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Clinical Toxicology of Mercury
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Sonal Sekhar Miraj, Pooja Gopal Poojari, Girish Thunga P, Mahadev Rao
On the physical examination, his body weight was 48.5 kg and height was 151 cm. Vital signs showed body temperature was 37.6°C, pulse rate was 126 beats/min, and blood pressure was 112/82 mmHg. Overall, general state of the child was good. However, while palpating extremities a diffused sensitivity was present. But, no rash, elevated temperature, swelling, or movement restriction at the joints were observed. At the both lower extremities and the gluteal area, substantial linear erythematosus and ulcerated lesions were present. Lab parameters of the child were as follows. His urinary analysis indicated density: 1034, pH: 5.1, protein: >310, sulfosalicylic acid (SAA) test: +++, ketone: trace, and glucose: negative. Hematological parameters were Hb: 14.1 g/dL, WBC count: 8,200/mm3, MCV:83 fL, MCH: 28.5 pg, MCHC: 35 g/dL, platelets: 438,000/mm3, RDW: 13%, and ESR: 16 mm/h. Liver enzyme levels showed AST: 110 IU/L, ALT: 89 IU/L, and LDH: 1030 IU/L. CK: 3020 IU/dL, blood lead (Pb) level: 22.5 mcg/L, blood Hg level: 132 mcg/L (normal: 0–100 mcg/L), rheumatoid factor (RF), C-reactive protein (CRP) and anti-nuclear antibody (ANA) tested to be negative. Moreover, serum levels of both C3 and C4 were normal. Levels of 5-aminolevulinic acid (ALA) and porphobillinogen (PBG) in urine were normal. Electromyography (EMG) demonstrated myogenic involvement, however, the EMG became normal after 2 months.
Major Histocompatibility Complex and Autoimmune Disease
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Ursula Holzer, Gerald T. Nepom
Juvenile idiopathic arthritis (JIA) is an umbrella term for a group of chronic childhood arthritides in children below sixteen years of age and persisting for at least six weeks and having no known cause.75 It includes clinically distinct forms of juvenile arthritis, which have genetic associations with different alleles of HLA class II. The most common form, oligoarticular arthritis, is defined as arthritis affecting four or less joints. The other forms are the extended oligoarthritis, polyarticular arthritis, divided in rheumatoid factor (RF) positive and negative, enthesitis related arthritis, psoriatic arthritis and “other arthritis”. The polyarticular form is defined by affecting five or more joints in the first six months. For the oligoarticular form of the disease, a significant disease susceptibilty exisits for the HLA-haplotypes DRB1*08-DQB1*0401-DQB1*0402 and DRB1*11-DQA1*0501-DQB1*0301.76,77 The class II genes HLA-DRB1*01 and DRB1*04 have been reported to increase the risk of polyarticular arthritis. DRB1 *04 has a particuarly high association with IgM rheumatoid factor-positive polyarticular arthritis, whereas DRB1*01 is associated with oligoarticular disease onset that converts to a polyarticular disease.8,79 Analysis of the distribution of the DPB1 alleles showed an increase in DPB1*0201 in the oligoarticular form of the disease.77,80,81
Vasculitis induced by drugs
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
Michiel De Vries, Marjolein Drent, Jan-Wil Cohen Tervaert
Cryoglobulinaemia refers to the presence of one or more antibodies which precipitate at temperatures below 37°C and solubilize on rewarming. Cryoglobulins are classified into three types based on whether they are monoclonal or not. Type II cryoglobulins are composed of monoclonal IgM and a poly-clonal IgG. The cryoglobulins have rheumatoid factor activity and can produce an immune-complex small-vessel vasculitis. Clinical manifestations of type II cryoglobulin-associated vasculitis are diverse. In many cases, this so-called ‘essential’ mixed cryoglobulinaemia is related to hepatitis C infection. Otherwise, cryoglobulinaemia in countries where hepatitis C prevalence is low is often a complication of a lymphoproliferative disorder and occurs sometimes years after cytotoxic therapy is administered, either because of an autoimmune disease or as treatment of a malignancy.97
Designing of an inflammatory knee joint thermogram dataset for arthritis classification using deep convolution neural network.
Published in Quantitative InfraRed Thermography Journal, 2022
Shawli Bardhan, Satyabrata Nath, Tathagata Debnath, Debotosh Bhattacharjee, Mrinal Kanti Bhowmik
Arthritis is a joint inflammatory disease that includes pain, stiffness, swelling, restriction in motion. In India, around 15% of the population suffers from arthritis [1], and in the United States, 22.7% of the adult population are affected through it in the year 2015 [2]. According to the observation of medical science, approximately 100 types of arthritis are there, and among them, Rheumatoid Arthritis (RA) and Osteoarthritis (OA) are the two most common types [3,4]. In India, the RA prevalence rate almost 0.9% and this range is 0.5% to 1% worldwide [5–8]. In the case of RA, the body immune system mistakenly attacks the healthy tissues and causes inflammation. Presence of RA in the body may also affect lunge, heart, blood vessels [9], skin, and eyes. On the other hand, 30.8 million adults are affected by OA in the United State [4]. The cartilage of joints breaks down due to OA and generates inflammation. In the advanced stage of OA, severe pain and permanent damage to joints may occur. Like RA, reactive arthritis (RE) is also a systemic rheumatic disease which may affect other body organs. The occurrence of inflammation due to RE is the result of a reaction to infection by certain bacteria in body joints. The most commonly affected large joints by arthritis in the human body are knee and hip. Presently, diagnosis of arthritis mainly depends on the subjective evaluation of medical experts and clinical tests like Erythrocyte Sedimentation Rate (ESR), C – reactive protein (CRP) and Rheumatoid factor. Image-oriented examination for arthritis includes X-ray, ultrasound, and Magnetic Resonance Imaging (MRI). But those imaging methodologies contains the ground truth of inflammation spreading is not available for analysis. Acquisition and creation of such a standardised dataset with the ground truth of inflammation and its analysis may be helpful for medical experts and future researchers.
Case series: rheumatological manifestations attributed to exposure to Libby Asbestiform Amphiboles
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Roger Diegel, Brad Black, Jean C. Pfau, Tracy McNew, Curtis Noonan, Raja Flores
The patient was first seen at the CARD in 2003. He reported coughing up phlegm each day, having suffered shortness of breath for several years and was experiencing sharp chest pains with a recent episode of pleurisy. He was diagnosed with asbestos-related pleural disease at this time. The patient was last in clinic October of 2015 when he reported still experiencing a chronic cough with phlegm production, dyspnea, wheezing and chest pain. Over time the patient’s pulmonary function showed a decline in DLCO (66%). The patient was diagnosed with polymyalgia rheumatica in 2000 and placed on prednisone. In 2001, he developed swelling in his peripheral joints, hands, wrists, ankles and feet and was diagnosed with seronegative rheumatoid arthritis with negative serology labs, negative ANA, negative rheumatoid factor, negative CCP. X-rays revealed no erosions. He was placed on methotrexate with prednisone, but after 6 months, developed hair loss and oral ulcers, and methotrexate was discontinued. He was placed on leflunomide, did well with leflunomide, and was able to taper off the prednisone. He was taking leflunomide for 1-l/2 years, but then started developing fluid around his heart and leflunomide was discontinued. The patient then went back on prednisone 20–25 mg daily from the early 2000s until 2014. In September 2014, he weaned off prednisone, so he could have a knee replacement. After the knee replacement in 2014, the patient started taking Lipitor, and the arthritis with swelling in his hands, wrists, ankles, and feet returned. The patient was placed back on prednisone at 10 mg with tapering doses and 10 mg weekly of methotrexate with good control of his arthritis symptoms. No other autoimmune diseases were present in the patient. The patient had been seen by different rheumatologists from 2000 until 2015, who concurred with the diagnosis of seronegative rheumatoid arthritis. However, subsequent testing showed a positive ANA at 1:2560 titer.