As allogeneic blood transfusion plays a role in clinical treatment effects, it also produces a number of immune-related side effects, such as the increased rate of postoperative infection, the rising relapse rate of malignant resection and so on. All those factors, such as CD200 surface molecule of allogeneic mononuclear cells, interleukin, sHLA and sFasL which are detached from the leukocyte surface during the period of storage, and serum bioactive molecules related to a certain degree with the occurrence of transfusion-related immunomodulation (TRIM). The clinical controlled trials, laboratory researches and animal models demonstrated that cloning deletion, induction of anergy and immune suppression are the three major mechanisms of TRIM. In this article, the research advances on mechanism of TRIM and the mediators inducing TRIM are reviewed.
Animals ; Humans ; Immunomodulation ; Immunosuppression ; Platelet Transfusion ; adverse effects ; Transfusion Reaction

A complex pathophysiological mechanism is involved in brain injury following cerebral infarction. The neurovascular unit (NVU) is a complex multi-cellular structure consisting of neurons, endothelial cells, pericyte, astrocyte, microglia and extracellular matrix, etc. The dyshomeostasis of NVU directly participates in the regulation of inflammatory immune process. The components of NVU promote inflammatory overreaction and synergize with the overactivation of autonomic nervous system to initiate stroke-induced immunodepression (SIID). SIID can alleviate the damage caused by inflammation, however, it also makes stroke patients more susceptible to infection, leading to systemic damage. This article reviews the mechanism of SIID and the roles of NVU in SIID, to provide a perspective for reperfusion, prognosis and immunomodulatory therapy of cerebral infarction.
Humans ; Endothelial Cells ; Stroke ; Neurons/physiology* ; Immunosuppression Therapy/adverse effects* ; Cerebral Infarction

Adult ; Antiviral Agents ; therapeutic use ; Colonic Neoplasms ; diagnosis ; etiology ; therapy ; Cyclosporine ; adverse effects ; Esophageal Neoplasms ; diagnosis ; etiology ; therapy ; Female ; Ganciclovir ; therapeutic use ; Humans ; Immunosuppression ; adverse effects ; Immunosuppressive Agents ; adverse effects ; Liver Neoplasms ; diagnosis ; etiology ; therapy ; Liver Transplantation ; adverse effects ; Lymphoproliferative Disorders ; diagnosis ; etiology ; therapy ; Middle Aged ; Pharyngeal Neoplasms ; diagnosis ; etiology ; therapy ; Survival Analysis ; Tacrolimus ; adverse effects ; Time Factors

Fibrosing cholestatic hepatitis is an aggressive and usually fatal form of viral hepatitis in immunosuppressed patients. We report three cases of fibrosing cholestatic hepatitis in various clinical situations. Case 1 was a 50-year-old man who underwent a liver transplant for hepatitis B virus (HBV)-associated liver cirrhosis. Two and a half years after the transplant, he complained of fever and jaundice, and liver enzymes were slightly elevated. Serum HBsAg was positive. Case 2 was a 30-year-old man in an immunosuppressed state after chemotherapy for acute lymphoblastic leukemia. He was a HBV carrier. Liver enzymes and total bilirubin were markedly elevated. Case 3 was a 50-year-old man who underwent renal transplantation as a known HBV carrier. One year after the transplant, jaundice developed abruptly, but liver enzymes were not significantly elevated. Microscopically lobules were markedly disarrayed, showing ballooning degeneration of hepatocytes, prominent pericellular fibrosis, and marked canalicular or intracytoplasmic cholestasis. Portal inflammation was mild, but interphase activity was definite and cholangiolar proliferation was prominent. Hepatocytes were diffusely positive for HBsAg and HBcAg in various patterns. Patients died of liver failure within 1 to 3 months after liver biopsy in spite of anti-viral treatment.
Adult ; Case Report ; Cholestasis, Intrahepatic/virology ; Cholestasis, Intrahepatic/immunology ; Cholestasis, Intrahepatic/etiology* ; Fibrosis ; Hepatitis B/complications* ; Human ; Immunosuppression/adverse effects ; Liver Transplantation ; Male ; Middle Age

OBJECTIVETo analyze the clinical features of mid- and long-term acute cardiac allograft rejection to improve the long-term clinical outcomes of the patients.

METHODSFourteen recipients (11 males and 3 females) underwent orthotopic heart transplantation with standard immunosuppressive therapy protocols (3 cases) or induction therapy protocols (11 cases). Cyclosporine, azathioprine or mycophenolate mofetil, and prednisolone were applied as the maintenance immunosuppressive regimen. Acute graft rejection episodes occurred within 3 to 6 months in 1 case, within 6 months to 1 year in 3 cases, within 1 to 2 years in 3 cases, within 2 to 5 years in 6 cases, and above 5 years in 1 case.

RESULTSNo significant difference was found in the incidence of late heart rejection between the patients receiving the two immunosuppressive therapy protocols. Immunosuppressants were withdrawn or spared in 8 recipients due to different causes. Nine recipients with steroid-sensitive acute cardiac allograft rejection were treated with steroid-pulse therapy, while the other 5 were treated with a short course of polyclonal antithymocyte antibodies because of steroid-resistant acute rejection; in 11 cases, azathioprine was converted to mycophenolate mofetil. Four of the 5 late deaths occurred in the recipients with steroid-resistant rejection. The surviving recipients had a good quality of life, and no recurrent episodes of rejection or infection were observed in the follow-up period.

CONCLUSIONSLate acute cardiac allograft rejection is associated mainly with patient compliance but not with early immunosuppressive therapy protocols. The episodes are rather severe and should be timely treated with steroid pulses or polyclonal antithymocyte antibodies.

Adolescent ; Adult ; Cyclosporine ; Female ; Graft Rejection ; etiology ; prevention & control ; Heart Transplantation ; adverse effects ; Humans ; Immunosuppression ; methods ; Male ; Middle Aged ; Mycophenolic Acid ; analogs & derivatives ; Young Adult

BACKGROUND: Optimal tacrolimus (TAC) trough levels for different periods after kidney transplantation (KT) has not been definitely established. This study aimed to investigate transplant outcomes of low-level (LL) and standard-level (SL) TAC according to post-transplant period. METHODS: A total of 278 consecutive kidney transplant recipients (KTRs) receiving TAC-based immunosuppression were divided into LL and SL-TAC groups (4–7 and 7–12 ng/mL for 0–2 months, 3–6 and 6–10 ng/mL for 3–6 months, 2–5 and 5–8 ng/mL for 7–12 months, respectively) according to TAC trough level at each period. We compared estimated glomerular filtration rate (eGFR), biopsy-proven acute rejection (BPAR), de novo donor-specific antibody (dnDSA), calcineurin inhibitor (CNI) toxicity, opportunistic infection, and allograft survival. RESULTS: SL-TAC group showed significantly higher mean eGFR at 0–2 months than LL-TAC group (72.1 ± 20.3 vs. 64.2 ± 22.7 mL/min/1.73m2; P = 0.003). Incidence of BPAR at 7–12 months was significantly lower in SL-TAC group than in LL-TAC group (0.0% vs. 3.9%; P = 0.039). Patients with persistent SL-TAC lasting 12 months showed higher eGFR at 7–12 months than those with persistent LL-TAC (65.5 ± 13.0 vs. 57.9 ± 13.9 mL/min/1.73m2; P = 0.007). No significant differences in dnDSA, CNI toxicity, serious infections, or allograft survival were observed. CONCLUSIONS: Maintenance of proper TAC trough level after 6 months could reduce BPAR without adverse drug toxicities in KTRs. Moreover, persistent SL-TAC during the first year after KT might have a beneficial effect on a trend for a lower incidence of dnDSA and better renal allograft function.
Allografts ; Calcineurin ; Drug-Related Side Effects and Adverse Reactions ; Glomerular Filtration Rate ; Humans ; Immunosuppression ; Incidence ; Kidney Transplantation ; Kidney ; Opportunistic Infections ; Tacrolimus ; Transplant Recipients

A 51-yr-old female was referred to our outpatient clinic for the evaluation of generalized edema. She had been diagnosed with idiopathic thrombocytopenic purpura (ITP). She had taken no medicine. Except for the ITP, she had no history of systemic disease. She was diagnosed with systemic lupus erythematosus. Immunosuppressions consisting of high-dose steroid were started. When preparing the patient for discharge, a generalized myoclonic seizure occurred at the 47th day of admission. At that time, the laboratory and neurology studies showed hyperglycemic hyperosmolar syndrome. Brain MRI and EEG showed brain atrophy without other lesion. The seizure stopped after the blood sugar and serum osmolarity declined below the upper normal limit. The patient became asymptomatic and she was discharged 10 weeks after admission under maintenance therapy with prednisolone, insulin glargine and nateglinide. The patient remained asymptomatic under maintenance therapy with deflazacort and without insulin or medication for blood sugar control.
Edema ; Epilepsies, Myoclonic/complications/drug therapy ; Female ; Humans ; Hyperglycemia/*chemically induced ; Immunosuppression ; Insulin/therapeutic use ; Lupus Nephritis/*complications/drug therapy ; Middle Aged ; Prednisolone/administration & dosage/*adverse effects/therapeutic use ; Purpura, Thrombocytopenic, Idiopathic/complications/*drug therapy

Reactivation of polyoma virus (BK virus) is a significant cause of morbidity in kidney transplant patients. This seemingly insignificant viral infection that affects the majority of population at a young age, once reactivated by immunosuppression, is a major factor contributing to graft loss. Screening techniques have been developed for early prediction of BK virus reactivation. These include plasma and urine assays for detection of BK virus DNA by PCR, urine cytology for detection of "decoy cells" and electron microscopy. Combining urine cytology and serology screening can be more effective for early detection of BK virus reactivation. Immunohistochemistry can be utilized as an additional tool to support the diagnosis. Once screening tests reveal a suspicious BK virus reactivation, tissue biopsy should be performed to confirm the diagnosis, rule out acute cellular rejection and plan treatment approaches. Treatment normally includes decreasing immunosuppression and the use of antiviral drug therapy. Unfortunately, disease outcome is often unfavorable and can culminate with eventual graft loss. Renal retransplantation has been performed with mixed results. As new data emerges, we will gain a better understanding of the disease caused by BK virus and respond with improved early diagnosis and treatment to preserve graft function.
Antiviral Agents/therapeutic use ; *BK Virus ; Humans ; Immunosuppression/*adverse effects ; Kidney Diseases/pathology/*virology ; *Kidney Transplantation ; Polyomavirus Infections/*complications/drug therapy/etiology ; Tumor Virus Infections/*complications/drug therapy/etiology

No abstract available.
Animals ; Antigen-Presenting Cells/immunology ; Graft Rejection/immunology/*prevention & control ; Graft Survival ; *Histocompatibility ; Humans ; Immunosuppression/*methods ; Intercellular Adhesion Molecule-1/immunology ; Isoantigens/*immunology ; Organ Transplantation/*adverse effects ; *Transplantation Tolerance

Infection of the central nervous system with Nocardia sp. usually manifests as supratentorial abscesses. Supratentorial and cerebellar abscesses from infection with Nocardia sp. following immunosuppression with long-term corticosteroids for idiopathic thrombocytopenia (ITP) have not been reported. An 83 years-old, human immunodeficiency virus (HIV)-negative, polymorbid male with ITP for which he required corticosteroids since age 53 years developed tiredness, dyspnoea, hemoptysis, abdominal pain, and progressive gait disturbance. Imaging studies of the lung revealed an enhancing tumour in the right upper lobe with central and peripheral necrosis, multiple irregularly contoured hyperdensities over both lungs, and right-sided pleural effusions. Sputum culture grew Nocardia sp. Neurological diagnostic work-up revealed dysarthria, dysphagia, ptosis, hypoacusis, tremor, dysdiadochokinesia, proximal weakness of the lower limbs, diffuse wasting, and stocking-type sensory disturbances. The neurological deficits were attributed to an abscess in the upper cerebellar vermis, myopathy from corticosteroids, and polyneuropathy. Meropenem for 37 days and trimethoprime-sulfamethoxazole for 3 months resulted in a reduction of the pulmonary, but not the cerebral lesions. Therefore, sultamicillin was begun, but without success. Long-term therapy with corticosteroids for ITP may induce not only steroid myopathy but also immune-incompetence with the development of pulmonary and cerebral nocardiosis. Cerebral nocardiosis may not sufficiently respond to long-term antibiotic therapy why switching to alternative antibiotics or surgery may be necessary.
Adrenal Cortex Hormones/*adverse effects/*therapeutic use ; Aged, 80 and over ; Cerebellar Diseases/*chemically induced/*diagnosis/pathology ; Humans ; Immunosuppression ; Male ; Muscular Diseases/*chemically induced/pathology ; Nocardia Infections/*diagnosis ; Purpura, Thrombocytopenic, Idiopathic/*drug therapy