
TNF-alpha blockers
-infliximab, adalimumab, golimumab
if TNF-alpha blockers don’t work for severe UC, what do you use?
VGEF blocker
-vedolizumab
UC maintenance therapy meds
5-ASA
Immunosuppressants (azathioprine or 6-MP) if 5-ASA not working
If TNF-alpha blocker induction works, then continue with agent for maintenance or azathioprine (same for Golimumab)
***Probiotics help with maintaining remission - maintains gut flora
what meds help with maintaining remission in UC?
probiotics - maintains normal gut flora
what is the surgical treatment for UC?
Colectomy
-generally curative in UC and most common rationale is failure of medical management
when would a UC pt get an EMERGENCY colectomy?
Life-threatening complications related to fulminant disease such as toxic megacolon unresponsive to medical treatment
-Toxic megacolon = dilation of colon and develop ileus unresponsive to meds and need surgery
when would a UC pt get an URGENT colectomy?
Severe disease admitted to hospital and not responding to intensive medical treatment
what type of surgery for UC is the most common and who is it for?
Elective surgery (most common)
- Refractory disease intolerant to long-term maintenance treatments (ex: long-term steroid dependence)
- Colorectal dysplasia or adenocarcinoma found on screening bx
- Long-term disease 7-10 years
when is surgery recommended for UC
failure of medical management
what are UC patients at an increased risk of?
colorectal cancer
-increasing the longer they have disease
what must UC pts be screened for and starting when?
must be screened for colorectal cancer beginning at 8 years after disease onset (even if well-maintained disease)
after initial screening colonoscopy for UC pts, what does further screening depend on? when do you screen for proctitis/proctosigmoiditis, left-sided colitis/pancolitis, UC w/PSC?
extent of disease
Proctitis/proctosigmoiditis
-usually screened every year
Left-sided colitis/pancolitis: Screened every 1-2 years
UC w/PSC: Annually from time of dx of PSC
UC risk factors for colorectal cancer
Duration and extent of disease (how poorly controlled is the disease)
Colonoscopic and histologic severity of inflammation
what is Crohn’s disease characterized as?
Intermittent bouts of low grade fever, diarrhea and RLQ pain (flares and remission cycle)
Also have perianal disease (abscess, tissue, fistula)
what type of inflammation is in Crohn’s disease, what’s it’s distribution and what does it cause?
Transmural inflammation in skip lesion distribution causes strictures, fistulas, ulcerations, abscess
where does Crohn’s affect?
COMMONLY AFFECTS SMALL BOWEL AND COLON - USUALLY TERMINAL ILEUM AND ASCENDING COLON
-small bowel (usually terminal) can only be affected and colon can only be affected
what other disease is associated with having Crohn’s disease?
perianal disease (abscesses, fistulas, fissures)
can extra intestinal manifestations occur in CD?
Yes, but not as common as they are in UC
Includes:
- arthalgia
- iritis/uveitis
- Pyoderma gangrenous or erythema nodosum
Crohn’s disease Risk Factors
Genetic factors: Need good fam hx (strongest risk factor)
Environmental factors:
- **Smoking – significantly exacerbates Crohn’s disease
- Sedentary lifestyle, exposure to air pollution, and consumption of western diet
Infectious factors:
-CD often occurs after infectious gastroenteritis
smoking and Crohn’s disease vs smoking and UC
smoking exacerbates Crohn’s disease
smoking lowers risk/milder disease in Ulcerative colitis
Crohn’s disease clinical presentation
MUCH BROADER SX’S VS UC B/C AFFECTS ANY PART OF GIT
- abdominal pain (intermittent and is RLQ)
- diarrhea (watery/NONBLOODY!!!)
- constitutional six’s (low grade fevers, weight loss/anorexia/malnutrition, weakness/fatigue/mailase - anemia, bone loss (d/t malnutrition w/ CD)
- small bowel obstruction presentation (N/V w/abd pain)
- anal fissure/skin tag/abscess/fistula (perianal presentation)
what types of sx’s are more common in CD vs UC?
Constitutional sx’s
- Low grade fevers
- Weight loss/anorexia/malnutrition
- Weakness/fatigue/malaise (anemia)
- Bone loss – d/t malnutrition associated with CD
what are Complications of Crohn’s?
Abscess, Small bowel obstruction, Fistulas (and and rectovaginal), Perianal disease, Carcinoma, Malabsorption, possible hx of other autoimmune d/o’s
how do you treat abscess in Crohn’s?
Broad spectrum abx s/p CT diagnosis and surgery or
Percutaneous drainage (done by interventional radiologist)
what is occurring in small bowel of obstruction in CD? how do you treat it?
SBO chronic structuring or severe inflammation -> closes off part of gut
If have strictures then need low fiber diet - high fiber diet can
cause bowel obstruction
Tx:
-IVF, NGT decompression and IV steroid but if refractory possible partial resection or stricturoplasty
how do you treat fistulas in CD?
If symptomatic - TPN (parenteral diet)/oral elemental diet may close fistula temporarily (tried initially)
Antibiologics 10 weeks (1/2 recur)
Surgical resection if medical management fails
how do you treat perianal disease in CD?
abx (flagyl or Cipro) but recurrence is common
Mesalamine (5-ASA) suppository or tacrolimus ointment for refractory fissure
Antibiologics
***Medical management of Crohn’s first line with surgical intervention last resort
how do you treat Carcinoma in CD?
• Increased risk of colon cancer (same time interval as UC), thus screening with colonoscopy required for early identification of dysplasia/malignancy
***Screen at 8 years of disease
how do you treat Malabsorption in CD?
s/p multiple resection or bacterial overgrowth w/fistulas, strictures or stasis
CD Classification
Montreal classification used to categorize CD
- L-classification: Defines extent of disease (where in the GIT it is)
- B-classification: Defines phenotype (structuring, penetrating)
3 components of CD diagnosis?
Same 3 diagnosing components as UC:
(1) Clinical sx’s and presentations
(2) Sigmoidoscopy/colonoscopy
(3) Biopsy results/Histologic examinations
what must you r/o in CD?
As with UC, must r/o important non-infectious causes (IBS – dx of exclusion, Behcet’s syndrome) and infectious causes (Yersinia – terminal ileum inflamed like in CD – looks like CD, enteroviruses, etc.) that mimic CD
what is the GOLD STANDARD FOR DX in CD?
Colonoscopy and mucosal bx is GOLD STANDARD FOR DX (colon & terminal ileum)
- Really bx from any area w/disease
- Aphthoid, stellate, linear ulcers
- Strictures
-***Segmental involvement w/ skip lesions
CD radiologic tests for dx
- CT/MRI enterography or enteroclysis
- Show inflammation (just like in UC), but doesn’t change tx or labs
- ***LINEAR ULCERS ARE CLASSIC
Labs in CD
CRP is high, ESR is high, fecal calprotectin (inflammatory marker good for trending flares & remissions), H/H is low (present with anemia of chronic disease), albumin is low, WBC is high
what is the first thing pts with CD should be counseled on?
All patients with CD should be counseled to QUIT SMOKING (#1)
CD diarrhea tx’s
Loperamide (Immodium) - if sure no infectious cause of the diarrhea
Terminal ileal disease or resection = bile acid sequestrant
Short gut = low fat diet
Mild Crohn’s disease tx?
Colon and small bowel disease = mesalamine (can’t be maintained on 5-ASA)
5-ASA derivatives, which are mainstay of UC, have shown to be less useful in treatment of CD b/c mesalamine releases only in the terminal ileum and colon
Moderate-Severe Crohn’s disease tx?
Steroid therapy (BUDESONIDE)
Immunosuppressant’s (AZATHIOPRINE - 6-MP; METHOTREXATE - induces remission)
TNF-alpha blockers (infliximab, adalimumab, certolizumab pegol)
Anti-integrins (VEDOLIZUMAB) - used after TNF-alpha blockers
Fistula disease (METRO OR CIPRO, SURGERY IF MEDS FAILS)
what does Methotrexate do in CD?
it’s a tx for moderate-severe Crohn’s disease
IT CAN INDUCE REMISSION AND CAN HOLD PTS IN REMISSION
what do the TNF-alpha blockers in CD treat?
Fistulas - that aren’t responding to abx and conventional therapy
50% refractory cases respond well to TNF-alpha blockade
Use induction dosage until remission and then maintenance dosage
is surgery curative in CD like in UC?
NO!!! SURGERY IS NOT CURATIVE IN CD
-high rate of disease recurrence after segmental bowel resection so try to preserve as much bowel as possible
what are the indications of surgery in CD?
Abscess that you can’t drain percutaneously, intractable fistula, toxic megacolon, fibrotic strictures w/ obstruction, refractory sx’s despite high dose steroids, perforation, intractable hemorrhage, cancer
when do you admit a pt for CD?
- Bowel obstruction
- Abscess (intra-abdominal or perirectal)
- Severe symptoms of diarrhea/dehydration, weight loss/weakness, abdominal pain and can’t control it
- Serious infection complication in immunocompromised population (steroids, TNF-alpha blockers, imunomodulators)
what must you regularly screen for in CD?
Regularly screen for active infection
-Tuberculosis, hepatitis, CMV, HIV, and C. diff
CD Colorectal cancer screening
In patients with more than a third of colon affected (Montreal classification L3), first screening colonoscopy should occur 8 years after onset, repeated every 1-2 years and then every 1-3 years once normal
Patients with PSC should undergo annual screenings
-Risk of cholangiocarcinoma – need to be evaluated for this (high morality; cancer of biliary tree)
what is celiac sprue?
***Allergic reaction to gluten
Immunologic/inflammatory response to ingested gluten (gliadin = alcohol-soluble fraction of gluten) affecting mucosa of GI tract
what is gluten?
Gluten = wheat, rye, barley
what does Celiac Sprue affect?
mucosa of proximal small bowel
celiac sprue is a disease of what?
Disease of significant malabsorption b/c nutrients absorbed in small bowel, so if small bowel not working -> malnutrition, electrolyte abnormalities
at what ages do most people present with celiac sprue?
childhood-adulthood
what are the 2 types of sx’s for Celiac Sprue?
GI sx’s and extraintestinal symptoms
CAN HAVE ONLY EXTRAINTESTINAL SX’S (NO GI SX’S)
what does the severity of GI sx’s of Celiac Sprue depend on?
Severity depends on how much of small intestine is involved & age @ presentation
- < 2 years old malabsorption presentation
(Much sicker, not hitting growth milestones, have weight loss, abd distention)
-Older age +/- GI sx’s, less weight loss, more atypical sx’s, “silent” sprue (no GI sx’s)
Celiac Sprue GI sx’s
- Diarrhea
- Borborygmus, Flatulence
- Weight loss
In infants and young children with untreated celiac disease, failure to thrive and growth retardation are common (classic malabsorption)
- Weakness and fatigue MOST COMMON (usually related to general poor nutrition)
- Severe abdominal pain
Extraintestinal sx’s of Celiac Sprue
- Fatigue, depression, Fe-deficiency anemia
- Anemia
- Osteopenia and osteoporosis d/t malnutrition
- Neurologic symptoms (includes motor weakness, paresthesia’s with sensory loss, and ataxia; Seizures may develop)
Skin disorders
-Dermatitis herpetiformis
Hormonal disorders – Amenorrhea, delayed puberty, and infertility in women and impotence and infertility in men
what skin disorders do celiac pts develop?
Dermatitis herpetiformis
-a condition with pruritic, papulovesicular skin lesions involving the extensor surfaces of the extremities, trunk, buttocks, scalp, and neck
Celiac Sprue Physical Exam
LOOKING FOR SIGNS OF MALABSORPTION
- A protuberant and tympanic abdomen
- Evidence of weight loss (loss of muscle mass or subcutaneous fat)
- Orthostatic hypotension (could be d/t diarrhea)
- Peripheral edema (protein malabsorption)
- Ecchymoses (vit K deficiency)
- Hyperkeratosis (vit A deficiency) or dermatitis herpetiformis
- Cheilosis and glossitis (Fe-deficiency)
- Evidence of peripheral neuropathy or ataxia (vit B12 or E deficiency) – has to do with vibratory sense would be decreased
-Chvostek or Trousseau sign, tetany (Hypocalcemia) -Can induce tetany w/BP cuff or twitching w/ tap on face
Dermatitis herpetiformis
Celiac Lab Dx
CBC – anemia (Fe, folate, B12)
CMP – malnutrition, electrolyte imbalance
Coags – PT prolonged d/t malabsorption of vitamin K
Stool – fat malabsorption (72hr fecal fat collection to detect steaorrhea)
Oral tolerance tests – lactose intolerance (often associated with celiac) -> Hydrogen breath test
what serologic test do you use to dx Celiac?
IgA TTG - 95% sensitive and specific
what other Serologic testing can you do for Celiac dx?
IgA level
- If negative IgA TTG, but strong clinical suspicion
- 3% w/ IgA deficiency
If <2 years or IgA deficiency
-IgA TTG combined with testing for IgG-deamidated gliadin peptide (high sp/sens)
-All levels antibodies become undetectable s/p 3-12 months gluten avoidance so can monitor for compliance
when do IgA antibodies become undetectable in Celiac?
All levels antibodies become undetectable s/p 3-12 months gluten avoidance so can monitor for compliance
what is the GOLD STANDARD DX for Celiac Sprue?
Endoscopy and mucosal biopsy prox + distal duodenum
what will you see on Endoscopy and mucosal biopsy of pros + distal duodenum in Celiac Sprue?
Atrophy or scalloping of duodenal folds
Histology
-Villi are atrophic or absent
-Hypertrophy of crypts
(Celluarlity of the lamina propria is increased with a proliferation of plasma cells and lymphocytes)
what is the best dx for Celiac?
BEST DX IS TO TAKE PT OFF OF GLUTEN B/C THEN SX’S GO AWAY TO MAKE SURE IT’S NOT SOMETHING OTHER THAN GLUTEN; ALSO BEST TX!!!
Celiac Sprue tx
Diet, Supplements, Steroids
Celiac Sprue diet tx
- Essential therapy = removal of ALL gluten (wheat, rye, barley, oats may be contaminated during processing)
- improvement in 2 weeks on diet
- associated w/lactose intolerance -> avoid diary until sx resolution
Celiac Sprue supplements tx
- B/c Celiac is a malabsorptive disease
- Will have electrolyte imbalances, low K, low Mg, etc.
Use: Vit A, B12, D, E
- Initial stages only required usually not long-term
- Once villi improve then won’t have to supplement with vitamins as much b/c malabsorption goes away
Celiac Sprue steroids tx
- Prednisone or budesonide 2 or more weeks for severe sx’s
- Unintentional or intentional gluten ingestion may trigger severe diarrhea, hypovolemia, electrolyte imbalance
what is lactose intolerance?
Common disorder d/t inability to digest lactose
All of our lactase we will ever get is when we are very young (breast milk when a baby), but then declines steadily with aging especially in people of non-european descent
what is Lactase?
Lactase is a brush border enzyme that digests lactose into galactose and glucose
Lactose intolerance most common in?
- Asian Americans – 90%
- Native Americans – 95%
- African Americans – 70%
what disorders can lactose intolerance develop secondarily to?
- Celiac sprue
- Crohns
- Giardia
- Viral gastroenteritis
- Malnutrition
- Short bowel syndrome
if you don’t have lactase, then how does the gut breakdown lactose?
by fermenting it which is done by producing a lot of gas
DDx of lactose intolerance
IBD, IBS, pancreatic insufficiency, mucosal malabsorptive disorders
Lactose intolerance clinical presentation
- Sx’s occur when ingested a raw milk product (ex: milk, cheese)
- Abdominal bloating
- Abdominal cramping
- Flatulence
- Diarrhea/loose stool (with higher intake of lactose)
- Nausea
- Borborygmi
- Severity of sx’s depends on quantity ingested and severity of deficiency
***EXCLUDE LACTOSE AND SX’S RESOLVE!!!
Lactose intolerance labs
Hydrogen breath test
After ingestion of 50g lactose a rise in breath H+ of greater than 20ppm w/in 90 min
Lactose intolerance tx
Goal of therapy is patient comfort and determining “threshold” of intake when symptoms occur
Spread lactose intake throughout the day in quantity <12 g (1 cup of milk) and most pts tolerate this w/o lactase
Lactase enzyme replacement
- Lactaid, Lactrase, Dairy Ease
- Quantity taken with lactose or number of capsules = degree of intolerance
- Some foods are pretreated with lactase (ex: Milk which = 70-100% lactose free)
Calcium supplementation if exclude dairy (prevent osteoporosis)
