Psoriatic arthritis with hyperuricemia: more peripheral, destructive, and challenging to treat.

OBJECTIVE: To study the impact of hyperuricemia on clinical presentation, severity, and associated comorbidities of psoriatic arthritis (PsA). METHODS: Retrospective bicentric case-control study performed in Strasbourg and Colmar, France, from 2009 to 2019. Patients with PsA (according to ICD-10 coding) and at least one available serum urate (SU) measurement were included. Demographic, comorbidities, clinical, and radiographic data were collected. Hyperuricemia was defined as SU level ≥ 360 µmol/L. RESULTS: We included 242 patients: 73 (30.2%) had hyperuricemia and 15 (6.2%) met 2015 ACR/EULAR criteria for gout. On univariate analysis, as compared with normo-uricemic patients, hyperuricemic patients were more frequently male (72.6% vs 39.1%, p = 1.6 × 10-6) with higher body mass index (30.9 vs 28.7 kg/m2, p = 0.015) and more comorbidities (Charlson comorbidity index: 2.6 vs 1.8, p = 0.005). PsA started at an older age (47.5 vs 43 years, p = 0.016) was more polyarticular (56.2% vs 41.9%, p = 0.049) than axial (9.6% vs 22.8%, p = 0.019) and more destructive (52.8% vs 37.4%, p = 0.032). PsA patients with joint destruction more frequently had hyperuricemia than did others (37.6% vs 25.8%, p = 0.047). Multivariable analysis confirmed the association of hyperuricemic PsA with peripheral joint involvement (odds ratio 2.98; 95% confidence interval 1.15-7.75; p = 0.025) and less good response to treatment (0.35; 0.15-0.87; p = 0.024). CONCLUSION: Patients with hyperuricemic PsA show poorer response to PsA treatment and have more peripheral and destructive joint damage than normo-uricemic patients. Key Points • Gout and psoriatic arthritis (PsA) can co-exist in the same patient. • Monosodium urate crystals might have a deleterious impact on PsA. • Hyperuricemic PsA is more polyarticular, less frequently axial, and more destructive than normo-uricemic PsA. • PsA with hyperuricemia should lead to more personalized medicine.

[A review of avascular necrosis, of the hip and beyond]. / Ostéonécroses aseptiques, une revue générale des ostéonécroses de la hanche, et au-delà.

Avascular necrosis is an ischemic or cytotoxic necrosis of epiphyseal bone, responsible for joint pain, altered life quality and frequently affecting young patients. Avascular necrosis can be unifocal or multifocal, underlining the possibility of a systemic origin. Avascular necrosis involves the femoral head in more than 75% of cases. Although avascular necrosis is irreversible, many risk factors must be sought, including corticosteroid treatment, hypercholesterolemia, sickle cell disease or alcohol abuse. MRI imaging is the main exploration for the diagnostic and staging of the disease, and should be performed in unexplained hip pain in young patients with normal X-rays. In the earlier stages of the disease (stage I and II of the Arlet and Ficat classification), joint surface is preserved, and conservative treatment is recommended. In the more advanced stages (III and IV of the Arlet and Ficat classification), the articular surface collapses and joint arthroplasty is the main treatment. However, there are some recent therapeutic advances, based on mesenchymal stem cells, which may contribute, in the future, to improve the bad functional prognosis of the disease.

Inactivation and mutagenesis of herpes virus by photodynamic treatment with therapeutic dyes.

Dyes which photosensitize membranes may be clinically useful for photodynamic treatment (PDT) of Herpes simplex virus (HSV) infections. It is important to determine whether the enveloped HSV can be inactivated via membrane damage without affecting the genetic material. Selection of appropriate PDT conditions, including the choice of dye, could minimize viral mutagenesis. We determined the mutagenesis caused by PDT employing three membrane-photosensitizing dyes of potential use in cancer photochemotherapy (Photofrin II, polyhematoporphyrin esters, zinc phthalocyanine tetrasulfonates) and a DNA-photosensitizing dye (proflavine sulfate). The effects were compared to those caused by exposure of HSV to ultraviolet radiation (UV). The procedure consisted of incubating HSV with microgram/ml (microM) concentrations of the dye, irradiating the samples with broad spectrum visible/near-UV radiation (Daylight fluorescent lamps) and assaying the survival of the treated HSV. Zinc phthalocyanine was the most potent dye per absorbed photon for inactivating HSV. In parallel with determination of survival, progeny of the surviving virus were grown for determination of mutagenesis. The progeny virus was harvested and subsequently assayed in the presence and absence of 40 micrograms/ml iododeoxycytidine (ICrd) to determine the frequency of mutation to ICrd resistance. Mutation frequencies were determined for progeny from the 1-4% survival level. For PDT with each membrane-photosensitizing dye, only zinc phthalocyanine increased the mutation frequency over the untreated control. This increase was less than 2-fold. Proflavine increased the mutation frequency 2-3 fold over the untreated control. Ultraviolet produced a 15-20 fold increase over the untreated control.(ABSTRACT TRUNCATED AT 250 WORDS)

Dye to use with virus challenge for testing barrier materials.

Can FD&C Blue no. 1 dye photoinactivate bacteriophages phi X174, T7, PRD1, and phi 6 under laboratory lighting conditions? At high levels of light, the dye (500 microM) photoinactivated only phi 6. Thus, this dye can be used at concentrations up to 500 microM with bacteriophages phi X174, T7, and PRD1 to test barrier material integrity.

Minimal effects of acrylonitrile on pulmonary and hepatic cell injury enzymes in rats with induced cytochrome P450.

Acrylonitrile (AN) has many industrial applications but is a known carcinogen in animals and a suspect human carcinogen. Its toxicity is generally associated with its bioactivation, the initial step of which is epoxidation by cytochrome P450. While the hepatotoxicity and pneumotoxicity of AN in naive rats is generally low, the purpose of this study was to investigate the pneumotoxicity and hepatotoxicity of AN in adult male Sprague-Dawley rats and evaluate interactions with agents that may alter its metabolism. Five agents, phenobarbital, beta-naphthoflavone, pyridine, ethanol, and acetone, were administered prior to AN as inducers of CYP2B, CYP1A, and CYP2E1. Pneumotoxicity was measured as increases in y-glutamyltranspeptidase (GGT) and lactate dehydrogenase (LDH) in bronchoalveolar lavage fluid (BALF). Hepatotoxicity was measured as increases in serum sorbitol dehydrogenase (SDH). AN (1 mmol/kg ip) had little effect on liver or lung, even when given following most of the inducing agents. AN (1.5 mmol/kg) caused an increase in GGT, but had little effect on SDH or LDH. Acetone plus AN caused an increase in mortality and some indication of pneumotoxicity, but lung and liver were histologically normal. Thus AN alone even at a high dose had no effect on the liver or lung and minimal effects following induction of cytochrome P450 by acetone.

The significance of diagnostic imaging in acute and chronic brain damage in boxing. A prospective study in amateur boxing using magnetic resonance imaging (MRI).

The significance and possible extent of structural damage to the central nervous system (CNS) due to boxing are investigated. Bleeding, especially microhematomas, is considered to be one probable cause of the chronic encephalopathy in boxers. In a prospective study, 13 amateur boxers were investigated with the help of MRI several times before and after their fights. The MRI investigations were accompanied by neurologic examinations before and after the fights. Among the 13 boxes, 5 demonstrated focal neurological signs following the fights, without evidence of small hematoma or other structural alterations. The number of head punches did not correlate with the occurrence of neurologic signs. These results indicate that up to now imaging methods cannot clarify the development of chronic encephalopathy.