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Rheumatology
Published in Kristen Davies, Shadaba Ahmed, Core Conditions for Medical and Surgical Finals, 2020
Gout is an inflammatory crystal arthropathy caused by the deposition of monosodium urate monohydrate in the synovium of joints. It is caused by a chronic hyperuricaemia (uric acid >450 μmol/L) although not all raised urate levels cause gout!
Septic Arthritis
Published in Firza Alexander Gronthoud, Practical Clinical Microbiology and Infectious Diseases, 2020
This group is the most common cause of an acutely hot swollen joint in adults and includes: Crystal arthropathy (gout and pseudogout) may mimic septic arthritis in presentation. Clues suggesting crystal arthritis include involvement of the first metatarsophalangeal joint, prior similar attacks and the presence of tophi. Diagnosis is confirmed by seeing crystals in the synovial fluid; however, the presence of crystals doesn't rule out a concomitant septic arthritis.Reactive arthritis secondary to an infection elsewhere in the body, such as urogenital (Chlamydia spp.) or gastrointestinal (e.g.. Campylobacter spp., Yersinia spp.). It may occur in the presence of recent conjunctivitis, mucus membrane lesions and urogenital or gastrointestinal symptoms.Rheumatoid arthritis is more often a symmetrical polyarthritis, but exacerbation of disease in a single joint can occur. The fact that patients with rheumatoid arthritis are at increased risk of developing septic arthritis makes the differentiation all the more difficult.
Crystal deposition disorders
Published in Ashley W. Blom, David Warwick, Michael R. Whitehouse, Apley and Solomon’s System of Orthopaedics and Trauma, 2017
Paul Creamer, Dimitris Kassimos
Crystal deposition diseases are common, although most are managed in primary care or by medical intervention. For the orthopaedic surgeon, their principal significance is as an important differential of acute monoarthritis: sepsis should always be excluded but an appreciation of acute crystal disease as an alternative cause may spare the patient prolonged antibiotics. Crystals may also be responsible for a destructive arthritis, requiring surgical intervention. Possible reasons to refer to rheumatology might include diagnostic uncertainty, severe recurrent attacks not responding to standard therapy, chronic tophaceous gout, or gout with renal disease or calculi. A number of drugs are now available to manage crystal arthropathy successfully in the long term and with careful treatment, outcomes can be excellent, especially for gout.
Emerging injectable therapies for osteoarthritis
Published in Expert Opinion on Emerging Drugs, 2022
It is possible that any signal supporting IL-1 inhibition in OA is in fact representative of those with a concomitant crystal arthropathy. Drugs targeting the IL-1 pathway have been shown to be of benefit in crystal arthropathies [52,53], and calcium pyrophosphate crystals and basic calcium phosphate crystals are in many joints with OA. For example, basic calcium phosphate crystals are found in 100% of cartilage samples from patients with OA undergoing arthroplasty [54]. Although these crystals do not directly cause OA, they may possibly activate an inflammasome pathway involving IL-1. This may in turn induce cartilage degeneration via proteases as described above [43]. More research into this possible subgroup needs to be performed to delineate the type of arthritis most responsive to IL-1 inhibition.
Aortitis which developed after the administration of granulocyte-colony stimulating factor
Published in Modern Rheumatology Case Reports, 2020
Tomoyuki Mukai, Shinichiro Kubo, Yoshitaka Morita, Mari Yamamoto, Masahiko Ikeda
G-CSF analogs can cause various adverse effects including rheumatic symptoms (Table 2) (17). Arthralgia and ostealgia are sometimes observed in the patients after G-CSF administration. Other rheumatic disease-related symptoms can be exhibited as crystal arthropathy, sweet syndrome, erythema nodosum, pyoderma gangrenosum, acute aortitis, capillary leak syndrome and interstitial pneumonia (Table 2) [17]. As we discussed above, though only limited cases with G-CSF-associated aortitis have been reported, considerable numbers of cases with G-CSF-associated aortitis might be overlooked. Some cases could be considered as chemotherapy-related aortitis or might recover spontaneously before the clinicians recognize the presence of aortitis due to its self-limiting nature. G-CSF-associated lumbago and arthralgia are relatively well-recognized among rheumatologists, whereas G-CSF-associated aortitis is likely to be under-recognized. Therefore, we should consider the possibility of aortitis when patients exhibit fever and inflammatory responses of unknown origin.