17 research outputs found
Henoch-Schönlein purpura in an older man presenting as rectal bleeding and IgA mesangioproliferative glomerulonephritis: a case report
<p>Abstract</p> <p>Introduction</p> <p>Henoch-Schönlein purpura is the most common systemic vasculitis in children. Typical presentations are palpable purpura, abdominal pain, arthritis, and hematuria. This vasculitic syndrome can present as an uncommon cause of rectal bleeding in older patients. We report a case of an older man with Henoch-Schönlein purpura. He presented with rectal bleeding and acute kidney injury secondary to IgA mesangioproliferative glomerulonephritis.</p> <p>Case presentation</p> <p>A 75-year-old Polish man with a history of diverticulosis presented with a five-day history of rectal bleeding. He had first noticed colicky left lower abdominal pain two months previously. At that time he was treated with a 10-day course of ciprofloxacin and metronidazole for possible diverticulitis. He subsequently presented with rectal bleeding to our emergency department. Physical examination revealed generalized palpable purpuric rash and tenderness on his left lower abdomen. Laboratory testing showed a mildly elevated serum creatinine of 1.3. Computed tomography of his abdomen revealed a diffusely edematous and thickened sigmoid colon. Flexible sigmoidoscopy showed severe petechiae throughout the colon. Colonic biopsy showed small vessel acute inflammation. Skin biopsy resulted in a diagnosis of leukocytoclastic vasculitis. Due to worsening kidney function, microscopic hematuria and new onset proteinuria, he underwent a kidney biopsy which demonstrated IgA mesangioproliferative glomerulonephritis. A diagnosis of Henoch-Schönlein purpura was made. Intravenous methylprednisolone was initially started and transitioned to prednisone tapering orally to complete six months of therapy. There was marked improvement of abdominal pain. Skin lesions gradually faded and gastrointestinal bleeding stopped. Acute kidney injury also improved.</p> <p>Conclusion</p> <p>Henoch-Schönlein purpura, an uncommon vasculitic syndrome in older patients, can present with lower gastrointestinal bleeding, extensive skin lesions and renal involvement which responds well to systemic steroid therapy. A history of diverticulosis can mislead physicians to the diagnosis of diverticular bleeding which is more common in this age group. The clinical manifestations of the disease, including characteristic skin rash, abdominal pain, joint inflammation and renal involvement raised the suspicious of Henoch-Schönlein purpura.</p
Zinc-containing sol-gel glass nanoparticles to deliver therapeutic ions
Zn-containing dense monodispersed bioactive glass nanoparticles (Zn-BAGNPs) have been developed to deliver therapeutic inorganic trace elements, including Si, Ca, Sr, and Zn, to the cells through the degradation process, as delivery carriers for stimulating bone regeneration because of their capacity to induce osteogenic differentiation. The solâgel-derived dense silica nanoparticles (SiO2-NPs) were first synthesized using the modified Stöber method, prior to incorporating therapeutic cations through the heat treatment process. The successfully synthesized monodispersed Zn-BAGNPs (diameter of 130 ± 20 nm) were homogeneous in size with spherical morphology. Ca, Sr and Zn were incorporated through the two-step post-functionalization process, with the nominal ZnO ratio between 0 and 2 (0, 0.5, 1.0, 1.5 and 2.0). Zn-BAGNPs have the capacity for continuous degradation and simultaneous ion release in SBF and PBS solutions due to their amorphous structure. Zn-BAGNPs have no in vitro cytotoxicity on the murine pre-osteoblast cell (MC3T3-E1) and periodontal ligament stem cells (PDLSCs), up to a concentration of 250 ”g/mL. Zn-BAGNPs also stimulated osteogenic differentiation on PDLSCs treated with particles, after 2 and 3 weeks in culture. Zn-BAGNPs were not toxic to the cells and have the potential to stimulate osteogenic differentiation on PDLSCs. Therefore, Zn-BAGNPs are potential vehicles for therapeutic cation delivery for applications in bone and dental regenerations
Oral sitafloxacin vs intravenous ceftriaxone followed by oral cefdinir for acute pyelonephritis and complicated urinary tract infection: a randomized controlled trial
Bannakij Lojanapiwat,1 Sireethorn Nimitvilai,2 Manit Bamroongya,3 SupunNee Jirajariyavej,4 Chirawat Tiradechavat,5 Aumnat Malithong,6 Chagkrapan Predanon,7 Dan Tanphaichitra,8 Boonlert Lertsupphakul9 1Department of Surgery, Maharaj Nakorn Chiang Mai Hospital, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand; 2Department of Internal Medicine, Nakhon Pathom Hospital, Nakhon Pathom, Thailand; 3Department of Surgery, Buddasothorn Hospital, Chachoengsao, Thailand; 4Department of Medicine, Taksin Hospital, Bangkok, Thailand; 5Department of Surgery, Udon Thani Hospital, Udon Thani, Thailand; 6Department of Medicine, BMA General Hospital, Bangkok, Thailand; 7Department of Surgery, Khon Kaen Hospital, Khon Kaen, Thailand; 8Department of Internal Medicine, Anandamahidol Hospital, Lopburi, Thailand; 9Department of Surgery, Maharaj Nakorn Si Thammarat Hospital, Nakhon Si Thammarat, Thailand Background: The conventional antibiotic regimen for community-acquired upper urinary tract infections with moderate severity in Thailand is parenteral ceftriaxone (CTRX) for several days followed by oral cephalosporin for 7–14 days. The aim of this study was to compare the efficacy and safety of oral sitafloxacin (STFX) with that of intravenous CTRX followed by oral cefdinir (CFDN) for the therapy of acute pyelonephritis (APN) and complicated urinary tract infection (cUTI).Methods: This open-label, randomized, controlled, noninferiority clinical trial included patients from nine centers across Thailand. Adult patients with APN or cUTI were randomly assigned to receive 100 mg of oral STFX twice daily for 7–14 days, or 2 g of intravenous CTRX for several days followed by 100 mg of oral CFDN three times per day for another 4–12 days.Results: A total of 289 adult patients with APN or cUTI (141 in the STFX group and 148 in the CTRX/CFDN group) were included in the intent-to-treat (ITT) analysis, and 211 patients (108 in the STFX group and 103 in the CTRX/CFDN group) were included in the per-protocol (PP) analysis. The baseline characteristics of patients in both groups were comparable. The causative pathogen in most patients with APN or cUTI was Escherichia coli. The clinical success rates at the end of treatment revealed the STFX regimen to be noninferior to the CTRX/CFDN regimen (86.6% vs 83.8% for ITT analysis and 97.2% vs 99.0% for PP analysis, respectively). Adverse events with mild-to-moderate severity were similar between groups.Conclusion: Oral STFX is noninferior to intravenous CTRX followed by oral CFDN in adult patients with APN and cUTI. Lower rates of resistance compared to CTRX and/or CFDN and oral administration suggest STFX as a more attractive treatment option in this patient population. Keywords: acute pyelonephritis, complicated urinary tract infection, sitafloxacin, ceftriaxone, cefdini
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Correction: HIV DNA reservoir increases risk for cognitive disorders in cART-naĂŻve patients (PLoS ONE)
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HIV DNA reservoir increases risk for cognitive disorders in cART-naĂŻve patients.
ObjectivesCognitive impairment remains frequent in HIV, despite combination antiretroviral therapy (cART). Leading theories implicate peripheral monocyte HIV DNA reservoirs as a mechanism for spread of the virus to the brain. These reservoirs remain present despite cART. The objective of this study was to determine if the level of HIV DNA in CD14(+) enriched monocytes predicted cognitive impairment and brain injury.MethodsWe enrolled 61 cART-naĂŻve HIV-infected Thais in a prospective study and measured HIV DNA in CD14(+) enriched monocyte samples in a blinded fashion. We determined HAND diagnoses by consensus panel and all participants underwent magnetic resonance spectroscopy (MRS) to measure markers of brain injury. Immune activation was measured via cytokines in cerebrospinal fluid (CSF).ResultsThe mean (SD) age was 35 (6.9) years, CD4 T-lymphocyte count was 236 (139) and log10 plasma HIV RNA was 4.8 (0.73). Twenty-eight of 61 met HAND criteria. The log10 CD14(+) HIV DNA was associated with HAND in unadjusted and adjusted models (pâ=â0.001). There was a 14.5 increased odds ratio for HAND per 1 log-value of HIV DNA (10-fold increase in copy number). Plasma CD14(+) HIV DNA was associated with plasma and CSF neopterin (pâ=â0.023) and with MRS markers of neuronal injury (lower N-acetyl aspartate) and glial dysfunction (higher myoinositol) in multiple brain regions.InterpretationReservoir burden of HIV DNA in monocyte-enriched (CD14(+)) peripheral blood cells increases risk for HAND in treatment-naĂŻve HIV+ subjects and is directly associated with CSF immune activation and both brain injury and glial dysfunction by MRS
HIV DNA reservoir increases risk for cognitive disorders in cART-naĂŻve patients.
ObjectivesCognitive impairment remains frequent in HIV, despite combination antiretroviral therapy (cART). Leading theories implicate peripheral monocyte HIV DNA reservoirs as a mechanism for spread of the virus to the brain. These reservoirs remain present despite cART. The objective of this study was to determine if the level of HIV DNA in CD14(+) enriched monocytes predicted cognitive impairment and brain injury.MethodsWe enrolled 61 cART-naĂŻve HIV-infected Thais in a prospective study and measured HIV DNA in CD14(+) enriched monocyte samples in a blinded fashion. We determined HAND diagnoses by consensus panel and all participants underwent magnetic resonance spectroscopy (MRS) to measure markers of brain injury. Immune activation was measured via cytokines in cerebrospinal fluid (CSF).ResultsThe mean (SD) age was 35 (6.9) years, CD4 T-lymphocyte count was 236 (139) and log10 plasma HIV RNA was 4.8 (0.73). Twenty-eight of 61 met HAND criteria. The log10 CD14(+) HIV DNA was associated with HAND in unadjusted and adjusted models (pâ=â0.001). There was a 14.5 increased odds ratio for HAND per 1 log-value of HIV DNA (10-fold increase in copy number). Plasma CD14(+) HIV DNA was associated with plasma and CSF neopterin (pâ=â0.023) and with MRS markers of neuronal injury (lower N-acetyl aspartate) and glial dysfunction (higher myoinositol) in multiple brain regions.InterpretationReservoir burden of HIV DNA in monocyte-enriched (CD14(+)) peripheral blood cells increases risk for HAND in treatment-naĂŻve HIV+ subjects and is directly associated with CSF immune activation and both brain injury and glial dysfunction by MRS
Plasma CD14<sup>+</sup> HIV DNA and plasma neopterin (left, <i>p</i>â=â0.0473, adjusted <i>r</i><sup>2</sup>â=â0.0662) and CSF neopterin (right, <i>pâ=â</i>0.023, adjusted <i>r</i><sup>2</sup>â=â0.123) by univariate regression.
<p>Plasma CD14<sup>+</sup> HIV DNA and plasma neopterin (left, <i>p</i>â=â0.0473, adjusted <i>r</i><sup>2</sup>â=â0.0662) and CSF neopterin (right, <i>pâ=â</i>0.023, adjusted <i>r</i><sup>2</sup>â=â0.123) by univariate regression.</p
Receiver operating characteristic (ROC) curve for level CD14<sup>+</sup> HIV DNA identifying HAND.
<p>ROC of CD14<sup>+</sup> HIV DNA onlyâ=â0.7922, ROC adjusting for CD4<sup>+</sup> T-lymphocyte and plasma HIV RNA: 0.8247.</p