Severity Of Systemic Symptoms Research Articles

PREVALENCE AND MANAGEMENT OF URINARY TRACT INFECTIONS IN TYPE 2 DIABETIC PATIENTS

Diabetes mellitus (DM) is a polygenic illness that affects many other organs. In people with type 2 diabetes, urinary tract infection is the most prevalent, the most severe, and has the worst consequences. They are also more frequently caused by microorganisms that are resistant to antibiotics. Immune system dysfunction, poor metabolic regulation, and inadequate bladder emptying owing to autonomic neuropathy may all contribute to these individuals' increased risk of urinary tract infections. The novel anti-diabetic sodium glucose cotransporter 2 inhibitors were not shown to raise the likelihood of symptomatic urinary tract infections appreciably. Urinary tract infection symptoms are comparable to those seen in people without diabetes, while some patients with diabetic neuropathy may exhibit changed clinical findings. The existence of symptoms, the severity of systemic symptoms, whether the infection is limited in the bladder or also includes the kidney, the presence of urologic abnormalities, concomitant metabolic disturbances, and renal function all influence treatment. There is no evidence that diabetic people with asymptomatic bacteriuria should be treated. Diabetes length, age, gender, method of drug administration, kind of medicines used in diabetes, poor glycemic control, obesity, unsanitary settings, sexual intercourse, and type of DM are all risk factors for UTI in diabetic patients. Antibiotic usage on a daily basis has rendered numerous harmful microorganisms resistant to their effects. In the long run, if UTI in diabetes people is not treated, it might lead to serious problems. Furthermore, the pattern of antibiotic resistance varies by geographical area. As a result, the use of susceptible antibiotics to treat UTI in diabetes patients has become critical. Medline and PubMed public database searches was carried out for papers written all over the world on UTI in diabetic patients. No predictive analytics technology was used. To evaluate the initial results and the methods of conducting the paper, the group members reviewed the data.

Vitamin D supplementation for primary dysmenorrhea: a double-blind, randomized, placebo-controlled trial.

ObjectiveRecent studies have shown a possible association between vitamin D deficiency and the severity of primary dysmenorrhea. The present study aimed to investigate the effect of vitamin D supplementation on pain and systemic symptoms in patients with primary dysmenorrhea.MethodsThis double-blind, randomized, placebo-controlled trial was conducted on female students aged 18 to 32 years with primary dysmenorrhea and vitamin D deficiency (25 [OH]D <30 ng/mL). The participants (n=116) received either 50,000 IU of vitamin D3 (cholecalciferol) or placebo capsules on a weekly basis for eight consecutive weeks. The outcomes were pain intensity (scored 0 to 10), number of days with pain, number of consumed pain-relief medications (per day), and severity of systemic symptoms (fatigue, headache, nausea/vomiting, and diarrhea; total score of 0 to 12).ResultsCompared with baseline, our participants who received vitamin D experienced significant reductions in pain intensity (−1.0 and −1.5 score at weeks 4 and 8, P<0.001), the number of days with pain (−1.0 day at weeks 4 and 8, P<0.001), the number of consumed pain-relief medications (−1.0 at weeks 4 and 8, P<0.001), and systemic symptoms severity (−1.0 score at weeks 4 and 8, P<0.001). No significant improvements were observed in the placebo group in terms of these outcomes.ConclusionVitamin D supplementation in women with primary dysmenorrhea and vitamin D deficiency could improve systemic symptoms and reduce pain intensity, the number of days with pain, and the need for consuming pain-relief medications.

Higher specificity of the new EULAR/ACR 2019 criteria for diagnosing systemic lupus erythematosus in patients with biopsy-proven cutaneous lupus.

The risk of developing systemic lupus erythematosus (SLE) in patients with cutaneous lupus erythematosus (CLE) varies, ranging between 5 to 23%, depending on the disease subtype. Interestingly, most of these patients do not manifest clinically significant internal organ features of SLE. The aim of our study was to evaluate the percentage of CLE patients who fulfilled SLE criteria introduced by the American College of Rheumatology (ACR 1997) and Systemic Lupus Erythematosus International Collaborating Clinics (SLICC 2012), as well as the new criteria developed by the European League Against Rheumatism and ACR (EULAR/ACR 2019). Patients were evaluated at baseline and during follow-up, and the severity of systemic symptoms was assessed. We retrospectively analysed the medical histories of 184 patients with CLE (75 with discoid lupus erythematosus and 109 with subacute cutaneous lupus erythematosus). The mean duration of follow-up after CLE diagnosis was 58 months (24-120 months). Of the analysed patients, 23.4%, 17.4% and 14.7% met the ACR 1997, SLICC 2012 and EULAR/ACR 2019 classification criteria for SLE at baseline, respectively. There was no significant difference in this proportion after follow-up. All of the CLE patients fulfilling SLE criteria demonstrated no-to-mild internal organ involvement and laboratory abnormalities such as cytopenia or complement levels were mild or only slightly decreased. The EULAR/ACR 2019 criteria are characterised by higher specificity for SLE diagnosis when compared to previously introduced criteria sets. We conclude that patients with CLE, even those meeting the criteria for SLE, have low risk of serious complications of SLE.

Urinary tract infections in patients with type 2 diabetes mellitus: review of prevalence, diagnosis, and management.

Urinary tract infections are more common, more severe, and carry worse outcomes in patients with type 2 diabetes mellitus. They are also more often caused by resistant pathogens. Various impairments in the immune system, poor metabolic control, and incomplete bladder emptying due to autonomic neuropathy may all contribute to the enhanced risk of urinary tract infections in these patients. The new anti-diabetic sodium glucose cotransporter 2 inhibitors have not been found to significantly increase the risk of symptomatic urinary tract infections. Symptoms of urinary tract infection are similar to patients without diabetes, though some patients with diabetic neuropathy may have altered clinical signs. Treatment depends on several factors, including: presence of symptoms, severity of systemic symptoms, if infection is localized in the bladder or also involves the kidney, presence of urologic abnormalities, accompanying metabolic alterations, and renal function. There is no indication to treat diabetic patients with asymptomatic bacteriuria. Further studies are needed to improve the treatment of patients with type 2 diabetes and urinary tract infections.

Histopathology of the exanthema in DRESS in correlation with markers of severe systemic involvement

Methods Skin biopsies performed in in-patients with a diagnosis of DRESS according to REGISCAR criteria, were independently evaluated by two Dermatopathologists. Epidermal and dermal parameters were scored (lymphocyte, eosinophil and neutrophil infiltrate, lymphocyte exocytosis, spongiosis and necrotic/vacuolated keratinocytes) and correlated with the severity of systemic symptoms (eosinophilia, liver cytolysis and cholestasis, evaluated respectively by serum ALT and GGT values) and the presence of circulating HHV-6 DNA.

Systemic Symptoms in the Progression of Cutaneous to Systemic Lupus Erythematosus

Patients with cutaneous lupus erythematosus (CLE) who develop systemic lupus erythematosus (SLE) may have few and mild systemic symptoms. To characterize the types and severity of systemic symptoms in a longitudinal cohort of patients with CLE. Prospective, longitudinal cohort study of 77 patients with CLE who presented between January 2007 and April 2011 at a university autoimmune skin disease clinic. Systemic symptoms and severity were determined from data recorded at each study visit and from medical records. Of 77 patients with CLE, 13 (17%) went on to meet criteria for SLE, with a mean (SD) time from CLE diagnosis to SLE of 8.03 (6.20) years. Of the 13 patients, 1 (8%) solely met the mucocutaneous American College of Rheumatology (ACR) criteria of malar rash, discoid rash, photosensitivity, and oral ulcers, and 3 (23%) met the mucocutaneous ACR criteria plus positive antinuclear and other antibody titers. After a mean (SD) follow-up time of 2.81 (1.34) years, only 5 of the 13 patients with CLE (38%) who progressed to meet SLE criteria developed moderate to severe additional systemic disease. Patients with CLE who developed SLE during our study did so mostly by meeting the mucocutaneous ACR criteria, and the majority developed none to mild additional systemic disease during the study period. Thus, our study suggests that a small percentage of patients with CLE eventually develop SLE and that even if they do, most patients will have mild systemic disease.

Giant Cell Arteritis - Beyond the Headache

Giant Cell Arteritis (GCA) is a chronic granulomatous vasculitis preferentially targeting large and mediumsized arteries but may be generalized; Vessel inflammation prominently involves the cranial branches of arteries originating in aortic arch. Headache is prevalent, appearing in two thirds of patients, classic in temporal region; may occur in occipital region or generalized accompanied in half a cases by “jaw claudication”. It is recognized today that this is in fact a systemic vasculitis with four possible phenotypes: large vessel vasculitis, cranial vasculitis, systemic inflammatory disease presentation and the polymyalgia rheumatica (PMR). Understanding the multiple aspects of Giant Cell Arteritis and the extensive involvement helps recognizing the dangerous complications: the vision loss, the aneurysms and dissecting aneurysms, the mesenteric insufficiency and the limb vascular occlusion and treat them. Scientific information now exists on the pathogenesis of GCA. Studies revealed the role of Th1 and Th17 cells and the network of cytokines and the implication in treatment. Studies in untreated and treated GCA patients have indicated that two cytokine networks contribute to the vasculitic immune pathology (IFN-γ axis and Il-17 axis). Also the majority of the studies have found a significant increased level of circulating IL-6 in patients with active disease Production of IL6 correlates with severity of systemic symptoms. The biopsy of temporal arteries is still the gold standard for diagnosis but the involvement of large vessels makes us look for the best studies to evaluate and re-evaluate after treatment that particular type of arteries. The review approaches studies that give information on vessel structure versus vessel inflammation (MRI/MRA, PET scan, and ultrasound). The first line of treatment is still the steroids, with a sense of urgency in complication to start sooner, use larger doses and decide on intravenous versus oral approach. Methotrexate and anti-tumor necrosis α inhibitors disappointed in studies and are not routinely recommended at this time. New treatments are connecting cytokine profile to its blocker trying to be more specific in managing a certain phenotype of GCA. Keywords: Giant cell arteritis, large vessel vasculitis, cranial arteritis, ischemic optic neuropathy, cytokines, temporal artery biopsy, positron emission tomography, glucocorticosteroids.

Do systemic symptoms predict the risk of kidney scarring after urinary tract infection?

Background and aims:In the NICE guideline on childhood urinary tract infection (UTI), it is assumed that the presence or severity of systemic symptoms, especially fever, predicts for renal scarring, and...

Severity of Mastitis Symptoms as a Predictor of C-Reactive Protein in Milk and Blood During Lactation

To investigate the presence of C-reactive protein (CRP) in breast milk and any relationship between changes in CRP in breast milk and blood, and the severity of systemic and breast symptoms experienced during mastitis. Mothers (n = 26) were followed prospectively from day 5 postpartum to the end of their lactation. Milk from each breast, blood, 24-hour urine samples and data on breast and systemic pathologies were collected at reference intervals during the first 3 months postpartum, daily during the occurrence of any breast inflammation and at 7 days after resolution of symptoms. CRP in blood was significantly increased during mastitis (p < 0.001, df:1,81; F = 31) and severity of systemic symptoms was a significant predictor for changes of CRP in blood (p < 0.01; df:3,42; F = 9.6). During mastitis both the symptomatic breast (p < 0.001; df:1,79; F = 19) and the contralateral asymptomatic breast (p < 0.004; df:1,75; F = 8.7) had a significantly higher milk CRP when compared with women with no mastitis. Although an increasing severity of breast and systemic symptoms in mastitis was predictive of an increasing CRP in milk and blood, respectively, the presence of CRP in similar concentrations in the mastitis and asymptomatic breast suggests it is of little use in making a differential diagnosis between infective verses noninfective forms of mastitis.

Soluble tumour necrosis factor receptor levels reflect coagulation abnormalities in systemic juvenile chronic arthritis.

The objective was to evaluate tumour necrosis factor (TNF) status in patients with systemic juvenile chronic arthritis (s-JCA). Plasma levels of TNF-alpha, and serum levels of soluble TNF receptor 1 and 2 (sTNFR1 and sTNFR2) were measured using specific immunoassays in 20 patients with s-JCA, 10 with polyarticular JCA and 15 with pauciarticular JCA, and in 20 controls comparable for age. In patients with active s-JCA, circulating levels of TNF-alpha, sTNFR1 and sTNFR2 were significantly (P < 0.001) higher than those of controls. The levels of sTNFR1 and sTNFR2, but not those of TNF-alpha, were associated with the persistence and severity of systemic symptoms and were significantly correlated with prolongation of partial thromboplastin time and decrease in prothrombin activity. In two patients evaluated during a s-JCA-associated macrophage activation syndrome, a marked increase in sTNFR1 and sTNFR2 was found. Our results suggest that in s-JCA, TNF is involved in systemic manifestations, in the subclinical coagulation abnormalities, and in the development of the macrophage activation syndrome.

Mapping Nucleotides in the 126-kDa Protein Gene That Control the Differential Symptoms Induced by Two Strains of Tobacco Mosaic Virus

The differential symptom determinants of the Holmes’ masked (M) and U1 strains of tobacco mosaic virus previously were mapped to the 5′-coterminal open reading frame (ORF) encoding the 126-kDa protein and the N-terminal two-thirds of the 183-kDa protein. Both proteins influence viral RNA accumulation, but the function of, and impact on, symptom formation by large domains within the 126-kDa gene, which are not conserved with sequences in analogous ORFs from other related viruses, are unknown. In the current study, cDNA clones representing each strain (i.e., MIC-TMV and U1-TMV) were mutated in these nonconserved domains to further define the nucleotides responsible for mosaic symptom induction onNicotiana tabacum.Progeny virus of a mutant containing only eight nucleotide substitutions from the MIC-TMV sequence to the U1-TMV sequence within the 126-kDa protein ORF of MIC-TMV induced U1-TMV-like symptoms. Single or multiple substitutions among these eight nucleotides further defined residues critical for symptom modulation. Complementary substitutions in the MIC-TMV and U1-TMV sequences did not always yield progeny virus that induced complementary visual symptoms. Progeny of some mutants contained second-site spontaneous mutations at specific positions shown to influence symptom phenotype. For a subset of the stable site-directed mutants, there was no correlation between severity of systemic symptoms and chlorotic lesion size or virus accumulation in these chlorotic lesions on inoculated leaves.

Electrophoretic mobility of different in pathogenicity strains of Tobamovirus group

Twenty four Tobamovirus strains divided according to their ability to overcome the resistance genes in tobacco and tomato as well as in their severity of systemic symptoms were tested. Significant differences between means of particle mobility of the virus groups were found especially about yellow mosaic strains which were distinguishable enough by the electrophoretic analysis.

Disease response to tobacco mosaic virus in transgenic tobacco plants that constitutively express the pathogenesis-related PR1b gene

Correlation of the temporal and spacial pattern of induction of the pathogenesis-related(PR) genes PR1a, PR1b, and PR1c with viral infections in certain tobacco cultivars has implicated PR proteins in viral disease resistance. To test whether the PR1 proteins of tobacco are involved in viral resistance, transgenic Nicotiana tabacum plants were constructed which constitutively express the PRib gene. This protein was secreted from cells of transgenic plants and accumulated in the extracellular space at levels equivalent to those found in nontransgenic plants in association with disease resistance. Transgenic plants derived from the cultivar (cv.) Xanthi (susceptible to tobacco mosaic virus [TMV] infection) exhibited no delayed onset or reduction in the severity of systemic symptoms after TMV infection. In transgenic plants derived from cv. Xanthi-nc (TMV resistant), the time of appearance, the size and general morphology, and the number of viral lesions produced were similar to the parental control plants after TMV infection. These data indicate that the PR1b protein of tobacco is not sufficient for TMV resistance, and imply that the PR1 proteins may not function as unique antiviral factors.

The Distribution of Some Genetic Determinants in the Two Nucleoprotein Particles of Cherry Leaf Roll Virus

SUMMARY Purified preparations of the two sedimenting nucleoprotein components (M and B) of tomato ringspot virus (TomRSV) and of strains of cherry leaf roll virus (CLRV) from elderberry (G) and from rhubarb (R) had little infectivity alone whereas mixtures of homologous components were very infective. However, whereas heterologous mixtures of the components of CLRV strains G and R were also very infective, heterologous mixtures of the components of CLRV-R and TomRSV were not. These results and serological evidence indicate that CLRV and TomRSV are not closely related to each other or to other nepoviruses with similar properties. Pseudo-recombinants produced by exchanging the nucleoprotein components of CLRV strains R and G were less stable than the parent isolates on storage in sap at 18 °C. Component M determined serological specificity whereas component B determined ability to infect Gomphrena globosa, and the lesion type and severity of systemic symptoms in Chenopodium and Nicotiana spp. Virulence also depended on the compatibility of M and B components and neither pseudo-recombinant was as virulent as the parent donating component B. Systemic infection and symptom production in Petunia hybrida required M and B components from strain R. In plant protection tests, the parent strains of CLRV protected tobacco plants against either parent and against the two pseudo-recombinants, whereas the pseudo-recombinants protected plants against either pseudo-recombinant but not against the parent strains. This suggests that determinants in both nucleoprotein components of either the protecting or challenging virus are involved.

Distribution of Determinants for Symptom Production, Host Range and Nematode Transmissibility between the two RNA Components of Raspberry Ringspot Virus

SUMMARY Raspberry ringspot virus has two RNA species, of mol. wt. about 2.4 × 106 (RNA-1) and 1.4 × 106 (RNA-2). In experiments with four naturally occurring strains, virus hybrids were made by mixing RNA-1 and RNA-2 preparations from different strains. Parent strains were regenerated by crossing appropriate hybrids. In the crosses, both serological specificity and transmissibility by the nematode Longidorus elongatus were determined by RNA-2, suggesting that the protein surface of the virus particles is involved in the transmission process. Ability of isolates to cause systemic yellowing in Petunia hybrida, previously found to be also controlled by RNA-2, was shown to be associated with distinctive ultrastructural changes in the chloroplasts. Severity of systemic symptoms in Chenopodium quinoa and other herbaceous hosts, ability to infect Lloyd George raspberry and ability to invade the non-inoculated leaves of Phaseolus vulgaris, were all determined by RNA-1. Both RNA species played a part in determining lesion type in inoculated leaves of Chenopodium amaranticolor and C. quinoa, and in some crosses the two kinds of hybrid were respectively less virulent and more virulent than either parent. The determinant for systemic symptoms in Petunia hybrida that is carried by RNA-2 was not expressed when in association with RNA-1 from the strain able to infect Lloyd George raspberry. Some genes of raspberry ringspot virus are probably pleiotropic.