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Rheumatoid vasculitis (RV) is an infrequent complication of longstanding severe rheumatoid arthritis (RA). The active vasculitis associated with rheumatoid disease occurs in about 1%-5% of the patient population. RV is a manifestation of "extra-articular" rheumatoid arthritis and involves the small- and medium-sized arteries in the body. Newer RA treatments, including biologic therapies, offer a broader array of potential therapeutic options, although no controlled trials exist to guide treatment. In general, following tissue confirmation of the diagnosis, the severity of organ involvement and disease manifestations can guide treatment decisions. We want to alert clinicians of this unique yet severe complication of RA which has high morbidity and mortality. We describe a thought-provoking case of a 44-year-old male with past medical history (PMH) of hypertension who presented with over three-month history of lower extremity (LE) swelling, discoloration, and ulceration. Arthralgias with constitutional symptoms (fatigue, weight loss), large pericardial effusion, was found to have leukocytoclastic vasculitis along with rheumatoid factor (RF) >650, and anti-cyclic citrullinated peptide (anti-CCP) antibodies >300, low C4 and normal C3. Pericardial fluid appeared serous, exudative, showed histiocytes, multinucleated giant cells and necrotic debris consistent with rheumatoid effusion. Skin, right shin, punch biopsy showed epidermal necrosis from underlying occlusive vasculopathy. Skin, left lower back, punch biopsy showed focal leukocytoclastic vasculitis. The patient was started on high dose steroids with marked improvement in the symptoms, Rituximab was planned awaiting QuantiFERON to be negative. Pan-CT angiography of the whole body was negative for any vascular changes ruling out polyarteritis nodosa (PAN).

Background The hormones of the hypophysis-thyroid axis (HTA), thyroid stimulating hormone (TSH), and thyroid hormones, L-thyroxine (T4) and 3, 3', 5-L-triiodothyronine (T3), modulate the metabolism, differentiation, and proliferation of almost every cell in the body. Several studies have examined the effect of HTA hormones on platelet count and mean platelet volume (MPV), but have reported inconsistent results. Our aim was to examine the association between HTA hormones and platelet count and MPV in a large cohort of the adult population of the United States. Methods We used the continuous National Health and Nutritional Examination Survey (NHANES) which made available data on HTA hormones (1999-2000, 2001-2002, 2007-2008, 2009-2010, and 2011-2012) to examine the association between HTA hormones and platelet count and MPV. Analyses were performed with adjustments for the complex survey sampling methods of NHANES data. Unadjusted and adjusted generalized linear regressions were performed to examine the relationship between HTA hormones and platelet count and MPV. Regression models were adjusted for age, sex, race, alcohol use, smoking status, serum c-reactive protein, red blood cell folate, diabetes mellitus, glomerular filtration rate, body mass index, and hypertension. Results Of the 10,619 individuals eligible for inclusion in the analyses, 5,267 (49.6%) were females and 2,132 (20.08%) were African Americans. The mean ± standard deviation of platelet count was 256.4 ± 67.1 109/L, MPV 8.04 ± 0.92 fL, serum T4 7.92 ± 1.68 mg/dL, and serum T3 114.08 ± 24.6 ng/dL. In unadjusted analyses, an increase in the serum levels of T4 or T3 was associated with a significant increase in the platelet count and MPV (all p-values < 0.05). In contrast, an increase in serum TSH level was associated with a significant decrease in the platelet count (p-value = 0.05) but had no effect on MPV. After adjustment for potential confounders, serum T4 levels were significantly associated with platelet count but not with MPV. Individuals in the lowest quartile of T4 had 18.73 x 109/L lower platelet count than individuals in the upper-most quartile (p-value = 0.03). Serum TSH and serum T3 levels had no effect on platelet count or MPV after adjusting for potential confounding variables. Conclusions We report that only serum T4 levels, and not TSH or T3 levels, are independently associated with platelet count and there is no independent association between HTA hormones and MPV. Our findings suggest a possible role of serum T4 on thrombopoiesis or on platelet lifespan.