Category Archives: Cox’s Conference

Cox’s Conference: Recurrent hypokalemia – Liddle Syndrome

In today’s Cox’s Conference, Dr. Jan Ramesh with expert discussant Dr. Biff Palmer presented a case of recurrent hypokalemia in the setting of lifelong hypertension that ultimately was diagnosed as Liddle Syndrome.

Continue reading Cox’s Conference: Recurrent hypokalemia – Liddle Syndrome

Cox’s Conference: Antiphospholipid Antibody Syndrome

At today’s Cox’s Conference, Dr. Josephine Harrington with expert discussant Dr. Srikanth Nagalla of antiphospholipid antibody syndrome.


-Antiphospholipid antibody syndrome should be suspected in a patient with unprovoked venous and arterial thromboses, especially in a young patient without provocation. Testing can also be considered in women with histories of pregnancy loss, intrauterine growth restriction, preeclampsia, and abruption in settings in which antiphospholipid syndrome is suspected (testing should be limited to lupus anticoagulant, anticardiolipin Ab, and beta 2 glycoprotein Ab)

-Diagnosis is based on clinical criteria of thromboses or pregnancy morbidity in the presence of antiphospholipid antibodies. The antiphospholipid antibodies used in the Sapporo classification are anticardiolipin (IgG and IgM), anti-beta2-glycoprotein (IgG or IgM), and lupus anticoagulant. Repeat confirmatory laboratory testing of the above antiphospholipid antibodies should be confirmed >= 12 weeks apart

-Remember that you need clinical features and laboratory features to diagnosis antiphospholipid antibody syndrome. Thus, there is no value in testing asymptomatic patients

-Multiple positive antiphospholipid antibodies, particularly triple positive (anticardiolipin, anti beta2 glycoprotein, and lupus anticoagulant) are at higher risk of thrombosis

Q: What is the importance of diagnosing antiphospholipid antibody syndrome, particularly in men, who will not have the pregnancy related complications?

A: Antiphospholipid antibody syndrome, due to its high risk of recurrence, typically requires indefinite anticoagulation. This is in contrast to unprovoked or provoked venous thromboses, for which discontinuation can be entertained. However, patient risk factors for bleeding, patient preference, and antibody positivity (e.g. triple positive vs single positive) should be taken into consideration. Moreover, the diagnosis of antiphospholipid antibody syndrome has implications on choice of anticoagulation. The evidence for the use of direct acting anticoagulants is scant, partially due to the rarity of disease limiting feasibility of large scale trials. The RAPS trial demonstrated non-inferiority of rivaroxaban when compared to warfarin; however, surrogate markers of thrombogenicity were used and long-term studies examining the actual thrombosis event rate of rivaroxaban vs warfarin are lacking. Thus, there is a general bias towards vitamin K antagonists in the treatment of antiphospholipid antibody syndrome. Additionally, the knowledge that antiphospholipid syndrome is driving thrombosis may yield additional treatment considerations for recurrent thrombosis while therapeutic on vitamin K antagonists. Hydroxycholroquine has been suggested to decrease the risk of thrombotic events and may be considered as add-on therapy to anticoagulation in such patients.

Q: Can anticoagulation be discontinued based on falling titers of antiphospholipid antibody titers later in life?

A: This is a great question whose answer is waiting to be discovered.