See the following review on Hypertriglyceridemic Pancreatitis:

• American Journal of Gastroenterology VOLUME 104 | APRIL 2009

Key teaching points:

• Protease inhibitors and NNRTIs can cause transaminitis, or worsen existing hepatitis
• Acute CMV can present in many ways,  including as a hepatitis. It differs from EBV and MAI, which can also present with hepatitis, in that it does not necessarily present with lymphadenopathy as EBV and MAI would.
• Treatment with ganciclovir is only indicated in severe disease with hemodynamic compromise or CNS (including retina/eye) involvement
• Counsel patients on transmission via bodily fluids and potential for congenital defects (hearing loss most commonly, but can be severe with multi-organ involvement) with maternal transmission of primary or existing infection trans-placenta or via breast feeding
• Think about reactivation of existing infections as well as acute primary infections in patients with advanced AIDS who are started on ART causing an immune reconstitution inflammatory syndrome (IRIS). Always try to continue ART through IRIS, although this may not be possible in life-threatening infections or complications of drug therapy.

Here is a nice review of drug allergy/hypersensitivity reactions.

Kikuchi’s disease is a rare disorder characterized by fever and lymphadenopathy and diagnosed by lymph node biopsy showing necrosis and histiocyte invasion. It is self-limiting. It has been associated with EBV, although no definitive causality has been established.

Subclavian Stenosis Epidemiology paper in JACC - http://content.onlinejacc.org/cgi/content/full/44/3/618

36 year old Haitian F with pmhx signficant for pseudotumor cerebri, R thyroid nodule who presented with fevers x 3 weeks and bilateral cervical lymphadenopathy.  Exam notable for bilateral enlarged cervical & supraclavicular nodes (largest 3 x 5 cm) with labs notable for normal WBC count with lymphocyte predominance and elevated ldh.  Full infectious workup including HIV & Tb studies negative as well as connective tissue disease workup which was negative.  Eventually, CT c/a/p performed notable for diffuse lymphadenopathy leading to a bone marrow biopsy which ultimately revealed acute lymphoblastic T cell leukemia with 53% blasts confirmed by excisional biopsy.  She was treated based on the ECOG2993 protocol but ultimately never achieved complete remission and passed awy.  Teaching objectives included fever of unknown origin and acute lymphoblastic leukemia.

Fever of Unknown Origin: http://www.ncbi.nlm.nih.gov/pubmed?term=9284789

Acute lymphoblastic leukemia (t-cell): http://www.ncbi.nlm.nih.gov/pubmed/19828704

Here is a little review about GI manifestations of lupus.

Rheumatology (1999) 38 (10):917-932

There are 3 types of Brugada syndrome, however type I is most common. It is related to a loss of function mutation in the SCN5A gene that encodes the myocyte sodium channel, leading to a shorter refractory period and conduction blockage which can precipitate a local reentry and subsequent VF/VT. First degree relatives should be screened with EKGs. Brugada syndrome (differentiated from the EKG pattern alone, which can be induced by fever or other sympathetic surges) is diagnosed by the EKG findings AND one of the following:

a)  Documented ventricular fibrillation
b)  Self-terminating polymorphic ventricular tachycardia (VT)
c)  Family history of sudden cardiac death at <45 years
d)  Type 1 ST segment elevation in family members
e)  Electrophysiologic inducibility of VT
f)  Unexplained syncope suggestive of a tachyarrhythmia
g)  Nocturnal agonal respiration

Arrhythmia inducing medications in Brugada syndrome are listed here: http://www.brugadadrugs.org/

Chest x-ray showed a large left pleural effusion with mediastinal shift to the right and CT showed 2 pleural based masses on the left as well as diffuse lymphadenopathy. Thoracentesis was performed with great care to drain slowly to reduce the risk of reexpansion pulmonary edema (risk only exists if collapse > 3 days, and is not related to volume of the effusion – nice review here). Cytology was negative as was ADA in search of possible TB although he had no risk factors. Lymph node biopsy showed a poorly differentiated squamous cell cancer. Palliative care was involved early – it has been shown to reduce hospitalization, improve quality of life and length of survival somewhat.

Remember that although smoking cessation returns risk of many diseases back to population risk, it does not do so completely for everything (i.e. lung cancer) and they are still at risk for earlier mortality (see article). Also, note that although this patient had not had any medical care for 20 years, there is no recommendation for routine lung cancer screening in patients and so his cancer would likely not have been diagnosed any earlier had he been in care, unless it was discovered incidentally – one big problem with lung cancer is that we often catch it too late! These recommendations may change in the future, so be on the look out for more articles like this one.

A paracentesis was performed in the middle of the night. Remember, paracentesis is a relatively safe procedure with < 1% chance of transfusion-requiring hemorrhage. Risk factors for SBP include large volume ascites, higher MELD scores and prior incidence of SBP. SBP occurs via translocation of bacteria from the GI tract to ascites or more commonly to the lymphatic system then ascites. Gram stain has little role given the low concentration of bacteria. Remember that > 250 PMNs in the ascites is diagnostic of SBP. Antibiotic of choice is a 3rd gen cephalosporin – cefoxatime or ceftriaxone – to cover GI flora.

This patient did not have SBP and it is thought that despite taking his diuretics, he was taking in a particularly salty diet. His ascites has not re-accumulated while in the hospital.