Diagnosis, management and outcomes of primary hypokalemic periodic paralysis during pregnancy.

Primary hypokalaemic periodic paralysis during pregnancy has been rarely reported. Four pregnant women with the acute onset of flaccid paralysis presented between January 2018 and December 2021. Focussed history and physical examination helped an appropriate radiological and laboratory investigation plan to be made. All women recovered within 4-7 days of potassium supplementation. Supplemental potassium continued until delivery. A pain management plan with continuous epidural infusion helped in avoiding stress-induced hypokalaemia. None of the women developed an episode of muscle weakness during the intervening period. In conclusion, a focussed history and targeted laboratory investigation are needed to diagnose primary hypokalaemic periodic paralysis. Early administration of oral or intravenous potassium is crucial in improving fetomaternal outcomes.

Rheumatoid arthritis autologous synovial fluid affects the plasticity and function of peripheral and induced T regulatory cells in vitro.

The synovial fluid (SF) microenvironment in rheumatoid arthritis (RA) may alter the stability and function of Tregs. In the present study, we assessed cytokine levels and percentage of Tregs, Tregs expressing CXCR3 (Th1-like Treg), CCR6 (Th17-like Treg) in RA peripheral blood (PB) and RA-SF using fluorescence cytometry. Effect of autologous SF on plasticity and function of RA-PB Tregs (pTregs; CD4+CD25hiCD127Lo/-) and induced vimentin-pulsed Tregs (iTregsVIM) was assessed in vitro. Cytokines and percentage of Th1-like and Th17-like Tregs were higher in RA-PB than OA-PB; higher in RA-SF than osteoarthritis (OA)-SF. Compared to OA-SF exposed OA-pTregs, RA-SF exposed RA-pTregs showed higher percentage of Th1-like (11% vs 20%) and Th17-like (16% vs 36%) Tregs; higher T-bet (p = 0.0001), RORγ (p = 0.0001) and lower FOXP3 (p = 0.0001) gene expression; and diminished percentage suppression of autologous T effector cells (36% vs 74%). RA-SF exposed iTregsVIM showed increased percentage of Th1-like and Th17-like Tregs compared to iTregsVIM exposed to AB serum (8% vs 0.1%; 21% vs 0.1%). IL-2, Tocilizumab and 5-azacytidine reduced the conversion of iTregsVIM (8% vs 2.4%; 21% vs 6.9%), when used in combination. To conclude, microenvironment in the RA synovial fluid is possibly responsible for conversion of pTregs into Th-like Tregs and their functional loss. A blockade of cytokine receptors and methyl transferases could inhibit Tregs conversion, providing clinical relevance for future Tregs targeting therapies.

Low C4A copy numbers and higher HERV gene insertion contributes to increased risk of SLE, with absence of association with disease phenotype and disease activity.

Low copy numbers (CNs) of C4 genes are associated with systemic autoimmune disorders and affects autoantibody diversity and disease subgroups. The primary objective of this study was to characterize diversity of complement (C4) and C4-Human Endogenous Retrovirus (HERV) gene copy numbers in SLE. We also sought to assess the association of C4 and C4-HERV CNs with serum complement levels, autoantibodies, disease phenotypes and activity. Finally, we checked the association of C4 and HERV CNs with specific HLA alleles. Genomic DNA from 70 SLE and 90 healthy controls of south Indian Tamil origin were included. Demographic, clinical and serological data was collected in a predetermined proforma. CNs of C4A and C4B genes and the frequency of insertion of 6.4kb HERV within C4 gene (C4AL, C4BL) was determined using droplet digital polymerase chain reaction (ddPCR). A four digit high resolution HLA genotyping was done using next generation sequencing. In our cohort, the total C4 gene copies ranged from 2 to 6. Compared to controls, presence of two or less copies of C4A gene was associated with SLE risk (p = 0.005; OR = 2.79; 95% CI = 1.29-6.22). Higher frequency of HERV insertion in C4A than in C4B increases such risk (p = 0.000; OR = 12.67; 95% CI = 2.80-115.3). AL-AL-AL-BS genotype was significantly higher in controls than SLE (9%vs1%, p = 0.04; OR = 0.15, 95% CI = 0.00-0.16). Distribution of HLA alleles was not different in SLE compared to controls as well as in SLE subjects with ≤ 2 copies and > 2 copies of C4A, but HLA allele distribution was diverse in subjects with C4B ≤ 2 copies and > 2 copies. Finally, there was no correlation between the C4 and the C4-HERV diversity and complement levels, autoantibodies, disease phenotypes and activity. In conclusion, our data show that, low C4A copy number and higher insertion of HERV-K in C4A increases the risk for SLE. C4 and C4-HERV CNs did not correlate with serum complements, autoantibodies, disease phenotypes and activity in SLE. Further validation in a larger homogenous SLE cohort is needed.

Semi-quantitative thigh magnetic resonance imaging scores in assessing disease activity and determining long-term clinical outcome in idiopathic inflammatory myopathies: a causal mediation analysis.

OBJECTIVES: To evaluate the relationship of thigh MRI (t-MRI) with manual muscle testing-8 (MMT-8), muscle enzymes and autoantibodies. To determine the causal and mediating factors resulting in poor recovery of MMT-8 in inflammatory myositis (IIM). METHODS: This was a single-centre retrospective study in IIM patients. t-MRI was semi-quantitatively scored for muscle oedema, fascial oedema, muscle atrophy and fatty infiltration. Spearman correlation of t-MRI scores was done with muscle enzymes at baseline, and MMT-8 at baseline and on follow-up. Causal mediation analysis was performed with age, sex, symptom duration, autoantibodies, diabetes and BMI as independent variables, follow-up MMT-8 as dependent and t-MRI scores as mediating variables. RESULTS: Baseline evaluation was done on 59 and follow-up on 38 patients. Median follow-up of the cohort was 31 (10-57) months. Baseline MMT-8 negatively correlated with muscle oedema (r = -0755), fascial oedema (r = -0.443) and muscle atrophy (r = -0.343). Creatinine kinase (r = 0.422) and aspartate transaminase (r = 0.480) positively correlated with muscle oedema. Follow-up MMT-8 correlated negatively with baseline atrophy (r = -0.497) and fatty infiltration (r = -0.531). On follow-up, MMT-8 males had positive total effect (estimate (95%CI)) via atrophy [2.93 (0.44, 4.89)] and fatty infiltration [2.08 (0.54, 3.71)]. Antisynthetase antibody had a positive total effect via fatty infiltration [4.50 (0.37, 7.59)]. Age had a negative total effect via atrophy [-0.09 (0.19, -0.01)] and fatty infiltration [-0.07 (-0.15, -0.01)]. Disease duration had a negative total effect via fatty infiltration [-0.18 (-0.27, -0.02)]. CONCLUSION: Baseline fatty infiltration and muscle atrophy resulting from older age, female sex, longer disease duration and absent anti-synthetase antibodies, partly mediate muscle recovery in IIM.

Conventional Tregs in treatment-naïve rheumatoid arthritis are deficient in suppressive function with an increase in percentage of CXCR3 and CCR6 expressing Tregs.

In rheumatoid arthritis (RA), immune homeostasis is maintained by T regulatory cells (Tregs) that in an inflammatory milieu can change towards T-helper-like phenotypes (Th-like Tregs). Our aim was to examine the phenotypic and functional characteristics of CD4+CD25+CD127lo/- Tregs, Th-like Tregs and T effector (Teff) cells in the peripheral blood (PB) and synovial fluid (SF) of treatment-naïve early RA, as compared to osteoarthritis (OA) and healthy control (HC) peripheral blood. Frequencies of Tregs, CXCR3, CCR6 expressing Tregs (Th-like Tregs), and Teff cells were analyzed using flow cytometry in RA (n = 80), OA (n = 20), and HC (n = 40). Cytokine concentrations of the respective T cell subsets in plasma and SF were measured using flow cytometric bead array. Tregs sorted from RA and HC PB using magnetic beads were analyzed for functional capacities by CFSE proliferation assay and FOXP3 gene expression using real-time PCR. We observed that the frequencies of Th17 cells in PB and SF were significantly higher in RA when compared to HC, whereas Tregs were lower in PB and high in SF compared to HC and OA respectively. Th1- and Th17-related pro-inflammatory cytokines IL12p70, INF-γ, TNF-α, and IL-6, and IL-17A were significantly higher in the plasma and SF of RA. Tregs expressing CXCR3 (Th1-like Tregs) and CCR6 (Th17-like Treg) were significantly higher in PB and SF of RA compared to controls and was positively associated with seropositivity and disease activity. Treg cells isolated from peripheral blood of RA showed decreased function and reduced FOXP3 gene expression compared to HC. In our study, we have demonstrated higher frequencies of Th1 and Th17 cells and increased circulatory and SF pro-inflammatory cytokines (IL12P70, INF-γ, IL-6, IL-17A, and TNF-α) in RA. This inflammatory milieu might alter total Tregs frequencies and influence conversion of Tregs into Th-like Tregs.

Kidney histopathology in predicting flares following drug withdrawal in proliferative lupus nephritis in clinical remission.

Residual renal histopathological activity at clinical remission in Proliferative Lupus Nephritis (PLN) can predict renal flare upon immunosuppression withdrawal. Data on the role of histological renal remission in predicting extra-renal flares is lacking. We assessed renal histopathology prior to drug withdrawal and the occurrence of renal and extra-renal flares over 52 weeks after drug withdrawal in PLN patients in long-term clinical remission. This is a subgroup analysis of a non-inferiority, open-label randomized (1:1) controlled trial. Patients with biopsy-proven Class III/IV LN in the past (biopsy 1), on immunosuppressants (IS) ≥ 3 years, in clinical remission for ≥ 1 year, on stable prednisolone dose (≤ 7.5 mg/day) plus a maintenance IS and hydroxychloroquine (HCQ) were subjected to a repeat renal biopsy (biopsy 2). Individuals with biopsy 2 having activity index (AI) < 4/24 were randomised to either prednisolone or IS withdrawal. Primary end-point was the proportion experiencing a flare [SELENA-SLEDAI flare index (SFI)] at week 52. Twenty-eight eligible patients underwent biopsy 2 and randomized to prednisolone (n = 15) and IS (n = 13) withdrawal. At biopsy 1, 12 (43%) had class III, 15 (53.5%) had class IV, and 1 (3.5%) had class III + V. At biopsy 2, PLN persisted in 4 (14.2%) while 18 (64.2%) were in histological remission (AI = 0) with 6 (21.4%) in class II. Following drug withdrawal, 9/28 (32%) had flares especially musculoskeletal (55.5%), mucocutaneous (44.4%), and renal (33.3%). Among the four persistent PLN patients, one of the two (50%) with AI = 1 had extra-renal flare while both the two with AI = 2 (100%) had renal and extra-renal flares. In those with histological remission (biopsy 2), 6/18 (66.6%) experienced extra-renal flare of whom one also had renal flare. Upon drug withdrawal, renal histopathology findings with any activity index can predict renal flare while histological remission is not enough to predict extra-renal flare, thus making it an unsuitable marker for deep SLE remission.

Performance of Clinical and Biochemical Parameters in Identifying Renal Histopathology and Predictors of One-Year Renal Outcome in Lupus Nephritis-A Single Centre Study from India.

Objectives: To assess the performance of clinical and biochemical parameters in identifying renal histopathology. To assess the performance of a combination of demographic, clinical, serological and histopathological parameters in determining renal response at one year. Methods: Data of biopsy-proven (ISN/RPS­2003 criteria) Lupus Nephritis (LN) were extracted from the institute database. Demographic, clinical and biochemical parameters at the time of biopsy were noted, and their associations with histopathological class, activity and chronicity scores were evaluated. Follow-up data at one year were collected. Complete, partial or no response (CR, PR, NR) for renal outcomes at one year and the predictors of NR were assessed. Results: Out of the 333 renal biopsies, 240 (71.8%) were Class III/IV. More patients with Class III/IV LN had hypertension (52.1%) and low eGFR (p < 0.001). Among Class III/IV, AS correlated weakly with UPCR (r = 0.31, p < 0.01), eGFR (r = −0.172; p < 0.01) and CS with eGFR (r = −0.212; p < 0.01). The presence of either hypertension, UPCR > 0.5 g/day, active urinary sediments or serum creatinine >1.3 g/dL had a sensitivity of >96% and specificity of <9% in detecting proliferative LN, crescents, interstitial inflammation and chronicity. NR was higher in males (aOR:3.9, 95% CI:1.4−11.0, p < 0.001), those with abnormal baseline creatinine (aOR: 1.9, 95% CI: 1.1−3.2, p < 0.001), higher renal SLEDAI (p < 0.05), higher AS, CS (p < 0.001) and interstitial inflammation (p < 0.005). In the binary logistic regression, the combination of male sex, baseline creatinine, UPCR and CS performed best in predicting NR (AUC: 0.762; 95% CI: 0.684−0.840, p < 0.001). Conclusions: Clinical and biochemical parameters alone have a poor specificity in identifying renal histopathology. A combination of demographic, clinical and histopathology parameters can better predict renal outcomes at one year.

Effect of skin phototype on quantitative nailfold capillaroscopy.

Objectives: To determine the impact of Fitzpatrick scale-based skin phototype on visualization of capillary density using nailfold capillaroscopy in healthy Indian adults. Methods: In this cross-sectional study, healthy adults were examined for nailfold capillaroscopy findings utilizing a portable capillary microscope at 800× magnification. Photographs of two contiguous areas measuring 1 mm2 each of the distal row of capillaries were captured. Images were captured from the central area of all fingers except thumb in both hands. Capillary density and morphology of nailfold capillaroscopies were assessed by two blinded assessors. The nailfold capillaroscopy parameters were compared between the Standard Fitzpatrick scale-based skin phototypes. Results: A total of 118 healthy adults were enrolled in the study. Type III, IV, V, and VI skin phototypes were seen in 27 (22.90%), 32 (27.19%), 29 (24.58%), and 30 (25.42%) participants, respectively. All participants (100%) had normal nailfold capillaroscopy morphology and architecture. Zero capillaries were visible in 11 fingers among 5 patients (4.24%) and all of them had Type VI phototype. The median capillary density per mm was 5.19 (interquartile range = 4.37-6.75) with 90 (76.27%) participants having less than seven capillaries. The median average capillary density was significantly different (p-value < 0.0001) across Type III (8.13, interquartile range = 6.44-8.88), Type IV (5.67, interquartile range = 4.41-6.98), Type V (4.94, interquartile range = 4.19-5.38), and Type VI (4.53, interquartile range = 3.72-4.91) phototypes (p < 0.05). Conclusion: The number of capillaries visualized during nailfold capillaroscopy decreases as the skin pigmentation increases. There is a need to redefine the nailfold capillaroscopy density and avascularity by taking skin phototype as one of the determinants before labeling a nailfold capillaroscopy finding with less visualized capillaries as abnormal.

Performance of timed function tests as outcome measures in idiopathic inflammatory myopathy-results from a single-centre cohort.

OBJECTIVE: To evaluate performance of timed function tests (TFTs) in assessing muscle strength and endurance as determined by Manual Muscle Testing 8 (MMT-8) and Functional Index 2 (FI-2), respectively, in idiopathic inflammatory myopathies (IIM). METHODS: This cohort study included 42 IIM patients satisfying 2017 EULAR/ACR criteria. Patients were classified as active (n = 18) or inactive disease (n = 24) based on clinical status at baseline. MMT-8, FI-2, 30 s rise from chair test, 30 s 1 kg arm rise test and 2-min walking distance (2MWD) were administered at baseline, 3 months and 6 months. Pearson rank correlation analysis and receiver operating curves were performed to assess the performance of timed function tests. RESULTS: All patients were followed up at 3 months and 39 completed 6 months' follow-up. All the three TFTs had excellent convergent (r > 0.7, P < 0.05) and divergent validity (P < 0.05). Only 2MWD had moderate to strong correlation with ΔMMT-8 at 3 and 6 months among those with active disease (P = 0.001). All the TFTs correlated with ΔFI-2 in active disease but only Δ2MWD correlated with ΔFI-2 in inactive disease at 6 months (r = 0.506, P = 0.036). At a cut-off of 5% improvement in MMT-8, 2MWD had an area under the curve (AUC) of 0.868 with 95% sensitivity with 2% improvement at 3 months. To detect a 10% ΔMMT-8, Δ2MWD at a cut of 8% and 7% had an AUC of 0.909 and 0.893 with a sensitivity of 92% at 3 and 6 months, respectively (P < 0.05). CONCLUSION: 2MWD is a reliable indicator of muscle strength, endurance and treatment response. The 2MWD can be self-administered by patients, making it a potential patient-reported outcome measure.

Atypical neurological manifestations in Wernicke's encephalopathy due to hyperemesis gravidarum.

OBJECTIVES: Hyperemesis gravidarum is known to induce nutritional, water and electrolyte deficiencies which can be fatal if not treated urgently. Thiamine deficiency may lead to a constellation of neurological symptoms that include Wernicke encephalopathy. Moreover, Wernicke encephalopathy is typically manifested as ocular paresis, ataxia and confusion. METHODS: Retrospective review of 6 women who developed neurological abnormalities following hyperemesis gravidarum and were treated with varying dosage of parenteral thiamine. RESULTS: Five women developed atypical neurological symptoms, namely, slurred speech, visual loss, seizure and aggressive behaviour while one woman developed typical clinical triad of Wernicke encephalopathy after hyperemesis gravidarum. Magnetic Resonance Imaging (MRI) scans revealed abnormalities suggestive of Wernicke encephalopathy in three women only. All women improved after parenteral thiamine administration during hospital stay and had a complete neurological recovery during 2 months follow up. DISCUSSION: Wernicke encephalopathy may not be necessarily associated with the typical neurological triad and may not have noticeable hyperintensity signal in dorsomedial thalami, mammillary bodies, hippocampus and periaqueductal region during magnetic resonance imaging. Atypical neurological signs and symptoms following hyperemesis gravidarum would invariably respond immediately to appropriate dosage of parenteral thiamine. A lower loading dosage of thiamine (100 mg thrice daily) appeared adequate for management in women with normal MRI scans.

Corneal ulcer in reactive arthritis.

A 20-year-old male presented with acute lower limb oligoarthritis and enthesitis followed by acute onset redness, watering, pain and decreased vision in the right eye. He had recent history of diarrhoea with fever. Erythrocyte sedimentation rate and high-sensitivity C-reactive protein (hsCRP) were raised and human leukocyte antigen-B27 was positive. The best corrected visual acuity (BCVA) in the right eye was 20/120 and it showed a paracentral shallow corneal ulcer of size 3 × 4 mm with underlying dense stromal infiltrates and haze. Microbiological evaluation of corneal scrapings was reported as Staphylococcus hominis. The epithelium healed on topical antibiotics in one week, but there were persistent punctate erosions and pleomorphic anterior stromal infiltrates and haze. The residual keratitis healed completely on topical steroids in ten days, with BCVA improving to 20/20. A diagnosis of reactive arthritis with immune-mediated keratitis was made.

Diagnosis of Undifferentiated Connective Tissue Disease in a Patient With Digital Gangrene and Positive Antinuclear Antibodies.

The occurrence of ischemia of the digits or digital gangrene is a well-known complication of systemic autoimmune diseases, such as systemic sclerosis, systemic lupus erythematosus, and anti-phospholipid syndrome, among others. The pathophysiological mechanisms are small vessel vasculitis, vasospasm of Raynaud's phenomenon, microthrombi due to antiphospholipid syndrome, and/or accompanying accelerated atherosclerosis. Digital ischemia can also occur in the context of disseminated bacterial infections and sepsis. We present here the case of a patient who had digital ischemia and positive antinuclear antibodies but without well-defined clinical features of a connective tissue disease. A diagnosis of undifferentiated connective tissue disease was made.

Liver Abnormalities in Systemic Lupus Erythematosus: A Prospective Observational Study.

Objectives In this study, we aimed to examine and analyze liver abnormalities among patients with systemic lupus erythematosus (SLE), including both newly diagnosed patients and those being followed up, as well as the prevalence of lupus hepatitis. Methods This was a prospective observational study. Clinical data, liver function tests (LFTs), and the findings from the ultrasonography of the abdomen among the patients were prospectively recorded and evaluated. Results Overall, 28 of the total 135 (20.7%) patients had liver abnormalities, including biochemical and those detected via ultrasonography. Ten patients had transaminitis, defined as aspartate aminotransferase (AST) or alanine aminotransferase (ALT) levels >2 times the upper limit of normal (ULN). Nine patients had elevated alkaline phosphatase (ALP) or gamma-glutamyl transferase (GGT) of >2 times ULN. In three patients, transaminitis was due to anti-tubercular therapy (ATT)-induced hepatitis; in seven (5.2%), no specific cause for transaminitis could be identified, and hence they were classified as cases of lupus hepatitis. On comparing clinical features between patients with (n=7) and without lupus hepatitis (n=128), the condition was more prevalent in newly diagnosed SLE patients compared to those who had been on follow-up [six (85.7%) vs. 30 (23.6%), p=0.002]. All seven patients with lupus hepatitis had complete resolution of the transaminitis on follow-ups. However, one patient who had received ATT (isoniazid, rifampicin, ethambutol, and pyrazinamide) died. Ultrasonography showed fatty liver in seven patients and chronic liver disease in one patient. Conclusion In this study, transaminitis due to lupus hepatitis was seen in newly diagnosed lupus patients and was not associated with disease activity. Before diagnosing lupus hepatitis, drug-induced liver disease has to be ruled out, and if persistent LFT abnormalities are present, further workup is suggested to rule out overlap with primary biliary cirrhosis and/or autoimmune hepatitis.

Association of Oxidative Stress with Disease Activity and Damage in Systemic Lupus Erythematosus: A Cross Sectional Study from a Tertiary Care Centre in Southern India.

To study oxidative stress in systemic lupus erythematosus (SLE) by estimating serum oxidised LDL (OxLDL), 8-hydroxy-2'-deoxyguanosine (8-OHdG), malondialdehyde (MDA), and total anti-oxidant status and to correlate with SLE disease activity and disease damage. Eighty SLE patients satisfying the Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) 2012 criteria and 80 healthy controls were studied. Exclusion criteria were infections, renal insufficiency, other connective tissue diseases, drug-induced lupus, smoking, alcohol consumption. Disease activity was measured by SLE disease activity index-2 K (SLEDAI), disease damage was quantified by SLICC-Damage Index (SDI). Sera was tested for OxLDL, 8-OHdG, and total antioxidant status (TAS) by double-antibody sandwich ELISA; MDA measured by Colorimetric assay. Oxidative stress markers were compared between group1- controls, group 2-mildly active SLE (SLEDAI ≤ 5), group 3- moderate to highly active SLE (SLEDAI ≥ 6). SLE patients had significantly higher MDA, 8-OHdG and lower TAS when compared to healthy controls, while OxLDL was similar in the three groups. MDA, 8-OHdG were significantly higher, TAS lower in group 3 compared to group 2. MDA had positive correlation with SLEDAI, TAS negatively correlated with SLEDAI. SLE with neuropsychiatric manifestations, vasculitis, anti-sdDNA antibodies had higher MDA, MDA/TAS ratio. SLE patients with thrombocytopenia, and vasculitis had higher OxLDL. Only OxLDL was significantly higher in those patients who have SDI > 1. SLE patients have increased oxidative stress measured by increases in MDA, 8-OHdG, and lower total antioxidant status that was associated with disease activity and some disease manifestations. However only OxLDL was associated with damage.

Aetiology and short-term outcome of acute respiratory distress syndrome: a real-world experience from a medical intensive care unit in southern India.

BACKGROUND: Acute respiratory distress syndrome (ARDS) is a highly fatal syndrome especially in resource constrained settings. In this study we prospectively studied the aetiology of ARDS and its short-term outcome. METHODS: Consecutive adults with suspected ARDS were screened. ARDS was diagnosed by the Berlin criteria. Aetiology was determined clinically, and by imaging and microbiological investigations. Patients presenting with fever, prominent cough and expectoration had a throat swab tested for influenza H1N1 virus. Outcome was discharge from hospital or death. RESULTS: A total of 42 patients, mean age 42.6 years, were studied. All received mechanical ventilation. Thirteen (31%) had pulmonary ARDS: H1N1 virus infection (n = 5), pneumonia (n = 7) and tuberculosis (n = 1). Twenty nine (69%) had extrapulmonary ARDS: sepsis (n = 16) and scrub typhus (n = 8). Thirty three (79%) died, of the nine survivors scrub typhus was diagnosed in seven patients. CONCLUSION: The aetiology of ARDS in tropical medical setting is infection related. ARDS due to scrub typhus appeared to be mild with good outcome.

Bilateral subretinal abscess in community-acquired meticillin-susceptible Staphylococcus aureus infection.

Subretinal abscesses due to endogenous staphylococcal blood stream infection is a rare occurrence. A young adult male presented with subretinal abscesses, necrotising pneumonia, pleural empyema, skin and soft tissue infection, muscle abscesses and deep vein thrombosis. Aspirate from one of the abscesses and blood culture revealed meticillin-susceptible Staphylococcus aureus. We present here a case of probable Panton-Valentine leucocidin (PVL) syndrome. PVL is a cytotoxin produced by S. aureus. Infection with PVL-positive S. aureus produces a clinical disease that is characterised by necrotising pneumonia and disseminated infection that often carries a high mortality. Our patient showed prompt clinical response to cloxacillin that was given for a total duration of 6 weeks. At the end of 6 weeks vision also recovered. The successful outcome in our patient was likely due to early and appropriate antibiotic therapy.

QT interval parameters, anti-Ro antibody status, and disease activity in systemic lupus erythematosus.

BACKGROUND: The QT interval a marker of ventricular depolarization and repolarization is reported to be prolonged in some proportion of patients with systemic lupus erythematosus (SLE). We studied electrocardiographic (ECG) abnormalities, in particular QT interval and its relationship with anti-Ro antibodies, disease activity, and serum interleukin 1ß (IL-1ß), interleukin 6 (IL-6) in SLE. METHODS: A 12-lead resting ECG was performed on 140 adult SLE patients fulflling SLICC/ACR classification criteria. All patients received hydroxychloroquine and prednisolone. Corrected QT (QTc) °440 milliseconds (ms) was defined as prolonged QTc. QT dispersion (QTd) °60 ms was defined as increased QTd. RESULTS: Eighty-four patients had some form of ECG abnormality. Prolongation of QTc and QTd was present in 24 (17.1%) and 50 (35.7%) respectively. Anti-Ro/SSA antibodies were present in 63 (45%). Prolongation of QTc in anti-Ro positive versus anti-Ro negative was 17.5% and 17% respectively, p=0.98. Prolongation of QTd in anti-Ro-positive versus anti-Ro-negative was 32% and 39% respectively, p=0.37. Prolonged QTc was observed in 15% patients with SLEDAI ˛4 compared to 17.5% patients with SLEDAI °5, p=0.78. The median serum concentrations of IL-1ß and IL-6 were similar in the groups with and without prolonged QTc, with and without prolonged QTd. On binary logistic regression analyses neither clinical nor laboratory factors were predictors of prolonged QTc. However, having valvular regurgitation and hypercholesterolemia was associated with significantly reduced odds of having prolonged QTd, adjusted OR 0.33 (CI 0.14-0.83), p=0.018 and 0.19 (CI 0.05-0.80), p=0.023 respectively. Those with high LDL cholesterol and hypertriglyceridemia had a significantly higher odds of having a normal QTd with adjusted OR of 4.34 (1.31-14.46) p=0.017and 5.59 (1.62-19.38) p=0.007respectively. CONCLUSION: Though 17% and 35% SLE patients have QTc and QTd prolongation, association with anti-Ro antibodies or disease activity was absent. A large proportion has other asymptomatic ECG abnormalities that may reflect subclinical cardiac involvement.

Community Acquired AKI: A Prospective Observational Study from a Tertiary Level Hospital in Southern India.

INTRODUCTION: Pattern of acute kidney injury (AKI) differs vastly from region to region in India. Moreover, prospective data on community-acquired AKI (CAAKI) using the KDIGO criteria for AKI are limited. Our objective was to study the etiology, clinical characteristics, and short-term outcome of CAAKI in adults. METHODS: This was a prospective observational study in the medical wards of a tertiary care hospital. Patients fulfilling the 2012 KDIGO AKI criteria of community acquired acute kidney injury (CAAKI) were included. Patients who developed AKI 48 hours after admission, those hospitalized >48 hours elsewhere, and patients with chronic kidney disease were excluded. The study did not include obstetric or surgical cases of AKI. Serum creatinine and urine output was monitored. Daily progress, in particular development of hypotension, oliguria, acute respiratory distress syndrome, sepsis, and renal replacement therapy, was noted. RESULTS: Of 186 CAAKI patients (mean age, 46.13 ± 15.2 years), 86/186 was infective etiology, 93/186 was non-infective etiology, 7/186 was due to intrinsic renal pathology. Pyelonephritis 33/186 (17.7%) was the most common infective etiology, and snakebite in 49 (26.3%) was the most common non-infective etiology; 28/186 (15.1%) died. On logistic regression, hypotension, mechanical ventilation, thrombocytopenia, and anuria were associated with mortality. CONCLUSIONS: Acute pyelonephritis and snakebite-related AKI emerged as the two most common medical causes of CAAKI in our region. Such environmental and infectious causes that largely are preventable causes of AKI are also associated with significant morbidity and mortality.

Procalcitonin levels in sepsis and its association with clinical outcome in southern India.

Procalcitonin has been found to be a good marker for the diagnosis of sepsis. However, data on procalcitonin levels to predict the clinical outcome in patients with sepsis are limited. The aim of our study was to estimate serum procalcitonin levels in patients with sepsis and to identify its relationship with the clinical outcome. This was a prospective observational study conducted on 112 patients with sepsis admitted to the medical wards and medical intensive care unit of a tertiary care teaching hospital. Serum procalcitonin was measured at baseline before antibiotic administration and on day 5. The clinical outcome studied was death or survival on day 28. Baseline mean serum procalcitonin was highest in patients with septic shock and lowest in patients having sepsis without organ dysfunction. Mean values of procalcitonin at baseline and on day 5 were significantly higher in non-survivors when compared with survivors. There was a significant difference in the change in procalcitonin levels from baseline to day 5 between survivors and non-survivors, with survivors having declining values on day 5 while non-survivors had increasing values from baseline. The baseline APACHE II and SOFA scores also showed a significant correlation with the baseline procalcitonin level. Declining values of procalcitonin therefore indicate a favourable clinical outcome in patients with sepsis.