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2020 National Conference | Cross-Specialty Panel Discussion Q&A

I often notice what I believe to be nail pitting in patients who have no psoriatic plaques but do have enthesopathy, which makes me consider PsA in the differential. Are there any diagnostic tools to confirm definitively that I am seeing nail pitting?

  • Nail pitting can be seen in other conditions, such as atopic dermatitis and alopecia areata. In psoriatic diseases, you may see nail pitting with the naked eye. A dermatoscope can be helpful in magnifying the nails for a closer look, but psoriasis patients may have other nail changes that can provide a clue for clinical diagnosis, including oil spots, which can be seen as round, yellowish-brown macules under the nail. Nail yellowing, thickening, and distal lifting are further symptoms that may be misdiagnosed as onychomycosis (fungal infection of the nails).


When you suspect a myositis, how often do you order a thigh MRI? Do you order that instead of an EMG?

  • I prefer an EMG of all four extremities, but, if the wait time for an appointment with the neurologist is too long, I order an MRI of the most affected extremity.


JAK inhibitors for dermatomyositis? Did I hear that correctly?

  • Yes, although they do not have an approved indication for PM or DM. Some small case studies treating refractory disease have used JAKs with promising results. 

Is the concern related only to HCTZ or does it extend to other thiazide diuretics, such as chlorthalidone?

  • All hypertensives have been implicated in drug-induced SCLE, including ACE inhibitors, calcium channel blockers, beta blockers, and diuretics 


Does subacute cutaneous lupus ever turn into systemic lupus?

  • Typically, SCLE is not characterized by systemic involvement, but 10% - 15% of cases can develop systemic disease, and most have mild symptoms. We should, however, screen patients at every OV to assess the systemic involvement. 


Are lupus vesicular lesions painful?

  • They are often itchy and sometimes cause a burning sensation (like a sunburn).


How do you differentiate between vesicles from SLE and those from zoster? Also, what are the merits of omeprazole compared to other PPIs?

  • An eruption of fluid-filled lesions, such as vesicles (<1 cm) or bullae (>1 cm), often occurs on sun-exposed areas in a patient with SLE while zoster typically affects a dermatome and is usually vesicular. The exception for zoster is when it is disseminated, in which case the vesicular eruption is generalized, and the patients are usually very ill. 

Is quinacrine available again?

  • Currently, there is a quinacrine shortage as it did not pass inspection and so has not been available for import to the US, but it can be found at a few compounding pharmacies. 

How often do you use dapsone?

  • I personally do not have a large number of patients on dapsone, but I do have a handful of patients with refractory disease for whom I have used dapsone.

I saw a patient for a new consult due to a rash, and the Bx favored the changes to be most consistent with the process of a connective tissue disease, such as lupus erythematosus. The serologies were all negative, and there are no other complaints besides the rash. The patient is on Remicade for UC and is well controlled. Do you think the rash is drug induced from the Remicade, even with negative ANA and ENAs?

  • Lupus-like reactions can occur secondary to drugs. Anti-histone levels may be elevated. The timing of the eruption relative to the start (or increased dosage) of Remicade needs to be explored. Furthermore, the morphology, distribution, and other features of the skin eruption must be taken into consideration in order to make a clinicopathological correlation. This case scenario needs additional information.

With joint symptoms appearing first in IBD, what are your first-line treatment choices?

  • For joint pain, I start with sulfasalazine and then methotrexate if there is no improvement. I also add curcumin 2,000 mg daily. There have been numerous studies showing that curcumin helps with joint pain associated with IBD. 

PPIs have been implicated in a variety of gut microbiome issues (D and B vitamin absorption, increased osteoporosis risk, etc.). From a GI perspective, is there any reason NOT to stop patients’ PPI if adding probiotics reduces their symptoms enough for PRN PPI use?

  • Continuing PPIs in the presence of gut microbiome issues is fine from a GI perspective, especially if the PPI is helping the patient’s upper GI symptoms.

Regarding a previous PPI question clarification, if there is concern about Barrett’s, is the PPI preventative (i.e., necessary for prevention) or just for symptom control? 

  • Once a patient is diagnosed with Barrett’s, we use a PPI for both prevention of dysplasia and management of symptoms.

When you talk about the patient with a new rash who is on biologics, you mention checking antibodies. What lab do you order?

  • When a patient on infliximab appears with a new rash, I recommend checking infliximab drug levels and infliximab antibodies. The infliximab antibodies will be helpful in discerning whether the patient has built up antibodies that could be the cause of the new rash. 

How much are NSAIDs contraindicated in IBD? Is it different for Crohn’s vs. UC?

  • NSAIDS are contraindicated in both Crohn’s disease and ulcerative colitis. There is no difference between the two regarding the contraindication of NSAIDS. NSAIDS can disrupt the GI tract’s mucosal lining and prompt an IBD flare. I always recommend to my patients to take only Tylenol and avoid NSAIDS. 

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