Clinic blood pressure (BP) is recognized as the gold standard for the screening, diagnosis, and management of hypertension. However, optimal diagnosis and successful management of hypertension cannot be achieved exclusively by a handful of conventionally acquired BP readings. It is critical to estimate the magnitude of BP variability by estimating and quantifying each individual patient’s specific BP variations. Short-term BP variability or exaggerated circadian BP variations that occur within a day are associated with increased cardiovascular events, mortality and target-organ damage. Popular concepts of BP variability, including “white-coat hypertension” and “masked hypertension”, are well recognized in clinical practice. However, nocturnal hypertension, morning surge, and morning hypertension are also important phenotypes of short-term BP variability that warrant attention, especially in the primary-care setting. In this review, we try to theorize and explain these phenotypes to ensure they are better understood and recognized in day-to-day clinical practice.

Lemierre syndrome is an uncommon condition classically described in acute oropharyngeal infection with septic thrombophlebitis of the internal jugular vein and metastatic septic embolism particularly to the lungs. It is commonly described in young healthy adults with isolation of Fusobacterium necrophorum. We describe a case of Lemierre syndrome in a 50-year-old man with newly diagnosed diabetes mellitus presenting with a neck abscess secondary to Klebsiella pneumoniae. Our patient made good recovery to appropriate antimicrobial therapy, prompt surgical drainage, and anticoagulation. Anticoagulation remains controversial and we review the literature for its role in Lemierre syndrome.

Inpatient anticoagulation care and outcomes were significantly improved by a pharmacist-managed anticoagulation service. The time to therapeutic INR was achieved appropriately and efficiently without compromising patient's safety.

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Patients with human immunodeficiency virus (HIV) are at risk of developing thrombosis and are 8 to 10 times more likely to develop thrombosis than the general population. Moreover, if they have hypercoagulable state they can have severe thrombosis and life-threatening thrombotic events. The purpose of this retrospective study is to analyze hypercoagulable state in HIV-seropositive patients who have been diagnosed with venous thromboembolism (VTE). This study is a subgroup study of a larger cohort group of HIV-seropositive patients with VTE followed up with our vascular medicine outpatient clinic. The patients included for this study were HIV-seropositive patients with hypercoagulable state, analyzed over the past 3 years, and followed prospectively. HIV-seropositive patients with arterial thrombosis were excluded. These patients had minimum, regular follow-up of 3 months, with a Doppler scan in the beginning and last follow-up. All the patients were analyzed for hypercoagulable state and the patients selected in this study were those who were tested positive for hypercoagulable state. All patients were analyzed for age, gender, race, site of thrombosis, coagulation factors, lipid panel, type of antiretroviral treatment, past or present history of infections or malignancy, CD4 absolute and helper cell counts at the beginning of thrombosis, and response to treatment and outcome. Patients with HIV with arterial thrombosis were excluded. The study was approved by the ethics committee. Five patients were included in this study. The mean age was 47.8 years (range 38 to 58 years). All were male patients with lower limb thrombosis. Most common venous thrombosis was popliteal vein thrombosis, followed by common femoral, superficial femoral, and external iliac thrombosis. Two patients had deficiency of protein S, two had high homocysteine levels, one had deficiency of antithrombin 3, and one had increase in anticardiolipin immunoglobulin G antibody. All the patients were taking nucleoside and nonnucleoside inhibitors but only one patient was taking protease inhibitors. There was no history of malignancy but two patients had past history of tuberculosis. The mean absolute CD4 counts were 244 cells/UL (range 103 to 392 cells/UL) and helper CD4 counts were 19.6 cells/UL (range 15 to 30 cells/UL). All were anticoagulated with warfarin or enoxaparin. There was complete resolution of deep vein thrombosis only in one patient on long-term anticoagulation but there was no resolution of thrombosis in the other four patients despite of therapeutic anticoagulation for more than 6 months. All the patients are alive and on regular follow-up. Thrombosis in HIV patients is seen more commonly in middle aged, community ambulant male patients. The most common hypercoagulable state was noted as deficiency of protein S and hyperhomocysteinemia. Eighty percent of the patients did not respond to therapeutic anticoagulation.

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