-
Clinical Transplantation Aug 2021COVID-19 epidemiologic studies comparing immunosuppressed and immunocompetent patients may provide insight into the impact of immunosuppressants on outcomes.
Comparative incidence and outcomes of COVID-19 in kidney or kidney-pancreas transplant recipients versus kidney or kidney-pancreas waitlisted patients: A single-center study.
BACKGROUND
COVID-19 epidemiologic studies comparing immunosuppressed and immunocompetent patients may provide insight into the impact of immunosuppressants on outcomes.
METHODS
In this retrospective cohort study, we assembled kidney or kidney-pancreas transplant recipients who underwent transplant from January 1, 2010, to June 30, 2020, and kidney or kidney-pancreas waitlisted patients who were ever on the waitlist from January 1, 2019, to June 30, 2020. We identified laboratory-confirmed COVID-19 until January 31, 2021, and tracked its outcomes by leveraging informatics infrastructure developed for an outcomes research network.
RESULTS
COVID-19 was identified in 62 of 887 kidney or kidney-pancreas transplant recipients and 20 of 434 kidney or kidney-pancreas waitlisted patients (7.0% vs. 4.6%, p = .092). Of these patients with COVID-19, hospitalization occurred in 48 of 62 transplant recipients and 8 of 20 waitlisted patients (77% vs. 40%, p = .002); intensive care unit admission occurred in 18 of 62 transplant recipients and 2 of 20 waitlisted patients (29% vs. 10%, p = .085); and 7 transplant recipients were mechanically ventilated and died, whereas no waitlisted patients were mechanically ventilated or died (11% vs. 0%, p = .116).
CONCLUSIONS
Our study provides single-center data and an informatics approach that can be used to inform the design of multicenter studies.
Topics: COVID-19; Humans; Incidence; Kidney; Kidney Transplantation; Pancreas; Retrospective Studies; SARS-CoV-2; Transplant Recipients
PubMed: 33998716
DOI: 10.1111/ctr.14362 -
Journal of Postgraduate Medicine 2023We describe a patient who presented with scrotal swelling followed by non-healing and discharging scrotal sinuses, following local trauma and was initially suspected to...
We describe a patient who presented with scrotal swelling followed by non-healing and discharging scrotal sinuses, following local trauma and was initially suspected to have an infected scrotal hematoma. An evaluation revealed it to be scrotal tuberculosis. He also complained of upper abdominal pain and on transabdominal ultrasonography was detected to have a mass in the head of the pancreas. Evaluation of the pancreatic mass revealed it to be pancreatic tuberculosis. Both lesions responded well to anti-tubercular therapy. This is an unusual case of two rare sites of extrapulmonary tuberculosis presenting simultaneously in the same individual. Care needs to be exercised while evaluating any non-healing ulcers or sinuses and mass lesions in countries endemic for tuberculosis as this disease can be a great masquerader.
Topics: Male; Humans; Tuberculosis; Pancreas; Genital Diseases, Male; Scrotum; Hematoma
PubMed: 36751759
DOI: 10.4103/jpgm.jpgm_558_22 -
Viruses Jan 2017Human enteroviruses (HEV), especially coxsackievirus serotype B (CVB) and echovirus (E), have been associated with diseases of both the exocrine and endocrine pancreas,...
Human enteroviruses (HEV), especially coxsackievirus serotype B (CVB) and echovirus (E), have been associated with diseases of both the exocrine and endocrine pancreas, but so far evidence on HEV infection in human pancreas has been reported only in islets and ductal cells. This study aimed to investigate the capability of echovirus strains to infect human exocrine and endocrine pancreatic cells. Infection of explanted human islets and exocrine cells with seven field strains of E6 caused cytopathic effect, virus titer increase and production of HEV protein VP1 in both cell types. Virus particles were found in islets and acinar cells infected with E6. No cytopathic effect or infectious progeny production was observed in exocrine cells exposed to the beta cell-tropic strains of E16 and E30. Endocrine cells responded to E6, E16 and E30 by upregulating the transcription of interferon-induced with helicase C domain 1 (IF1H1), 2'-5'-oligoadenylate synthetase 1 (OAS1), interferon-β (IFN-β), chemokine (C-X-C motif) ligand 10 (CXCL10) and chemokine (C-C motif) ligand 5 (CCL5). Echovirus 6, but not E16 or E30, led to increased transcription of these genes in exocrine cells. These data demonstrate for the first time that human exocrine cells represent a target for E6 infection and suggest that certain HEV serotypes can replicate in human pancreatic exocrine cells, while the pancreatic endocrine cells are permissive to a wider range of HEV.
Topics: Cytopathogenic Effect, Viral; Echovirus 6, Human; Gene Expression Profiling; Humans; Immunity, Innate; Immunologic Factors; Islets of Langerhans; Organ Culture Techniques; Pancreas, Exocrine; Viral Load; Viral Structural Proteins
PubMed: 28146100
DOI: 10.3390/v9020025 -
Diabetes Feb 2021Type 1 diabetes (T1D) is characterized by insulin deficiency resulting from the selective destruction of pancreatic β-cells by self-reactive T cells. Recent evidence... (Review)
Review
Type 1 diabetes (T1D) is characterized by insulin deficiency resulting from the selective destruction of pancreatic β-cells by self-reactive T cells. Recent evidence demonstrates that innate immune responses substantially contribute to the pathogenesis of T1D, as they represent a first line of response to danger/damage signals. Here we discuss evidence on how, in a relapsing-remitting pattern, pancreas remodeling, diet, microbiota, gut permeability, and viral/bacterial infections induce the accumulation of leukocytes of the innate arm of the immune system throughout the pancreas. The subsequent acquisition and presentation of endocrine and exocrine antigens to the adaptive arm of the immune system results in a chronic progression of pancreatic damage. This process provides for the generation of self-reactive T-cell responses; however, the relative weight that genetic and environmental factors have on the etiopathogenesis of T1D is endotype imprinted and patient specific. With this Perspectives in Diabetes, our goal is to encourage the scientific community to rethink mechanisms underlying T1D pathogenesis and to consider therapeutic approaches that focus on these processes in intervention trials within new-onset disease as well as in efforts seeking the disorder's prevention in individuals at high risk.
Topics: Animals; Diabetes Mellitus, Type 1; Humans; Immunity, Innate; Insulin-Secreting Cells; Pancreas; T-Lymphocytes
PubMed: 33472941
DOI: 10.2337/dbi20-0026 -
Annals of Medicine Oct 1997There is strong evidence that the aetiology of insulin-dependent diabetes mellitus (IDDM) is due to a complex interaction between genes and the environment and that the... (Review)
Review
There is strong evidence that the aetiology of insulin-dependent diabetes mellitus (IDDM) is due to a complex interaction between genes and the environment and that the pathogenesis is autoimmune. In early perinatal life the immune system is induceable and exposures in this period may initiate autoimmunity. Recent findings of time and space clustering of birth dates for later diabetic cases together with the early observation of a very high prevalence of diabetes in cases with rubella embryopathy suggest that foetal virus exposure may be important. Recent findings from Sweden and Finland suggest that enterovirus exposure during foetal life may initiate autoimmunity which may lead to diabetes. Other immune events, such as maternal-foetal blood group incompatibility and pre-eclampsia in the mother have also been associated with IDDM risk. Other more unspecific events in the perinatal period, such as a short gestational age, caesarean section and neonatal respiratory disease, are also indicated to increase the risk. In addition, food components such as nitrosamine components, cow's milk protein and gliadin have been proposed to initiate the slowly progressing autoimmune beta-cell destruction. Most of these epidemiological findings are supported by experimental studies in the nonobese diabetic mice but their exact mechanisms of action are still unclear. It is concluded that new evidence is accumulating indicating that perinatal exposures may be important for the initiation of beta-cell destruction. As such risk factors may be targets for primary prevention strategies further studies are urgently warranted.
Topics: Diabetes Mellitus, Type 1; Female; Humans; Infections; Islets of Langerhans; Maternal Exposure; Pregnancy; Prenatal Exposure Delayed Effects; Sweden; Viruses
PubMed: 9453289
DOI: 10.3109/07853899708999371 -
Scientific Reports Jul 2018Hypoglycaemia is an important complication of Plasmodium falciparum malaria infection, which can be lethal if not treated. A decrease in blood sugar (BS) level has been...
Hypoglycaemia is an important complication of Plasmodium falciparum malaria infection, which can be lethal if not treated. A decrease in blood sugar (BS) level has been correlated with disease severity, parasitaemia and the use of certain antimalarial drugs. This study explored the relationship between pancreatic pathology, including the expressions of insulin and glucagon in the islets of Langerhans, and the BS levels in P. falciparum malaria patients. Pancreatic tissues from malaria patients were divided into three groups, namely those with BS < 40 mg/dl, BS = 40-120 mg/dl, and BS > 120 mg/dl. In P. falciparum malaria, pancreatic tissues showed numerous parasitised red blood cells (PRBCs) in the capillaries, oedema, acinar necrosis and the presence of inflammatory cells. The islet size and the expression of insulin were significantly increased in P. falciparum malaria patients with hypoglycaemia. In addition, insulin expression was positively correlated with islet size and negatively correlated with BS levels. This pioneer study documents an increase in insulin expression and an increase in islet size in hypoglycaemic patients with P. falciparum malaria. This could contribute to the pathogenesis of hypoglycaemia and provides evidence for the potential need to effectively manage the hypoglycaemia seen in malaria infection.
Topics: Blood Glucose; Case-Control Studies; Glucagon; Humans; Hypoglycemia; Insulin; Islets of Langerhans; Malaria, Falciparum; Pancreas
PubMed: 29993021
DOI: 10.1038/s41598-018-28797-w -
World Journal of Gastroenterology Oct 2016The diagnostic approach to a possible pancreatic mass lesion relies first upon various non-invasive imaging modalities, including computed tomography, ultrasound, and... (Review)
Review
The diagnostic approach to a possible pancreatic mass lesion relies first upon various non-invasive imaging modalities, including computed tomography, ultrasound, and magnetic resonance imaging techniques. Once a suspect lesion has been identified, tissue acquisition for characterization of the lesion is often paramount in developing an individualized therapeutic approach. Given the high prevalence and mortality associated with pancreatic cancer, an ideal approach to diagnosing pancreatic mass lesions would be safe, highly sensitive, and reproducible across various practice settings. Tools, in addition to radiologic imaging, currently employed in the initial evaluation of a patient with a pancreatic mass lesion include serum tumor markers, endoscopic retrograde cholangiopancreatography, and endoscopic ultrasound-guided fine needle aspiration (EUS-FNA). EUS-FNA has grown to become the gold standard in tissue diagnosis of pancreatic lesions.
Topics: Endoscopic Ultrasound-Guided Fine Needle Aspiration; Endoscopy; Endosonography; Evidence-Based Medicine; Hemorrhage; Humans; Infections; Neoplasm Staging; Pancreas; Pancreatic Neoplasms; Pancreatitis; Prevalence; Randomized Controlled Trials as Topic; Reproducibility of Results; Sensitivity and Specificity; Ultrasonography
PubMed: 27818584
DOI: 10.3748/wjg.v22.i39.8658 -
Journal of Virology May 1984Rous-associated virus 7 (RAV-7) is a subgroup C avian leukosis virus which does not transform cells in vitro or carry an oncogene. When injected into 1-day-old hatched...
Rous-associated virus 7 (RAV-7) is a subgroup C avian leukosis virus which does not transform cells in vitro or carry an oncogene. When injected into 1-day-old hatched chicks, RAV-7 causes a low incidence of lymphoid leukosis after a latent period of several months. In contrast, infection of 10-day-old chicken embryos with RAV-7 leads to a disease syndrome characterized by stunting, obesity, atrophy of the bursa and the thymus, high triglyceride and cholesterol levels, reduced thyroxine levels, and increased insulin levels (Carter et al., Infect. Immun. 39:410-422, 1983; J.K. Carter and R.E. Smith, Infect. Immun. 40:795-805, 1983). Histopathological examination of tissues from affected chicks revealed an accumulation of lipid in the liver and an extensive infiltration of the thyroid and pancreas by lymphoblastoid cells. In the present investigation, the subgroup specificity of this syndrome was investigated. Other subgroup C avian leukosis viruses (transformation-defective B77, transformation-defective Prague C strain of Rous sarcoma virus, and RAV-49) caused stunting, infiltration of the thyroid and pancreas, increased liver weights, decreased thyroxine levels, and increased insulin levels, but they did not cause a uniform, profound increase in triglyceride and cholesterol levels. Avian leukosis viruses of subgroup A [myeloblastosis-associated virus 1 causing osteopetrosis [MAV-1(O)] and RAV-1], subgroup B [MAV-2(O), MAV-2 causing nephroblastoma [MAV-2(N)], and RAV-2], subgroup D (RAV-50), and subgroup F (ring-necked pheasant virus and RAV-61) did not cause a syndrome identical to that induced by RAV-7. All of the viruses examined induced some stunting and a reduction in thyroxine levels which correlated with the stunting. The two subgroup F viruses caused an infiltration of the thyroid which may have been secondary to severe lung involvement. We conclude that the RAV-7 syndrome is unique, particularly in the induction of a hyperlipidemia.
Topics: Animals; Avian Leukosis Virus; Body Weight; Chick Embryo; Chickens; Hyperlipidemias; Insulin; Liver; Organ Size; Pancreas; Species Specificity; Thyroid Gland; Thyroxine
PubMed: 6323732
DOI: 10.1128/JVI.50.2.301-308.1984 -
The American Journal of Pathology Mar 2013Chagas disease, caused by Trypanosoma cruzi, is an important cause of morbidity and mortality primarily resulting from cardiac dysfunction, although T. cruzi infection...
Chagas disease, caused by Trypanosoma cruzi, is an important cause of morbidity and mortality primarily resulting from cardiac dysfunction, although T. cruzi infection results in inflammation and cell destruction in many organs. We found that T. cruzi (Brazil strain) infection of mice results in pancreatic inflammation and parasitism within pancreatic β-cells with apparent sparing of α cells and leads to the disruption of pancreatic islet architecture, β-cell dysfunction, and surprisingly, hypoglycemia. Blood glucose and insulin levels were reduced in infected mice during acute infection and insulin levels remained low into the chronic phase. In response to the hypoglycemia, glucagon levels 30 days postinfection were elevated, indicating normal α-cell function. Administration of L-arginine and a β-adrenergic receptor agonist (CL316, 243, respectively) resulted in a diminished insulin response during the acute and chronic phases. Insulin granules were docked, but the lack of insulin secretion suggested an inability of granules to fuse at the plasma membrane of pancreatic β-cells. In the liver, there was a concomitant reduced expression of glucose-6-phosphatase mRNA and glucose production from pyruvate (pyruvate tolerance test), demonstrating defective hepatic gluconeogenesis as a cause for the T. cruzi-induced hypoglycemia, despite reduced insulin, but elevated glucagon levels. The data establishes a complex, multi-tissue relationship between T. cruzi infection, Chagas disease, and host glucose homeostasis.
Topics: Adipose Tissue, White; Animals; Blood Glucose; Chagas Disease; Disease Models, Animal; Fluorescent Antibody Technique; Glucagon; Gluconeogenesis; Glucose; Homeostasis; Insulin; Liver; Male; Mice; Pancreas; Trypanosoma cruzi
PubMed: 23321322
DOI: 10.1016/j.ajpath.2012.11.027 -
PloS One 2017With increasing interest in the use of triploid salmon in commercial aquaculture, gaining an understanding of how economically important pathogens affect triploid stocks...
With increasing interest in the use of triploid salmon in commercial aquaculture, gaining an understanding of how economically important pathogens affect triploid stocks is important. To compare the susceptibility of diploid and triploid Atlantic salmon (Salmo salar L.) to viral pathogens, fry were experimentally infected with Salmonid alphavirus sub-type 1 (SAV1), the aetiological agent of pancreas disease (PD) affecting Atlantic salmon aquaculture in Europe. Three groups of fry were exposed to the virus via different routes of infection: intraperitoneal injection (IP), bath immersion, or cohabitation (co-hab) and untreated fry were used as a control group. Mortalities commenced in the co-hab challenged diploid and triploid fish from 11 days post infection (dpi), and the experiment was terminated at 17 dpi. Both diploid and triploid IP challenged groups had similar levels of cumulative mortality at the end of the experimental period (41.1% and 38.9% respectively), and these were significantly higher (p < 0.01) than for the other challenge routes. A TaqMan-based quantitative PCR was used to assess SAV load in the heart, a main target organ of the virus, and also liver, which does not normally display any pathological changes during clinical infections, but exhibited severe degenerative lesions in the present study. The median viral RNA copy number was higher in diploid fish compared to triploid fish in both the heart and the liver of all three challenged groups. However, a significant statistical difference (p < 0.05) was only apparent in the liver of the co-hab groups. Diploid fry also displayed significantly higher levels of pancreatic and myocardial degeneration than triploids. This study showed that both diploid and triploid fry are susceptible to experimental SAV1 infection. The lower virus load seen in the triploids compared to the diploids may possibly be related to differences in cell metabolism between the two groups, however, further investigation is necessary to confirm this and also to assess the outcome of PD outbreaks in other developmental stages of the fish when maintained in commercial production systems.
Topics: Alphavirus; Alphavirus Infections; Animals; Aquaculture; Diploidy; Kidney; Liver; Muscle, Skeletal; Myocardium; Pancreas; RNA, Viral; Reverse Transcriptase Polymerase Chain Reaction; Salmo salar; Triploidy; Viral Load
PubMed: 28949966
DOI: 10.1371/journal.pone.0179192