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I Have Spots and My Skin Burns

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I Have Spots and My Skin Burns I have spots and my skin burns Patient presentation History Differential diagnosis Examination Investigations Discussion Treatment Final Outcome References Evaluation - Questions & answers MCQs Patient presentation Peter, a 60 year-old Caucasian policeman, complains of a painful burning sensation in his lower extremities lasting for several months. Lower limbs petechiae (small purple/red hemorrhagic spots) appeared one week ago. Acknowledgement This case study was provided by Prof. Olivier Boyer (M.D., Ph.D., Head of the Department of Immunology and Biotherapy, Rouen University Hospital, France) and Dr. Maëlle Le Besnerais (M.D., Assistant Professor of Internal Medicine, Rouen University Hospital, France) of the Faculty of Medicine of Rouen, Normandy University, France. The authors would like to thank David Saadoun, Odile Goria, Lucie Guyant-Maréchal and Fabienne Jouen for their critical reading of this case study, Isabelle Duval for the development of pictures and Laetitia Demoulins for technical assistance. We are grateful to Nikki Sabourin-Gibbs, Rouen University Hospital, for her help in editing the manuscript. Immunopaedia.org.za History Peter complains of chronic fatigue and aching joints which started several months ago. He denies significant alcohol consumption and intravenous drug abuse. He received a blood transfusion after a gunshot injury to his arm 35 years ago. He reports distal paraesthesia (tingling or numbness) of both legs and painful burning in both feet which has progressed to the lower and upper limbs. Knee pain wakes him up at night. Past medical history None No allergies Surgical history Appendix removed at 10 years old Arm gunshot injury 35 years ago Family history His father has hypertension and type 2 diabetes Travel history He traveled to Thailand 25 years ago Social history Policeman, married, two children Medication None Differential diagnosis IgA vasculitis Polyarteritis nodosa ANCA-associated vasculitis (eg. granulomatosis with polyangiitis [formerly Wegener’s], microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis [formerly Churg and Strauss syndrome]) Vasculitis associated with an autoimmune disease (eg. systemic lupus erythematosus, rheumatoid arthritis, Sjögren’s syndrome) Infection (eg. rickettsial infections, malaria, babesiosis) Immunopaedia.org.za Infection related vasculitis (eg. bacterial endocarditis, poststreptococcal vasculitis and glomerulonephritis, Hepatitis C virus (HCV) associated mixed cryoglobulinemia vasculitis) Serum sickness Drug-induced small vessel vasculitis (hypersensitivity vasculitis) Examination Vitals Heart rate: 83/min Blood pressure: 114/72 mmHg Temperature: 37.8°C Oxygen saturation: 97% General He looks tired No pallor Livedo reticularis (mottled reticulated vascular pattern that appears as a lace-like purplish discoloration of the skin) Symmetrically distributed palpable purpura (red/purple discolored spots on the skin that do not blanch on applying pressure) in the lower extremities Bilateral supramalleolar (above the ankle joint) skin ulcers Cardiovascular Normal heart sounds All pulses present Respiratory No dyspnea (shortness of breath), no cough Respiratory rate 17/min No chest deformity Good bilateral air entry No crackling sound on the lungs or wheezing Abdomen Mild hepatomegaly (enlargement of the liver) Neurological Immunopaedia.org.za Normal cognition No meningism No paralysis of cranial nerves Normal motor strength Superficial hypoesthesia (decreased sensitivity to stimuli) of lower limb under knees associated with dysesthesia (unpleasant, abnormal sense of touch) Loss of joint position and vibration sense and sensory ataxia (failure of muscle coordination) Tendon reflexes were absent at the ankles bilaterally and reduced at the knee No sphincter disorder Investigations Examination Value Normal limits White blood cell 7.41 (4-12 x109/L) Hemoglobin 10.9 (12.1-15.2 g/L) Platelets 175 (140-450 x109/L) C reactive protein (CRP) 5 (0-8 mg/l) Sodium 136 (135-147 mmol/L) Potassium 4.2 (3.3-5.0 mmol/L) Urea 6.2 (2.5-6.4 mmol/L) Creatinine 96 (62-115 mmol/L) Creatinine kinase 183 (25-195 IU/L) Total protein 62 (60-80 g/L) Albumin 37 (35-50 g/L) Corrected calcium 2.35 (2.1-2.6 mmol/L) Phosphate 1.3 (1.0-1.5 mmol/L) Magnesium 1.1 (0.8-1.3 mmol/L) Aspartate aminotransferase 56 (10-35 IU/l) Alanine aminotransferase 70 (10-35 IU/l) Immunopaedia.org.za Examination Value Normal limits γ-glutamyl transferase 86 (10-38 IU/l) Alkaline phosphatase 127 (35-105 IU/l) Bilirubin 18 (2-18 µmol/l) Prothrombin time 85 (75-100%) Thyroid stimulating hormone 11.3 (9-30 mIU/L) Antinuclear antibodies Negative Autoimmune hepatitis-specific antibodies (anti mitochondrial, anti smooth muscle, Negative anti-LKM, anti-LCI) Anti neutrophil cytoplasmic antibodies Negative (anti-Myeloperoxydase (MPO) and anti Proteinase 3 (PR3)) Anti-citrulline antibodies Negative CH50 50 (85-140 IU/ml) C3 0.46 (0.5-1.53 g/L) C4 0.02 (0.2-1 g/L) Rheumatoid factor 459 <20 IU/ml Serum protein electrophoresis Hypogammaglobulinemia Cryoglobulin See below Proteinuria 0.09 <0.15 g/24h HIV Negative HBs antigen Negative Anti-HBs antibodies Negative Anti-HBc antibodies Negative Immunopaedia.org.za Examination Value Normal limits Anti-HCV antibodies Positive HCV polymerase chain reaction 1.12x107 (<15 IU/ml) HCV genotyping 1b Cryoglobulin Examination type III (polyclonal IgG, IgM κ/λ) 2670 (<50 mg/l) Figure 1: Immunofixation electrophoresis of Peter’s cryoglobulinemia. The first lane is protein electrophoresis (ELP). The next lanes are immunofixation performed with anti- heavy chain antibodies for IgG (G), IgA (A), IgM (M), and anti- light chain antibodies for kappa (κ) and lambda (λ). A type III polyclonal IgG, IgM κ/λ cryoglobulin is observed. EKG: normal Chest X-ray: normal Computed tomography: mild hepatomegaly Evaluation of liver fibrosis by Fibroscan: 8 kPa (moderate fibrosis without cirrhosis) EMG: electromyography shows a severe length-dependent axonal sensitive polyneuropathy of the Immunopaedia.org.za lower limbs Skin biopsy: leukoclastic vasculitis with fibrinoid necrosis and thickening of the vessel wall associated with inflammatory infiltrate consisting of neutrophils as well as destruction of neutrophils, nuclear dust, and neutrophilic debris Figure 2: Histological analysis of a skin biopsy (H&E staining) showing leukoclastic vasculitis with fibrinoid necrosis associated with inflammatory infiltrate. [Jordan A. et al (2011). Pathology of the Cutaneous Vasculitides: A Comprehensive Review, Advances in the Etiology, Pathogenesis and Pathology of Vasculitis] Discussion The cause of the presenting condition is Hepatitis C Virus (HCV) associated mixed cryoglobulinemia vasculitis. Cryoglobulins are defined by the presence of circulating immune complexes that precipitate as serum is cooled below core body temperature, and that resolubilize when serum is rewarmed. Cryoglobulinemia refers to a condition with circulating cryoglobulins in the serum. Cryoglobulinemia vasculitis refers to small to medium size vessel vasculitis resulting from the pathogenicity of cryoglobulin-containing immune complexes. The prevalence of clinically significant cryoglobulinemia is estimated at around 10 per million. Mixed cryoglobulinemia vasculitis more frequently occurs in patients aged 45–65 years, mainly in women (sex ratio women:men is 2–3:1) with no predominant ethnicity. Significant proportions of patients with chronic infection or autoimmune diseases have detectable Immunopaedia.org.za levels of cryoglobulins in their serum (about 40-65% of HCV infection, 15-20% of HIV infection, 15-25% of autoimmune diseases). The different types of cryoglobulins Classification of cryoglobulinemia is based on the clonality and type of immunoglobulins. Classification Type I (monoclonal): isolated monoclonal lg (typically IgG or IgM, and less commonly lgA or free light chains), and found in conditions like monoclonal gammapathy of unknown signification, multiple myeloma and Waldenstrom’s macroglobulinemia. It accounts for 10-15% of all cryoglobulinemias. Type II (mixed): mixture of monoclonal IgM and polyclonal IgG, with the IgM component having positive rheumatoid factor activity. Also called essential mixed cryoglobulinemia, this type is mostly found in patients with chronic hepatitis C, autoimmune diseases (Sjögren’s syndrome, Lupus etc.), and B-cell lymphoma. This is the most common type and accounts for 40-60% of all cryoglobulinemias. Type III (mixed, polyclonal): mixed cryoglobulinemia consisting of polyclonal IgG and polyclonal IgM. Also a common type, mostly in association with autoimmune diseases, accounting for 25-30% of all cryoglobulinemias. Both type II and type III are referred to as mixed cryoglobulinemia since they both consist in a mixture of IgM and IgG. Typically, type III precedes type II during disease evolution. Immunopaedia.org.za Figure 3: (A) Aspect of a cryoprecipitate at +4°C (arrowed), (B) the different types of cryoglobulins as determined by immunofixation. The first lane is protein electrophoresis (ELP). The next lanes are immunofixation performed with anti-heavy chain antibodies for IgG (G), IgA (A), IgM (M), and anti-light chain antibodies for kappa (κ) and lambda (λ). (B.1) type 1 IgM κ, (B.2) type 2 polyclonal IgG and IgM and monoclonal IgM κ, (B.3) type 3 polyclonal IgG and IgM (κ/λ). Figure 4: Types of cryoglobulins and their main causes. Type I and type II/III cryoglobulins result from different clinical contexts, i.e. B cell lymphoproliferation versus Immunopaedia.org.za infection/autoimmunity, respectively.
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