Case Presentation: A 15-week G2P3 pregnant 33-year-old woman with past medical history of chronic hepatitis C, current intravenous drug use (IVDU) presented from a correctional facility complaining of abdominal pain and hematuria. Exam revealed a gravid uterus and bilateral pedal edema. Patient responding only to pain and not following commands. Temp 102.8 F, HR 120’s beats/min, RR 30-35 breaths/min BP 112/51 mmHg, O2 saturation 90% on room air. Laboratory: WBC 12.5 , procalcitonin 0.65, negative SARS-CoV-2 PCR and Hepatitis C RNA viral load of 24 (low). Urine drug screen with cocaine. Total body MRI showed bilateral airspace opacities consistent with multifocal pneumonia versus septic emboli. She was treated with broad-spectrum antibiotics. TTE showed vegetations on the tricuspid, aortic and mitral valves. All blood cultures were positive for methicillin sensitive Staphylococcus aureus (MSSA). She developed a diffuse palpable purpuric rash (macules and petechiae) of the abdomen and botharms and legs. Polyarthralgias limited ambulation. Pathology from a skin biopsy showed pustular leukocytoclastic vasculitis (LCV). Direct immunofluorescence of frozen sections revealed faint granular anti-C3 staining in superficial dermal vessels and no immunoreactivity for IgG, IgA, IgM and fibrinogen, consistent with septic vasculitis due to immune complex depositions. C3 and C4 complement levels were within normal limits.
Discussion: Cutaneous purpuric lesions are often associated with systemic diseases such as Chronic Hepatitis B and C and are less commonly associated with Infective endocarditis most commonly associated with complement deposition in small vessels. LCV is a histologic term that refers to a neutrophil mediated vasculitis of the small vessels (venules and arterioles), major clinical findings of LCV include non-blanching palpable purpura usually after inciting insult [1]. Definitive diagnosis is made through punch skin biopsy. Because our patient had Hepatitis C and infective endocarditis, the appearance of a purpuric rash raised the question of cryoglobulinemic vs complement-mediated vasculitis.Cutaneous purpura is the most common skin manifestation of IE, prevalence varying from 8%-40% [2]. Although classically associated with hepatitis C, the presence of cryoglobulins in patients with IE has previously been reported [3]. Immune complex deposition can cause inflammation that affects the small vessels, most notably in the skin and joints causing fatigue, purpura, and arthralgia [4]. Although Infective endocarditis may cause cryoglobulinemia (which typically features with a purpuric lower extremity rash and renal dysfunction) more often the rash in endocarditis is due to complement deposition.
Conclusions: lthough leukocytoclastic vasculitis and cryoglobulinemia can be associated with Hepatitis C infections our patient had nearly undetectable Hepatitis C RNA. Her renal dysfunction and acute palpable purpuric rash associated with IE-related sepsis from MSSA bacteremia and the pathology showing C3 depositions and no cryoglobulins in the small vessels of the skin strongly suggest complement mediated LCV triggered by the underlying endocarditis. Corticosteroids commonly prescribed with Hepatitis C are contraindicated. Acute bacterial endocarditis presenting with purpuric rash should encourage early skin biopsy and particularly in those with IVDU and a history of hepatitis to assure the appropriate management of this very serious too often fatal disease.[4][5]
