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Vol. 66, No. 4 2015
Northeast Florida Medicine
DCMS online
. org
Inflammatory Bowel Disease
including fungal infections, disseminated histoplasmosis,
and coccidiomycosis.
3
Infliximab has been implicated in
the development of disseminated herpes zoster. Alveolar
hemorrhage, lupus-like reactions, and ARDS have all been
reported in patients exposed to infliximab therapy.
13
Renal and Urologic Manifestations
Renal manifestations can occur in anywhere from 4-23
percent of patients with IBD.
15
Several types of glomerulo-
nephritis have been reported including IgA nephropathy,
minimal change glomerulonephritis, and membranoprolif-
erative glomerulonephritis (MPGN). When the intestinal
tract is put into remission, these renal diseases commonly
improve. Tubulointerstitial nephritis can be drug induced,
such as that with the use of 5-ASA products, but it is also
a recognized extraintestinal manifestation of IBD. A rare
but serious disorder, more commonly seen with Crohn’s
than ulcerative colitis, is amyloidosis. It is characterized by
extracellular deposition of proteolytic fragments of serum
amyloid A. In the kidney, it presents with proteinuria, which
can lead to nephrotic syndrome and renal failure. The main
goal to prevent progression of amylodosis is to control the
underlying inflammatory condition.
The most common renal complication in IBD is neph-
rolithiasis with a prevalence of 5 to 15 percent.
15
Patients
with Crohn’s are more frequently involved. Typically this is
in patients that have ileocolonic involvement. Most of these
kidney stones are calcium oxalate or uric acid stones. Bile
acid malabsorption with fatty acids reaching the colon is the
most important cause of calciumoxalate stone formation. As
a consequence of free fatty acids binding the calcium within
the colon lumen, increased amounts of free oxalate are then
reabsorbed, increasing the risk of oxalate stones. Calcium
supplementation is recommended. Decreased urine pH as
a result of diarrhea and low urine volumes may lead to uric
acid stone formation. Therefore, to prevent uric acid stones,
fluids are mandatory and a purine reduced diet is encour-
aged along with alkalinization of the urine. Finally, patients
with Crohn’s disease may develop enterovesical fistulae and
perivesical abscesses. Obstructive uropathy may occur as
a result of retroperitoneal inflammation with fibrosis and
scarring in long-termCD. Asmentioned, drug-induced renal
complications from the 5-ASA products are important. Cy-
closporin and tacrolimus can induce acute renal dysfunction
as a result of renal vasoconstriction. Glomerulonephritis has
been described as a result of anti-TNF therapy.
15
Neurologic Manifestations
In recent years, neurologic symptoms in IBD patients are
gainingmore attention.MRI studies have revealed intracere-
bral focal whitematter lesions, mimickingMultiple Sclerosis
(MS), in up to 42 percent of patients with asymptomatic
Crohn’s and 46 percent of patients with asymptomaticUC.
16
Peripheral neuropathies are themost common features.These
neuropathies do not follow intestinal activity, nor do they
respond to IBD specific treatments. Central Nervous System
involvement in IBDcan include demyelinating diseases such
as MS or ischemic optic neuropathy. B12 deficiency from
ileal Crohn’s can lead to a peripheral polyneuropathy. This
can also be seen in patients who have had ileal resection
from chronic disease. Drug-induced neurotoxicity is also
important. The use of metronidazole, sulfasalazine, and the
calcineurin inhibitors can induce a peripheral neuropathy.
These patients can have tremor, psychosis, paresthesias,
ataxias, and a variety of motor defects. Anti-TNF therapies
may be associated with a Guillain-Barre-like syndrome or a
chronic demyelinating polyneuropathy.
16
The description of
progressivemultifocal leukoencephalopathywith the alpha-4
integrin inhibitor Natalizumab has thwarted its use.
Anemia
Anemia is a common extraintestinal symptom in patients
with IBD, seen in up to a third of patients.
3
One major
cause is the chronic disease itself associated with activation
of cell mediated immunity. Chronic intestinal blood loss,
inadequate dietary intake or malabsorption of iron, B12,
folate are reasons for anemia, as well as drug-induced
toxicity from medication such as azathioprine or 6-MP
or methotrexate.
Iron deficiency anemia can be profound. Iron supplemen-
tation can be attempted by mouth, but commonly has to
be given intravenously to restore bone marrow function to
most of these patients. Occasionally, erythropoietin therapy
may be needed. B12 and folate deficiency lead to macrocytic
megaloblastic anemia. In Crohn’s disease, this is related to
ileal involvement. Deficiencies in B12 can appear up to two
years after surgery when extensive storage of B12 in the
liver is depleted. Vitamin supplementation, parenterally, is
mandatory in these patients.
Metabolic Bone Disease
Osteoporosis and osteopenia are common in patients with
IBD (20-50 percent).
17
Hip fractures may be more common
in these individuals due to age, steroid treatment, smoking,
low physical activity, and inflammatory cytokines. Bone
densitometry (DEXA scanning) helps define the presence
of osteoporosis. Factors contributing to osteopenia and os-
teoporosis are the chronic inflammation caused by increased
circulating levels of cytokines including IL-1, IL-6, andTNF.