Ankylosing spondylitis and IBD

VA morning report had a great case yesterday of a young patient with back pain and GI bleeding that was found to have Anklyosing Spondylitis and associated IBD! Thanks to Dr Bhushan, we have a great review article to share with you all. Here are some highlights:

  • 5-10% of patients with Ankylosing Spondylitis are associated with IBD (either Crohn’s or UC)
  • Inflammation of the axial skeleton is the major hallmark of AS, occuring in more than 90% of patients and is typically characterized by inflammatory low back pain and morning stiffness due to sacroilitis or spondylitis
  • AS can also exhibit peripheral synovitis +/- enthesitis. Peripheral joint involvement is generally oligo-articular and asymmetric and is generally non-erosive, self-resolving joint pain
  • Although 75-90% of AS patients have associated HLA-B27 molecule, only 50-70% of AS and IBD patients are HLA-B27 positive
  • Although 5-10% of AS patients have overt IBD, up to 40-60% of AS patients have subclinical gut inflammation – current guidelines do not recommend screening asymptomtic patients with colonoscopy
  • The clinical implications of this fact are that NSAID therapy can pose a severe problem in AS patients with underlying IBD (the mainstay of medical therapy in AS is NSAIDs)
  • Treatment options for AS asscociated with IBD include physiotherapy, local corticosteroids and anti-TNF agents
  • Unfortunately, conventinoal disease-modifying anti-rheumatic drugs such as MTX, azathioprine or sulfasalazine (all effective for IBD) do not show improvement in axial AS symptoms
  • Anti-TNF agents such as infilximab and etanercept are highly effective in treating active AS and are recommended for patients with active AS that cannot tolerate NSAIDs
  • Interestingly, only inflximab has been showed to have clinical efficacy in IBD sx (not etanercept). The mechanism for this difference is unclear.
  • Check out the whole article here!

DRESS Syndrome

Over at the University, we discussed the variety of drug-related reactions, particularly DRESS Syndrome. Take a look, it may come up in potpourri some day!


  • Drug Reaction with Eosinophilia and Systemic Symptoms
  • <1/100,000 people in the general population
  • Highly variable clinical presentation
  • No strict diagnostic criteria


  • Antiepileptic agents (eg, carbamazepine, lamotrigine, phenytoin, phenobarbital)
  • Allopurinol
  • Sulfonamides (particularly sulfasalazine)
  • Dapsone, minocycline, and vancomycin
  • HLA-B 5801: allopurinol
  • HLA-A 3101: carbamazepine

Drug Rash:

  • Initially presents as a morbilliform eruption
  • Face and upper part of the trunk and extremities are involved initially
  • Progresses to a diffuse, confluent, and infiltrated erythema with follicular accentuation
  • Often involves more than 50 percent of the BSA – extent of involvement suggests severity
  • Can progress to exfoliative dermatitis, vesicles, pustules


  • Leukocytosis with eosinophil counts >700/microL (in 50 to 90 percent of cases)
  • Atypical lymphocytosis with large activated lymphocytes, lymphoblasts, or mononucleosis-like cells (in 30 to 70 percent of cases)
  • Increased serum ALT (in up to 80 percent of cases)
  • HHV-6 infection (in 40 to 60 percent of tested patients)

Systemic Symptoms:

  • Fever, malaise, lymphadenopathy
  • Liver: mild transaminitis to frank hepatitis and acute liver failure. Severe hepatitis is responsible for the majority of deaths associated with DRESS.
  • Kidney (acute interstitial nephritis)
  • Lungs (eos on BAL, interstitial pneumonitis)
  • Heart (eosinophilic myocarditis, pericarditis)
  • Gastrointestinal tract (diarrhea, mucosal erosions, bleeding)
  • Pancreas (pancreatitis)
  • Thyroid (autoimmune thyroiditis, appearing often late, as a sequel of DRESS)
  • Brain (encephalitis, meningitis)
  • Muscle (myositis)
  • Peripheral nerves (polyneuritis)
  • Eye (uveitis)


  • Mainstay: withdrawal of the offending drug
  • Exfoliative dermatitis: fluids, electrolytes, and nutritional support
  • High potency topical corticosteroids for symptomatic management
  • Supportive care of organ involvement
  • Usually resolves in 6-9 weeks, but can last up to 6 months


Is my patient at risk for MRSA pneumonia?

Today at Parkland Morning Report we talked about selection of antibiotics for suspected pneumonia and when to cover for MRSA. There are several studies that have looked at risk factors for MRSA pneumonia, but there is no general consensus. This seems to imply that risk factors depend on the location of the community and hospital. Below are some risk factors associated with MRSA pneumonia (includes HAP/HCAP and community acquired):

  • Immunocompromised
  • Active or post-influenza infection
  • Recent antibiotic use (particularly cephalosporins and fluoroquinolones)
  • Multilobar infiltrate – cavitary and necrotic lesions
  • IV Drug Use
  • Pleural Effusion
  • Dialysis patient

Check out this interesting case-control study from 2013 in Respiratory Medicine that looked at risk factors for MRSA pneumonia at an academic university hospital. The study looked at risk factors associated with MRSA pneumonia, both hospital/health care and community acquired forms.

Risk factors for methicillin-resistant Staphylococcus aureus in patients with community-onset and hospital-onset pneumonia

Enter your publications, presentations, or abstracts!

Have you published an article, abstract, or manuscript recently? Have you presented at a local, state, or national conference? If so, send us the information below! We want to know all of the amazing things you have done and let the rest of the program know as well!

Does my patient still need bladder cancer surveillance?

At VA morning report today we had a patient who was >10 years out from TURBT for his bladder cancer and so we asked “does this patient still need surveillance?” As internists, we share the responsibility of cancer surveillance post treatment so this is an important question to ask!

  • GU cancers account for 22% of new cancer cases in the US (in 2000)
  • For non-muscle invasive bladder cancers the treatment is TURBT +/- intravesicular therapy (often BCG)
  • Bladder cancer patients are at risk for recurrance in organs that share the genitourinary epithelium such as renal pelvis, ureter, prostate, bladder
  • For follow up, the recommendations are to perform cytoscopy and urine cytology starting 3 m after therapy and q 3 months for two years, then q 6 m for two years. After that the recommendation is for yearly cytoscopy and urine cytology lifelong
  • Three studies have looked at the need for lifelong follow up with data showing that there is a high rate of recurrance early on with significant decline in risk as time progresses (eg one study looked at 86 pts with high risk bladder cancer and found 31% had progression at 5 years and 5% had progression at 10 yrs)
  • The AUA guidelines however currently support lifelong follow up:
  • The high frequency of local recurrence and the potential for stage progression especially for high-risk disease highlights the importance of vigilant surveillance with cystoscopy for patients with nonmuscle invasive bladder cancer. Furthermore the potential for disease recurrence and progression even in the long term typically requires and necessitates lifelong follow-up
  • Check out this article that summarizes follow up  for bladder cancer, prostate cancer, RCC and testicular cancer:
  • Full AUA guidelines:

Eculizumab – When is it used?

Today at Parkland Morning Report we discussed about the utility of the medication, eculizumab, for hemolytic uremic syndrome. Below are some interesting articles regarding treating thrombotic thrombocytopenic purpura, hemolytic uremic syndrome (HUS), and eculizumab. Key points below:

  • Eculizumab is a recombinant, humanized, monoclonal anti-C5 antibody. It binds to C5 which halts the complement cascade and inhibits production of protein complexes that kill cells.
  • Blocks terminal complement activation, thus patients may have higher risk to infections from encapsulated bacteria such as Neisseria meningitides, Haemophilus influenzae and pneumococci as vaccination is recommended.
  • Used to treat paroysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS).
  • Atypical HUS is distinguished from classic HUS in that it primarily involves the kidneys and seems to have a clear link to dysregulation of the complement system.
  • In regards to administration, patients typically receive 4 weekly IV doses for induction, then a maintenance dose every 2 weeks for aHUS. Duration is unclear as some patient remain on therapy indefinitely. Alternative therapy is plasma therapy.
  • Eculizumab side effects include constipation, nausea, vomiting, tachycardia, fever.
    How I treat thrombotic thrombocytopenic purpura and atypical haemolytic uraemic syndrome
    Update on hemolytic uremic syndrome: Diagnostic and therapeutic recommendations

JNC 8 – Hypertension Guidelines

As firm D rotates through clinic week and provide excellent care for their PCIM and PRIME patients (I’m looking at you, Bujanda), I thought a quick run-down of the most recent, evidence-based hypertension guidelines was in order!

  • In patients 60 years or older who do not have diabetes or chronic kidney disease, the goal blood pressure level is now <150/90 mm Hg.
  • In patients 18 to 59 years of age without major comorbidities, and in patients 60 years or older who have diabetes, chronic kidney disease (CKD), or both conditions, the new goal blood pressure level is <140/90 mm Hg.
  • First-line and later-line treatments should now be limited to 4 classes of medications: thiazide-type diuretics, calcium channel blockers (CCBs), ACE inhibitors, and ARBs.
  • Second- and third-line alternatives included higher doses or combinations of ACE inhibitors, ARBs, thiazide-type diuretics, and CCBs. Several medications are now designated as later-line alternatives, including the following: beta-blockers, alpha-blockers,  central alpha2/-adrenergic agonists (eg, clonidine), direct vasodilators (eg, hydralazine), loop diruretics (eg, furosemide), aldosterone antagoinsts (eg, spironolactone).
  • When initiating therapy, patients of African descent without CKD should use CCBs and thiazides instead of ACE inhibitors.
  • Use of ACE inhibitors and ARBs is recommended in all patients with CKD regardless of ethnic background, either as first-line therapy or in addition to first-line therapy.
  • ACE inhibitors and ARBs should not be used in the same patient simultaneously.
  • CCBs and thiazide-type diuretics should be used instead of ACE inhibitors and ARBs in patients over the age of 75 years with impaired kidney function due to the risk of hyperkalemia, increased creatinine, and further renal impairment.

Take a look at the source: 2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults

Fungal Tests

Today at Parkland Morning report we discussed about different fungal tests with Dr. Lee from the Infectious Disease department at UT Southwestern. Below are some key points from today’s discussion:

  • The clinical presentation, patient’s history, and risk factors should ultimately guide what fungal tests you order.
  • Candida and Cryptococcal spp. can be detected by standard blood cultures. There is research currently looking at the utility of fungal blood cultures.  (1)
  • Galactomannan serum assay tests for Aspergillus antigen and is used to aid in the diagnosis of invasive aspergillosis. This test is particularly useful if cultures or histopathological evidence cannot be obtained. The galactomannan can be detected 7-14 days before clinical signs develop. A negative result does not rule out Aspergillus infection. Some antibiotics such as piperacillin, amoxicillin, and augmentin can cause false-positive results. (2)
  • A “fungal comp fix” assay refers to antibody testing to fungal infections. The fungal antibody panel tests for IgG and IgM for Blastomycosis, Coccidoidomycosis,and Histoplasmosis, although they won’t discriminate between the acute vs chronic antibody form. A positive result means current or past infection. Some labs are eliminating panels as you have to order antibodies for each species.  (3)
  • Urine histoplasmosis antigen has a high sensitivity (>90%) in disseminated disease. It has even higher sensitivity when combined with serum test. Poor sensitivity in chronic and self-limited disease. (4)





How to diagnose a patient

Below is an interesting article from Dr. Gupreet Dhaliwal, an associate professor in Internal Medicine from UCSF. He discusses techniques and skills in reasoning in trying to come up with the right diagnosis for a patient. Special thanks to Brian Davis (PGY-02) for sharing this!

UTSW Internal Medicine

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