Study Objective: To ascertain the prevalence of monoclonal gammopathy in an inception cohort of patients with low bone mineral density. Design: We conducted a prospective cohort study of 115 patients (median age 69 [47–90]; 102 female) who were newly diagnosed (January-June 2022) with osteopenia (47% of cohort) or osteoporosis (OP) (53%) from the DXA clinic. Screening comprised serum protein electrophoresis (SPEP), serum free light-chain assay (sFLC), and urine Bence Jones protein testing (uBJP). Results were available for 109, 108, and 96 participants, respectively. Participants with prior diagnosis of low bone density or monoclonal gammopathy were excluded. Results: 59% of the cohort had a history of fragility fracture. Monoclonal proteins were detected in 2 out of 115 patients (1.7%) with abnormal sFLC results in both cases. One patient’s work-up revealed multiple myeloma, and another patient was diagnosed with a low-grade B-cell non-Hodgkin lymphoma. No cases of MGUS were identified in this cohort. Conclusion: Among 115 newly diagnosed osteopenia/OP patients, the prevalence of underlying monoclonal gammopathy was low (1.7%). We identified isolated cases of multiple myeloma and an indolent B-cell lymphoma, but no MGUS, in this sample. These findings illustrate that while routine screening of all low bone density patients will yield few positives, it can uncover serious but treatable haematologic conditions in a minority. The study also highlights the value of using a combination of tests (serum electrophoresis plus free light-chain and urine protein assays) to improve detection of monoclonal gammopathies in patients with low bone density.
Hyperuricemia has moved from a niche biochemical finding to a clinically relevant cardio-renal-metabolic risk state. This review synthesises contemporary evidence on uric acid biology, epidemiology, and management. We outline sources and biochemistry of urate, the hepatic xanthine oxidoreductase pathway, and the coordinated roles of renal and intestinal transporters that set steady-state serum levels, emphasising URAT1, GLUT9, NPT1, NPT4, and ABCG2, as well as the organic anion transporters OAT1 and OAT3, which import uric acid from the blood into proximal tubule cells. We summarise definitions, diagnostic thresholds, and global prevalence with sex-specific ranges, then differentiate asymptomatic hyperuricemia from crystal disease. Clinical sections integrate mechanistic links between soluble and crystalline urate and organ injury: inflammasome-mediated gout; tubulointerstitial injury, arteriolopathy, and obstructive pathways in kidney disease; oxidative stress, endothelial dysfunction, and vascular remodelling in hypertension, atherosclerosis, and coronary events; and metabolic pathways involving fructose metabolism, insulin resistance, and hepatic lipogenesis that connect hyperuricemia to metabolic syndrome and MAFLD. We appraise clinical evidence across cohorts, imaging, genetics, and randomised trials, distinguishing strong causal domains such as gout and uric acid nephrolithiasis from associative domains where treatment decisions should be individualised. A practical, phenotype-driven treat-to-target framework is presented that prioritises xanthine oxidase inhibition, adds uricosuric therapy for underexcretion, embeds lifestyle therapy, and applies safety strategies including HLA-B*58:01 screening in high-risk ancestries. We conclude with research gaps and priorities, including transporter-targeted strategies, intestinal urate quantification, pragmatic trials in enriched phenotypes, and clarity on long-term cardiovascular and renal outcomes.
Background: Infections cause significant morbidity and mortality in systemic lupus erythematosus (SLE). This study describes infection prevalence, patterns, and their association with disease severity and flares in a single-centre Sri Lankan SLE cohort. Methods: This retrospective descriptive study at the National Hospital of Sri Lanka included SLE patients aged ≥14 years meeting American College of Rheumatology (ACR) and the European Alliance of Associations for Rheumatology (ACR/EULAR) criteria. Data on diagnosis, organ damage (Systemic Lupus International Collaborating Clinics [SLICC]/ACR Damage Index), treatment, flares, and infections were collected from medical records. Univariate logistic and Cox regression analyses assessed risk factors for infections, with odds ratio (OR) and hazard ratio (HR) reported with 95% CIs. Results: Two hundred patients (females = 92.5%; mean age = 37.3 years [SD = 2.1]; mean diagnosis age = 23.8 years; mean SDI = 3.38 [SD = 0.41]) were studied. Skin damage occurred in 59.5%. 47.0% had flares; median duration to first flare 67.5 months (IQR = 21.8–124.5). Infections occurred in 45.5% (rate 45.9/1000 patient-years). Infection risk increased with age (OR = 1.03,1.01–1.06), disease duration (OR = 1.03,1.01–1.06), damage score (OR = 1.2,1.04–1.34), flares (OR = 2.9,1.61–5.09) and comorbidities (OR = 2.1,1.20–3.75). Multiple analyses showed that flares (HR = 2.43,1.55–3.81) and the presence of comorbidities (HR = 1.64,1.03–2.62) increased infection hazard. 29.5% experienced infections while on prednisolone. Conclusions: This study found a high infection rate among patients with SLE, with increased risk associated with older age and longer disease duration. Modifiable factors, including steroid use, comorbidities, and disease flares, were also significantly associated with infections. Optimising disease control, minimising unnecessary steroid exposure, and appropriate management of comorbidities may help reduce the infection burden in SLE patients.
Objective: To investigate the clinical characteristics and outcomes of thrombotic thrombocytopenic purpura (TTP) in patients with systemic lupus erythematosus (SLE) compared to idiopathic TTP (I-TTP). Methods: This retrospective cohort study included adult patients with SLE-TTP ( n = 9) and I-TTP ( n = 7) treated at a tertiary care centre in East India from January 2019 to July 2024. Patients with SLE-TTP fulfilled the 2019 American College of Rheumatology criteria for SLE, and TTP was defined if microangiopathic haemolytic anaemia and thrombocytopenia (platelet count <100,000 cells/µl) were present with an intermediate-to-high-risk PLASMIC score. Clinical characteristics, treatment details and outcomes were extracted from medical records. Treatment response was assessed using complete remission criteria and survival analysis. Results: The SLE-TTP group consisted of all female patients with a median age of 27 years, significantly younger compared to the I-TTP cohort (median age of 55 years, P = .01). Haematological parameters were comparable between groups. Complete response rate was achieved in eight out of nine patients (89%) in SLE-TTP and five out of seven patients (71%) in the I-TTP group ( P = .4). The median time to complete response was 27 and 45 days for SLE-TTP and I-TTP groups, respectively ( P = .31). Conclusion: SLE-TTP patients were younger at diagnosis compared to I-TTP. The findings are exploratory, and further research with a larger sample size and additional biomarkers is warranted to enhance understanding and management of SLE-TTP and I-TTP.
Peripheral spondyloarthritis (pSpA) includes many cases of PsA, ReA, IBD-SpA, and a subset without features of psoriasis, IBD and preceding infection, referred to as ‘pure’ pSpA. It is well documented that peripheral manifestations contribute considerably to the morbidity of SpA. However, despite a lot of advances in the treatment of axSpA with the introduction of newer biological agents targeting IL-17, IL-23, and JAK pathways, pSpA (excluding psoriatic arthritis) remains an area devoid of much research, with only a few clinical trials. In this narrative review, we tried to look into this entity of pSpA, excluding psoriatic arthritis (non-psoriatic pSpA). Future studies should focus on genetics, the development of specific biomarkers, exclusive classification criteria, specific outcome measures, imaging modalities and randomised control trials in pSpA.
