Foods to avoid with Lupus

Natural Lupus Treatment System

Dr. Levin was not a victim of the autoimmune disease called lupus but of a heart issue which required surgery. While he was recovering through cardiac rehabilitation he got involved with a colleague who practiced allopathic and alternative medicine. After running his own clinic for more than 40 years before retirement he now began to see a different side of medicine one which would lead him to create the e-book Natural Lupus Treatment System. With these materials, users will learn why alternative treatment methods work better than conventional ones, how to treat all types of lupus, a simple vitamin regimen and nutrition method that will heal their body, and much more. Actually there is no cure yet discovered for lupus, however, you will find methods to control and manage its signs and symptoms. The aim of the treatments of lupus generally would be to let the patient experience more comfort and lesser pain. Read more here...

Proven Lupus Treatment By Dr Gary Levin Overview


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Mapping the Systemic Lupus Erythematosus Susceptibility Genes

Systemic lupus erythematosus (SLE) is a prototype systemic, autoimmune inflammatory disease that can involve virtually any organ or tissue type. The disease has a strong familial tendency but, like most human illness, has a complex pattern of inheritance that is consistent with multiple susceptibility genes as well as environmental risk factors. Association studies have been performed, especially for the major histocompatibility complex on chromosome 6 and for various complement components. Several large familial studies have begun to report results for genetic linkage. Linkage has been established for many genetic intervals. SLE is a complex clinical illness, and investigation of the genetics of the illness based on clinical manifestations revealed linkages not found without consideration of the phenotype of the disease. Key Words Autoantibodies autoantigens complement genetic association genetic linkage HLA systemic lupus erythematosus Systemic lupus erythematosus (SLE) is a complex...

TCR Chain Abnormalities in Human Systemic Lupus Erythematosus

A growing number of studies have revealed that the expression of many genes is abnormal in T lymphocytes of patients with systemic lupus erythematosus (SLE). Although aberrant expression of signaling molecules may arise intrinsically or in response to the environment, these abnormalities play a significant role in the pathogenesis of this autoimmune disease. Modern research on lymphocyte signaling abnormalities in SLE has been directed toward identifying defective expression of various signaling molecules, understanding the molecular basis of the deficiency, and dissecting the T-cell signaling abnormalities that result from abnormal gene expression. The developments suggest that interplay of abnormal transcriptional factor, aberrant messenger RNA processing editing, ubiquitination, proteolysis, oxidative stress, and changes in chromatin structure invariably contribute to the abnormal expression of numerous signaling molecules in SLE T cells. The contribution of each of these...

Systemic Lupus Erythematosus

Recently, Mellemkjaer et al. 15 published the largest study about the association between lupus and malignancy. They studied malignancy in 1585 SLE patients for 10,807 person-years of follow-up. They observed statistically significant risks of 5.2-fold to develop lymphoproliferative neoplasm and 1.3-fold for cancer of all sites. In 1966, Abu-Shakraet al. 14 studied 724 Table 2. Systemic lupus erythematosus Table 2. Systemic lupus erythematosus

Answers To Case 18 Acute Pericarditis Caused by Systemic Lupus Erythematosus

Summary A young woman presents with nonexertional pleuritic chest pain that is relieved with sitting forward. In addition, she has a pericardial friction rub and ECG changes consistent with acute pericarditis. She has no radiographic evidence of a large pericardial effusion and no clinical signs of cardiac tamponade. Regarding the etiology of her pericarditis, she has pancytopenia and an active urinary sediment, which could be caused by infection but may also represent a connective tissue disease such as systemic lupus erythematosus (SLE).

Mitochondrial Hyperpolarization and ATP Depletion Predispose Lupus T Cells to Necrosis

In response to treatment with exogenous H2O2, a precursor, or ROI, lupus T cells failed to undergo apoptosis, and cell death preferentially occurred via necrosis. As noted in ref. 24, H2O2 triggered a rapid increase of AWm and ROI production, which was followed by apoptosis of PBLs in healthy subjects. By contrast, H2O2 failed to elevate AWm, ROI production, and apoptosis, but rather elicited necrosis in patients with lupus. Both CD3 CD28-induced H2O2 production and H2O2-induced apoptosis require mitochondrial ROI production. Therefore, diminished CD3 CD28-induced H2O2 production and H2O2-induced apoptosis together with deficient elevation of AWm and ROI levels reveal deviations of key biochemical checkpoints in mitochondria of patients with SLE.

TCell Signaling Abnormalities in Human Systemic Lupus Erythematosus

Abnormal expression of key signaling molecules and defective functions of T lymphocytes play a significant role in the pathogenesis of systemic lupus erythematosus (SLE). T-cell receptor (TCR) CD3-mediated stimulation of SLE T cells shows increased protein tyrosine phos-phorylation of cellular proteins, with faster kinetics, heightened calcium response, and decreased interleukin (IL)-2 production. The molecular mechanism of T-cell signaling abnormalities in SLE T cells is complex and cannot be explained fully by the current theories of T-cell signaling. Current research on lymphocyte signaling abnormalities in SLE has been directed toward investigating various factors that contribute to abnormal tyrosine phosphorylation, intracellular calcium response, and cytokine production. Latest developments suggest multiple components, including altered receptor structure, supramolecular assembly, modulation of membrane clustering, aberrant cellular distribution, and precompartmentalization with...

Conclusions The Selection of Murine Lupus Models

The diverse array of inbred and genetically altered mice provides many models for systemic lupus erythematosus, each with particular clinical manifestations and unique pathogenesis (Tables 1-4). Investigators should therefore choose models based on areas or phenomena of interest within the lupus autoimmune spectrum For instance, studies focusing on anti-dsDNA antibody responses, T-cell autoreactivity, or hemolytic anemia may find the best supporting literature and precedence in the NZ systems. In contrast, studies of diversification and diversity of autoantibody repertoires and multisystem autoimmune disease may prefer MRL models. Congenic autoimmune-prone CD95-mutant animals, like MRL Mp-lpr lpr, may provide particularly rapid assay systems, but investigators should beware of possible confounding from the concomitant, severe lymphadenopathic process. Finally, studies with interests Targeted Genes With Lupus-Like Phenotypes in some specific genes might benefit from the lupuslike...

Diagnosis of Murine Lupus

At present, there is no consensus as to the diagnosis of lupus in murine models, but in general, most studies judge experimental interventions based on the presence of antinuclear antibodies, including anti-dsDNA, and immune-deposit-related glomerulonephritis. Thus, minimal analysis includes assessment of the fluorescent antinuclear antibody test and anti-dsDNA antibodies and histo-pathological analysis of kidneys, often including immunofluorescence for IgG. The assessment of other organs, such as salivary glands or joints, has not been broadly studied or codified. In some investigations, serial analysis has been performed for antinuclear antibodies and or specific autoantibodies (Subheading 3.2.), serum creatinine and urea nitrogen, urine proteinuria (Subheading 3.3.), and even kidney biopsies (249) unfortunately, such use remains nonstandardized, and the predictive value of any of these tests is incompletely known (250). Consequently, most experiments are performed as...

CyA in Systemic Lupus Erythematosus

Some evidence suggest that patient with systemic lupus erythematosus (SLE) have a higher incidence of malignancy, especially hematopoietic 63-65 , breast, lung, and gynecological cancers 66,67 even if not all reports agree with this observation 68, 69 . None of the available lupus cohort studies have demonstrated a clear correlation between immunosuppression and higher cancer risk, but there is a reasonable concern of a possible increased risk with the additional exposure to immunosuppressive drugs. As a matter of fact, a high incidence of cervical atypia in women with SLE treated with cytotoxic drugs has been reported 70 ,

Lupus Prone Mice With Defined Mutations

(Canale-Smith syndrome 239-241), CD95 ligand (242), and caspase-10 (243). These syndromes share in common the development of severe lymphadenopa-thy because of CD3+CD4CD8- T cells and the high incidence of often lupuslike autoimmune disease. CD95 defects alone generally do not convey autoimmunity per se, but rather accelerate and amplify any underlying autoimmune diathesis For example, C57BL 6-lpr animals develop mild inflammatory disease consisting of lymphadenopathy, anti-single-stranded DNA (anti-ssDNA) antibodies, and mild, if any, glomerular disease MRL Mp-lpr animals develop widespread inflammation, including lymphadenopathy, autoantibodies of multiple specificities including anti-dsDNA, antiribonucleoprotein, anticardiolipin, and antiribosomal P, immune complex glomerulonephritis, as well as sialadenitis and hepatitis (see Subheading 1.2. 155-157). Thus, these mutations have often been used in murine lupus to accelerate the in vivo assay. Several other mutant animal models have...

Prevalence Of Cancer In

Mortality studies have also found cancer to be an important primary cause of death among patients with SLE. In a recent mortality studies of 665 SLE patients followed-up at a North American lupus clinic, malignant tumors were found in 12 (9.7 ) out of 124 deceased SLE patients. In 6.5 of the total deaths, metastatic cancer was found to be the primary cause 14 .

Other Tests of Tubular Function

Wegener's, vasculitis, rapidly progressive glomerulonephritis Pauci-immune rapidly progressive glomerulonephritis Goodpasture syndrome, renal allograft in Alport syndrome Postinfectious glomerulonephritis Membranoproliferative glomerulonephritis types 1 and 2 Membranoproliferative glomerulonephritis type2 > type 1 Systemic lupus erythematosus Systemic lupus erythematosus Drug-induced systemic lupus erythematosus Scleroderma, CREST syndrome Primary and secondary cryoglobulinemia Monoclonal gammopathies

Specific Cancers And

The development of neoplasia in patients with SLE was not related to specific clinical features or a certain subtype of SLE. Lymphoproliferative tumors were identified in patients with mild and severe forms of SLE, in patients with discoid lupus and in patients with subacute cutaneous lupus (SCLE) 12, 13, 15, 16, 20 .

Causes Of Cancers In

UVB is the strongest risk factor for basal cell and SCC of the skin. Patients with SLE were found to develop SCC of the skin into chronic disceid lesions, suggesting that UVB is a common etiologic agent for discoid lupus and skin cancer in the same patient 51, 52 , Thirty percent of sera of patients with SLE were found to react with retroviral gag protein p24 67 . Similarly, 24 of sera of patients with SLE were found to bind type C retroviral particles 67 . Ito et al. 68 reported that a patient with lupus nephritis developed adult T-cell leukemia associated with human T-cell leukemia virus (HTLV) type 1.

Genetichereditary susceptibility

Inherited renal disease is an infrequent cause of ESRD, cystic kidney disease being the most prevalent accounting for about 3 of all cases 61 . However, experimentally inbred strains of rats are selected because of their known susceptibility to toxic injury, an example of which is the Fischer 344 rat 63 . This selective animal susceptibility has led to speculation that a similar situation might exist for humans. A possible relationship between occupational exposure and genetic susceptibility comes from a study conducted by the Michigan Renal Registry 64 . The study design was a case-control involving 325 men with ESRD in which an occupational exposure was sought. The results found that the strongest association for ESRD patients was a family history of renal disease (odds ratio 9.30). Patients with ESRD that were excluded from consideration included diabetic nephropathy, polycystic kidney disease, heroin nephropathy, lupus nephropathy, nephropathy due to malignancy, Alport's syndrome,...

Annexins And The Antiphospholipid Syndrome

The anti-phospholipid syndrome refers to a range of autoimmune conditions which are characterised by venous or arterial thrombosis, recurrent strokes, pulmonary embolism, recurrent pregnancy loss or obstetric complications and the presence of circulating antibodies with specificity to a range of phospholipids including phosphatidylserine and cardiolipin. The syndrome is the leading cause of vascular thrombosis in children. It sometimes accompanies other autoimmune conditions such as systemic lupus erythematosus (SLE).

Antiphospholipid Antibodies

Antiphospholipid antibodies are a heterogenous family of acquired circulating IgG antibodies that react with various anionic phospholipids including cardiolipin, phosphatide acid, and phosphatidylcholine. They have the common property of inhibition phos-pholipid-dependent coagulation reactions in vitro and are often detected as a prolonged PTT. Clinically, their presence is highly associated with a thrombotic diathesis. Some clinicians consider them a risk factor for recurrent clotting of hemodialysis vascular accesses. The lupus anticoagulant testing is most specific for these antibodies. It is important to recognize that IgG and or IgM anti-cardiolipin antibody titers do not necessarily parallel the anticoagulant activity in vitro. Of related interest, a primary antiphospholipid syndrome characterized by otherwise unexplained thrombosis in large arteries and veins has been associated with the presence of these antibodies.

Inflammatory Vascular Diseases

Systemic lupus erythematosus (SLE) affects individuals from adolescence to old age. The small cerebral arteries undergo fibrinoid necrosis, mononuclear infiltration, hyalinization, and fibrosis. The lumen is often occluded by a thromboembolus. Characteristic visceral manifestations are verrucous endocarditis, glomerulo-nephritis, and interstitial pneumonia. Patients may harbor lupus anticoagulant antibodies and present the antiphospholipid antibody syndrome.

The Prevalence of Neoplasia is Increased in PM and Especially DM

Additional established associations also seem, with rare exceptions, reassuring in terms of cancer risk. These include childhood DM, myositis associated with a defined connective tissue disease such as systemic lupus erythematosus or scleroderma, and myositis occurring as a feature of mixed connective tissue disease 1, 14, 17, 18, 37 10 , Similarly, the presence of antisynthetase ab, which characterizes a subset of myositis frequently featuring with interstitial lung involvement, carries a very low risk of cancer both in literature 10 and in our experience. Unsurprisingly, the same is true for the presence of interstitial pneumonitis. In a series of 63 DM patients, none of the 8 with interstitial pneumonitis had cancer, compared with 18 out of the 55 patients without 41 . Nevertheless, the theoretical risk of pulmonary neoplasia occurring as a long-term complication of pulmonary fibrosis must be kept in mind for patients with connective tissue diseases 17 .

Genetic Influences on Pharmacokinetics

Another example in which drug-metabolism genotype is important is with the enzyme N-acetyl transferase and the drugs procainamide and hydralazine. The relationship between the genetics and pharmacokinetics of these drugs was among the earliest pharmacogenomic examples. Both of these drugs cause a lupus-like syndrome, and it was recognized decades ago that those who developed this lupus-like syndrome were much more likely to have decreased acetylation as compared with those who did not experience this toxicity (4,15,16). Thus, slow acetylators, a genetically-determined phenotype, are at increased risk of drug-induced lupus. In the case of procainamide, fast acetylators may also experience genotype-related adverse events. Specifically, procainamide is metabolized to N-acetylprocainamide (NAPA), an active metabolite that also possesses antiarrhythmic activity. Fast acetylators accumulate much higher concentrations of NAPA, and as a result are at somewhat increased risk of NAPA-induced QT...

Types And Aspects Of Renal Failure

Renal failure is classified as either acute or chronic. Acute renal failure occurs suddenly, often secondary to sudden acute illness or to therapy. Acute renal failure is characterized by loss of sodium in blood and increased fraction of sodium excretion in the urine (FENa), especially when compared to creatinine clearance. Loss of sodium is due primarily to decreased tubular function, which helps regulate sodium and other electrolyte levels as well as water balance. Glomerular filtration rate is usually less than 20 mL min. Chronic renal failure occurs over a longer period of time, with renal insufficiency progressing through several clear-cut stages. Chronic renal failure may also be secondary to an underlying illness. Chronic renal failure is often caused by chronic illness with complications that affect the kidney, such as the immunologic damage of systemic lupus erythematosus or the nonimmuno-logic damage of diabetic nephropathy or multiple myeloma.

Xenobioticinduced immune disregulation

Some drugs such as hydralazine or procainamide may induce lupus like diseases with antinuclear antibodies and proteinuria. D-penicillamine not only causes glomerulopathies, but also myasthenia, poly-myositis or lupus, suggesting that this compound provokes immune disregulation. Gold salts also are capable of inducing various immunopathological disorders such as pneumonitis, anemia, thrombocytopenia and hepatitis.

Hydralazine and procainamideinduced autoimmunity

Methylation of deoxycytosine residues of gene promoters takes place during cell ontogeny and silences genes through fixation of methylcytosin binding proteins and changes in chromatin structures (developed in 64 ) this pattern is maintained through subsequent mitoses by methyltransferases. It was shown that antigen specific T-cell clones, incubated with inhibitors of these enzymes, overexpressed LFA-1 and became able to proliferate in the presence of autologous antigen presenting cells, even in the absence of the nominal antigen. Autoreactivity is probably the consequence of the increase in LFA-1 expression since antigen specific T-cells transfected with LFA-1 also became autoreactive 63 . The injection of T-cells rendered autoreactive by incubation with procainamide 65 or with hydralazine 66 or of T-cells transfected with LFA-1 63 into a non-irradiated syngeneic normal recipient triggers an autoimmune disease 66 . This disease is marked by anti-DNA antibody production,...

Interpretation of the Renal Biopsy

The reproducibility of the pathologist's interpretation has been assessed during evaluation of standardized classification schemes such as the NIH modified semiquantitative histologic scoring system for lupus nephritis and the Banff classification system for interpretation of renal transplant biopsies. In one study 5 pathologists each assessed multiple samples in a blinded fashion findings were only moderately reproducible. It seems that the more detailed the classification system, the greater the likelihood of inter-and intra-pathologist differences in interpretation.

Calreticulin in Neoplasia

Calreticulin has been implicated in the pathogenesis of some autoimmune disease conditions. In systemic lupus erythematosus (SLE), calreticulin might support the formation of the Ro SS-A autoantigen complex (reviewed by Eggleton et al. 1997), and this could be related to its response to heat shock and stress factors.

Detection Of A Malignant Disease

From all the reports on p53 autoantibodies it seems to come up that p53 autoantibodies are in general associated with a malignant disease, whereas, healthy blood donors are rarely positive for p53 autoantibodies. Two individuals were found to express p53 autoantibodies although no tumor was detected. Both individuals were heavy smokers and diagnosed for chronic cough or a benign obstructive tracheal tumor. Both developed lung cancer within 5 or 15 months, respectively 27 . In a study of patients with prostate carcinoma, a healthy control patient was also positive for p53 autoantibodies 28 , Later, it turned out that this patient died from an undetected lung cancer. Thus, these studies might indicate that p53 autoantibodies may be early markers for malignancy and that this type of analysis allows for the detection of an unknown cancerous malignancies. However, there are also reports that p53 autoantibodies were found in patients with nontumorous diseases such as autoimmune diseases....

Autoimmune Disease Process

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease of unknown etiology. SLE is characterized by the involvement of multiple organ systems and the production of autoantibodies directed against nuclear components, including ssDNA, ds-DNA and histones 1-2 , The hallmark of autoimmunity is the activation and proliferation of lymphocytes directed against self-antigen. Abnormalities in lymphoid cell function include (i) changes in the ratio of T-cell subset population (ii) increased T-helper and decreased T-suppressor functions (iii) restricted usage of T-cell receptor genes (iv) defect in programmed T-cell death mechanisms, (v) increased population of active T cells (vi) increased expansion of B cells leading to the production of autoantibodies and (vii) abnormalities in the signal transduction pathway in lymphocytes. Defect in the signal transduction cascade mechanisms in lymphocytes from SLE patients have been shown to result in the aberrant expression of many genes and...

AntiCD137 mAbs Disrupt Hematopoiesis in Mice

We have found that repeated anti-CD137 treated lupus prone NZB W F1 mice develop multi-focal hepatitis. Cessation of anti-CD137 treatment led to the resolution of hepatitis. To determine whether development of hepatitis was or was not related to the susceptibility of NZB W F1 mice to autoimmune disease, we repeatedly injected normal naive mice with therapeutic doses of anti-CD137. Like NZB W F1 mice, we found that normal mice also developed hepatitis. Further

Less Enzyme Or Defective Protein

Isoniazid-induced neurotoxicity Drug-induced lupus erythematosus Phenytoin-isoniazid interaction Isoniazid-induced hepatitis Arylamine-induced bladder cancer Increased susceptibility to drug-induced hemolysis Glucose-6-phosphate dehydrogenase deficiency Other defects in glutathione formation or use Hemoglobinopathies Hereditary methemoglobinemia Hypoxanthine-guanine phosphoribosymtransferase-

Preisers disease scaphoid ischemic necrosis

Although Preiser 100 has been criticized for including patients who have a history of trauma in his original 1910 publication 101 , scaphoid is-chemic necrosis without trauma is still commonly referred to as Preiser's disease. Although atrau-matic ischemic necrosis of the scaphoid has been associated with systemic lupus erythematosus, systemic sclerosis, steroid ingestion, and cytotoxic chemotherapy 102-105 , several cases have been reported in which no apparent cause could be identified 106-109 .

An Environmental Factor Can Preferentially Costimulate Autoimmune Response and Disease in Neonatal Mice

Pinworm infection also influences the neonatal response to a peptide of the lupus Ag, Ro60 (Fig. 2). Neonatal but not adult mice, infected with rodent pin-worm, produced a strong and diversified autoAb response when injected with the human Ro60 (316-335) peptide. Although adult SJL mice immunized with the Ro60 peptide (316-335) in CFA produced Abs indicative of intramolecular and intermolecular spreading (Deshmukh et al. 1999), this was not observed in adult BALB c mice (Fig. 2D). However, as shown in Fig. 2A-C, a single injection of the Ro60 (316-335) peptide in water, in pinworm-infected neonatal BALB c mice, induced Ab against both human and murine Ro60. In addi- Fig. 2A-D The influence of pinworm infection on the murine antibody response to the human lupus autoantigen Ro60. Mice with pinworm infection were injected with human Ro60 peptide 316-335 (or peptide 19, arrows) in water. The human and murine Ro60 peptides 316-335 differ from each other by three amino acid residues. The...

Monoclonal Gammopathies

This monoclonal immunoglobulin may not only be directed against proteins of the coagulation pathway (usually factor VIII) but may also be an antibody against the phospholipid of tissue thromboplastin, resulting in a 'lupus-like' anticoagulant Antiphospholipid Syndrome. The first such case was described by Thiagarajan 91 in 1980. This was an IgM which reacted specifically with phos-phatidylserine and phosphatidylinositol and prolonged the PTT and RVVT in vitro. Lupus anticoagulants are generally polyclonal immunoglobulins. Bellotti et al. 101 in their study of three patients with monoclonal gammopathies and lupus-like anticoagulants included one each with MGUS, myeloma and lymphoma. Only the patient with lymphoma had any APS related complaints, viz., recurrent TIA.

Neonatal Immunization Induces Autoimmune Disease Besides Autoimmune Ovarian Disease

AIG develops in neonatal rats that are injected with the gastric parietal cell H+K+ ATPase Ag in water (Claeys et al. 1997). Lupus autoAbs and nephritis develop in mice injected neonatally with a peptide that mimics double-stranded DNA in IFA (Singh et al. 1996). In double transgenic mice expressing influenza virus hemagglutinin and its cognate T cell receptor (TCR), a state of tolerance of the transgenic CD8+ T cells is preceded by transient neonatal autoimmune response (Morgan et al. 1999). In addition, tolerance to the allogeneic lymphocytes is preceded by an early and transient graft-versus-host response to the donor MHC class II alloAg (Schurmans et al. 1991), and by a transient lupus-like disease that becomes fatal in mice with bcl-2 overexpressing B cells (Lopez-Hoyos et al. 1996).

Autoimmune Diseases Associated With Thymoma

The various autoimmune diseases that occur in patients with thymoma include mainly myasthenia gravis (MG), pemphigus, systemic lupus erythematosus (SLE), pure red cell aplasia (PRCA), and other conditions that seldom appear concomitantly with this tumor. Thymoma is one of the neoplasms associated with pemphigus. Pemphigus vulgaris is more common in patients with nonthymic neoplasms, whereas in patients with thymoma, it is as common as pemphigus foliaceus 12 . However, Souteyrand et al. 13 have previously reviewed 20 cases of patients with thymoma and pemphigus, and in their report pemphigus erythematosus was the predominant type (55 of the cases). Interestingly, patients with nonthymic neoplasms usually have pemphigus before the detection of malignancy, whereas the majority of patients with thymoma have it before the development of pemphigus 14 . Since thymoma is associated with other autoimmune conditions as well, it is not surprising that many of pemphigus patients have additionally...

Pharmacological Targeting of Mitochondrial Dysfunction in SLE

Mitochondrial hyperpolarization predisposes for increased ROI production (38). Oxidative stress affects the activity of transcription factors activation protein (AP-1) and NF-kB (64,65) and, further downstream, may lead to the skewed expression of IL-2, TNF, and IL-10 (48). Increased spontaneous apoptosis of lymphocytes has been linked to increased IL-10 production, release of Fas ligand, and overexpression of Fas receptor in SLE (61). Because increased ROI levels confer sensitivity to H2O2-, NO-, TNF-, and Fas-induced cell death (14,15), elevated baseline AWm, ROI production, and intracellular pH may have key roles in altered activation and death of lupus T cells. Although mitochondrial hyperpolarization was not affected, IL-10 antibody or IL-12 normalized ROI production and intracellular alkalinization in lupus PBLs (37). Therefore, IL-10 antagonists may partially correct signaling dysfunction in lupus. A proapoptotic 1,4-benzodiazepine (Bz-423) has been found to promote...

Indications for Renal Biopsy

The renal biopsy may also be useful in evaluating proteinuric conditions in patients with systemic disease. The best example is lupus nephritis. In this setting, even though diagnosis is rarely the issue, the specific morphology of renal involvement guides the choice of therapy. A standardized set of criteria (World Health Organization classification of lupus nephritis) has been developed to assist the clinician in deciding on appropriate treatment regimens. Additionally, an NIH-modified semiquantitative histologic scoring system for lupus nephritis with scales grading the inflammatory activity and chronicity of biopsy lesions has been described and correlated with clinical outcomes.

Relationship Between Diagnosis And Prognosis

Non-Plaque-Induced Gingival l esions Non plaque-induced gingivitis can be seen in patients with a variety of bacterial, fungal, and viral infections.' Since the gingivitis in these patients is not usually attributed to plaque accumulation, prognosis is dependent on elimination of the source of the infectious agent. I Hematologic disorders such as lichen planus, pemphigoid, pemphigus vulgaris, erythema multiforme, and lupus erythematosus also can manifest in the oral cavity as atypical gingivitis (see Chapter 21). Prognosis tor these patients is linked to management of the associated der-matologic disorder. Finally, allergic, toxic, and foreign body reactions, as well as mechanical and thermal trauma can result in gingival lesions. Prognosis for these cases is dependent on elimination of the causative agent.

Pacing for Children and Adolescents Including Congenital Heart Block

Congenital complete AV block is a rare anomaly that results from abnormal embryonic development of the AV node and is not associated with structural heart disease in 50 of cases. Congenital complete heart block is also associated with maternal lupus erythematosus. Most of the children with isolated congenital complete AV block have a stable escape rhythm with a narrow complex. Pacing is generally indicated in children with complete heart block if the heart rate in the awake child is less than 50 beats per minute or if associated with left ventricular systolic dysfunction or ventricular arrhythmias. The indications for pacing in congenital complete AV block have been clarified by a prospective study demonstrating improved survival and reduced syncope, myocardial dysfunction, and mitral regurgitation even among asymptomatic patients.34,35 Exercise testing does not predict future cardiac events in this population.

Role Of Cas In Skin Diseases

CAs have been implicated in the pathogenesis of human autoimmune diseases (Nishimori and Onishi 2001). The description of a disease called autoimmune exocrinopathy (Strand and Talal 1980) and dry gland syndrome (Epstein et al. 1982) in the past and autoimmune epithelitis (Moutsopulos 1994) recently was supported by the concept of an autoimmune reaction against a common target antigen, such as CA II, expressed by the ductal epithelial cells of exocrine organs. Serum antibodies reactive to CA II have been reported in patients with several autoimmune diseases of multiple exocrine organs, including systemic lupus erythematous and Sj gren's syndrome (Inagaki et al. 1991 Itoh and Reichlin 1992). Autoantibodies to CA I, primarily expressed in red blood cells, have also been observed in the sera of patients with Sj gren's syndrome, and in these patients anti-CA II and anti-CA I antibodies were not cross-reactive (Kino-Ohsaki et al. 1996). One possible explanation is that serum antibodies...

Leukocyte Adhesion Deficiency

The primary role of C1 is to cleave C2 and C4 proteolytically to generate the classical pathway C3 convertase, C4b2a. Deficiencies in C1, C2, or C4 cause diminished C3 convertase production by the classical pathway. This is not usually a serious problem because the alternative pathway can generate an alternative pathway C3 convertase with the same function. Deficiencies of these early complement components often occur in patients with systemic lupus erythematosus (SLE), although the explanation for this association remains unclear.

Adverse reactions

The thionamide drugs are all liable to cause minor and major adverse effects. Minor are rash, urticaria, arthralgia, fever, anorexia, nausea, abnormalities of taste and smell. Major are agranulocytosis, thrombocytopenia, acute hepatic necrosis, cholestatic hepatitis, lupus-like syndrome, vasculitis.

Interferon And Autoimmunity

Given the possible effects of interferons on the immune system it is perhaps not surprising that autoimmune disorders have been reported as a consequence of interferon-a therapy. For example, autoimmune haemolytic anaemia, autoimmune thyroid disorders and thrombocytopenic purpura have all been described 18 . Interferon-a therapy is also associated with autoantibody production including antibodies to nuclear antigens 19 , thyroid antigens and epithelial cells. Ronnblom et al. 20 described a patient with a malignant carcinoid tumour who developed SLE during interferon-a therapy. Interestingly, this patient had a further course of interferon-a therapy which resulted in the recurrence of anti-DNA antibodies and clinical evidence of active lupus. This report stimulated the authors to prospectively study 135 patients with malignant carcinoid tumours treated with interferon-a and they found 25 patients who developed clinical evidence of autoimmune disorders 18 . This included 18 patients...

Combination Chemotherapy

Recently, our unit has observed 6 patients with haema-tological malignancy (5 had a lymphoma and 1 had acute myeloid leukaemia) who developed an autoimmune connective tissue disease following combination chemotherapy 24 , Three patients developed SLE and 1 each developed lupus profundus, limited cutaneous systemic sclerosis and Churg-Strauss syndrome. Only 1 of these patients received interferon-a and his SLE developed 5 years after this therapy. These connective tissue diseases manifested themselves between 1 and 63 months after the first chemotherapy course and all cases responded to modest doses of prednisolone and or hydroxychloroquine, though the patient with Churg-Strauss syndrome received prednisolone and azathioprine. Three of the 6 patients have subsequently died from recurrent malignancy.

Receiver operating characteristic ROC curve a

Control hyperglycemia in type 2 diabetes mellitus surfactant - a substance that reduces the surface tension of the moist surfaces of solid tissue sweat test - test for cystic fibrosis that involves measuring the subject's sweat for abnormally high sodium chloride content systematic error - error that occurs predictably once a pattern of recognition is established predictable errors of the same sign and magnitude systemic lupus erythematosus - chronic autoimmune inflammatory disease involving multiple organ systems tachometer - device that measures speed in revolutions per minute tachycardia - racing heart rate tagged - labeled with some component that allows

Synopsis Of The Novel

In part 2 it is mid-April, and Rabbit and Janice return to springtime Brewer. While Janice looks for a job, Rabbit reflects on his dismal past, visiting his ill lover, Thelma, whose disease, systemic lupus erythema-tosus, has depleted her family's income and spirit. Rabbit learns from her that Nelson is a cocaine addict, causing Rabbit additional worry about AIDS. He visits Springer Motors, discovering Nelson has taken down his old basketball star photos, has hired a woman, and that the homosexual AIDS-inflicted bookkeeper refuses to show him the books. Janice takes Penn State extension real estate courses, while Rabbit frets about Nelson. They talk about Nelson's drug addiction and bleeding the company then receive threatening calls from his unpaid drug dealers. They are guilt-ridden for raising Nelson to be so troubled. Rabbit asks his friend Charlie Stavros for advice, and they discuss Brewer's drug problem at large. Late one evening after the drugged-up Nelson attacks Pru, she...

Antinuclear Antibodies

Perhaps the most common use for ANA testing in clinical nephrology is detection of renal involvement due to systemic lupus erythematodes (SLE). Screening testing usually identifies a homogenous pattern at titers > 1 60. In general, absolute levels of ANA do not correlate well with clinical disease activity. The presence of anti-double-stranded DNA (anti-ds DNA) antibodies, which bind to epitopes in the double helical structure of DNA, are highly specific for SLE but are seen in only 60 of patients. The presence of anti Smith (Sm), anti ribonucleoprotein particles

Measurement of Cytokines in Autoimmune Disease

The immune system alterations that characterize systemic autoimmune diseases, with systemic lupus erythematosus (SLE) the prototype, extend to virtually all components of the innate and adaptive immune responses. A current paradigm suggests that a host microenvironment that favors maturation of antigen-presenting cells can promote activation of autoantigen-specific lymphocytes and result in chronic immune system activation and tissue damage (1-3). This scenario involves dendritic cells, T cells, and B cells, as well as the products of inflammatory cells of the innate immune system, including monocytes and neutrophils. The effector functions implemented by these immune system cells are induced and mediated by cytokines, along with autoantibodies and products of the complement system. SLE is characterized by production of autoantibodies, and abundant data indicate that those autoantibodies are both antigen driven and depend on T-cell help. The T-cell-derived signals that drive B-cell...

Musculoskeletal Symptoms

There were further reports of the syndrome occurring after chemotherapy for breast cancer but also following treatment for non-Hodgkin's lymphoma 6, 7 as well as ovarian cancer 8 . A more recent series by Warner et al. 9 describes 23 women with breast cancer who developed postchemotherapy rheumatism bringing the total number of patients in the literature to 46. They described one group of 8 patients in whom there were no preexisting rheumatic symptoms, and a further 15 who had rheumatic complaints prior to chemotherapy but in whom the symptoms markedly worsened or new features appeared. Four patients in the first group developed a polyarthritis and 3 had fibromyalgia after chemotherapy. The most notable patient in the second group was a woman who had autoimmune haemolytic anaemia prior to her breast cancer but who developed systemic lupus erythematosus 15 years after oophorectomy and chemotherapy. The main difference from Loprinzi et al.'s report was that...

P53 Autoantibodies and Cancer Speciiicity Diagnosis and Monitoring

The presence of p53AAb is generally indicative of malignancy. Nevertheless, rare exceptions become known. In autoimmune diseases (AID), p53AAb can be detected in patients with systemic lupus erythematosus (SLE) 57, 58 , Sjogren's syndrome and systemic sclerosis (scleroderma) 57 , Additionally, we found seropositive individuals among patients with Graves' disease, Wegener's granulomatosis, and other vasculitis 58 , The role of p53AAb in AID is yet unknown. Furthermore, is there an association between p53AAb generation and p53 protein accumulation in patients with AID Recently, extensive apoptosis was demonstrated in most of the epidermis of cutaneous lupus erythematosus lesional skin showed a marked increase in p53 protein-positive keratinocytes 59 . Skin samples from 44 patients with scleroderma, however, revealed no abnormal expression of p53 59 although Kovacs et al. 57 found a p53AAb-positive patient.

Epigenetic Basis Of Disease

As has been mentioned previously, DNA methylation plays an important role in stabilizing the genome particularly at the repeat sequences. In case of the Fragile X syndrome, an increase in the trinucleotide repeat length leads to silencing of the FMR1 gene locus. In contrast to this, decrease in repeat lengths of the D4Z4 repeat leads to hypomethylation at 4q3S locus leading to Facioscapulohumeral muscular dystrophy (FSHD). Systemic lupus erythmatosus (SLE) is caused by a loss of DNA methylation in T cells due to reduced activity of DNMT1 while


Gender Some disorders are more common in men, such as abdominal aortic aneurysms. In contrast, women more commonly have autoimmune problems, such as chronic idiopathic thrombocytopenic purpura or systemic lupus erythematosus. Also, the possibility of pregnancy must be considered in any woman of child-bearing age.


An additional mechanism of antibody mediated damage includes its penetration to the tissues to produce deleterious effects. This is suggested by the observation of IgG in epithelial cells of skin biopsy from lupus patients. Several cell populations (predominantly neurons) have been shown to engulf IgG by pinocytosis through in vitro studies.

Solid Tumors

Urinary bladder cancer and squamous cell carcinoma (SCC) were found to be associated with SLE. A strong association was suggested between bladder cancer and treatment with cyclophosphamide for SLE 48 , However, in 5- and 10-year follow-up studies, none of 38 patients with lupus nephritis who were treated with cyclophosphamide developed bladder cancer 49-50 ,


Women with medical conditions such as diabetes, asthma, thyroid disease, hypertension, lupus, thromboembolism, seizures should be referred to providers with experience in managing high risk pregnancies. Women with psychiatric disorders should be comanaged with a psychiatrist and counselor therapist so that the patient can benefit from pharmacologic and behavioral therapy. These patients may require more frequent visits. Patients who have drug, tobacco, or alcohol dependence should be educated about the risks and referred to rehab treatment centers to quit the drug prior to conception. Women should also be educated about proper nutrition and exercise during pregnancy. Preconception counseling may also address issues such as financial readiness, social support during pregnancy and the postpartum period, and issues of domestic violence.

Glomerular Nephritis

Glomerular nephritis may be caused by immunologic damage such as systemic lupus erythematosus, poststreptococcal damage, or hypersensitivities to drugs. The cause also may be nonimmunologic in origin, such glomerular nephritis that is produced by diabetic nephropathy. Chronic glomerular nephritis is a slower developing disease and may be idiopathic, and is characterized by gradual uremia and loss of functioning nephrons. systemic lupus erythematosus - chronic autoimmune inflammatory disease involving multiple organ systems

Nephrotic Syndrome

Diabetic nephropathy is one cause of nephrotic syndrome. The syndrome also may be caused by a primary defect of the kidney, or it may be secondary to diabetes, carcinomas, systemic lupus erythematosus, or drug therapies. The syndrome may result from autoimmune renal damage, such as from systemic lupus erythematosus or toxic reactions to bee stings or from chronic glomerular nephritis or nonim-munologic disorders, such as renal vein thrombosis, serious infections, and toxic reactions to drugs or carcinomas. Nephrotic syndrome is characterized as a renal condition compromising the integrity of basement glomerular membrane and tubular epithelium, often resulting in large porous openings.6


Abnormal T-cell effector functions in systemic lupus erythematosus (SLE) are present and may be associated with disease immunopathogenesis. Our work has led to the characterization of a signaling defect, involving protein kinase A (PKA), leading to abnormal T-cell effector functions in SLE. PKA is a component of the adenylyl cyclase cyclic adenosine monophos-phate PKA (AC cAMP PKA) pathway, a principal signal transduction system in T cells. The aim of this chapter is to provide a comprehensive, technical, step-by-step approach to studying PKA function in T cells. The methods detailed here are (a) chromatographic fractionation of PKA-I and PKA-II isozymes and PKA phosphotransferase activity in purified T cell populations, (b) Western immunoblotting to identify the presence of regulatory (R)-subunit proteins of PKA, and (c) isolation of RNA, and quantification of PKA R subunit-specific transcripts by competitive polymerase chain reaction. Although our emphasis in the chapter is T cells,...


Include degenerative neurological illnesses (e.g. Parkinson and Huntington diseases), stroke, metabolic conditions (e.g. vitamin B12 deficiency), endocrine conditions (e.g. hyper- and hypothyroidism, hyper- and hypoadrenocorticism), autoimmune conditions (e.g. systemic lupus erythematosus), viral or other infections (e.g. hepatitis, mononucleosis, human immunodeficiency virus), and certain cancers (e.g. carcinoma of the pancreas). The associated physical examination findings, laboratory findings, and pattern of prevalence or onset reflect the aetiolog-ical general medical condition, the management of which is more complex and the prognosis less favourable if major depressive disorder is present.


Ethosuximide (Zarontin) (t 2 55 h) differs from other antiepilepsy drugs in that it blocks a particular type of calcium channel that is active in absence seizures (petit mal), and it is used specifically for this condition. Adverse effects include gastric upset, CNS effects and allergic reactions including eosinophilia and other blood disorders, and lupus erythematosus.

Concluding Remarks

In this review we have highlighted the pluripotent effects of anti-CD137-mediated costimulation with emphasis on T-dependent B cell function in normal and autoimmune prone mice. We have shown that anti-CD137 treatment of normal mice during antigen priming, but not thereafter, suppresses the induction of T-dependent humoral immunity as well as CD8 T cell immunity. We suggest that the mechanism through which this occurs may involve CD137-mediated signaling in dendritic cells and other CD137-expressing APC. In studying lupus prone mice, contrary to our observations in normal mice, we find that we can suppress established T-dependent humoral autoimmune responses. On the other hand, as in normal mice, we fail to suppress established T-dependent humoral immunity to conventional antigens in NZB W F1 mice, and we speculate how this may occur. We have also included some of our unpublished studies on the regulatory function of B cells and their suppression of anti-tumor immunity. These data,...

Bone Marrow Toxicity

Thrombocytopenia is the commonest hematologic complication of IFN therapy, and a reduction in platelet count below 100,000 is seen in up to 15 of patients at 3 mU tiw. Thrombocytopenia is common in advanced liver disease, because of a blunted response to thrombopoetin, and this response may be aggravated by IFN (41,42). Severe thrombocytopenia, less than 50,000, is seen in less than 1 of patients, and is both dose-dependent and more common in patients with advanced fibrotic disease. The authors recommend halving the IFN dose at a platelet count of50,000, and cessation of therapy at 30,000 platelets. We have not seen significant bleeding from thrombocytopenia, but have seen a patient with systemic lupus erythematosus, who had an autoimmune thrombocytopenia induced by IFN, with the development of antiplatelet antibodies and significant gastrointestinal bleeding. In patients who are on combination therapy, there appears to be a beneficial effect of ribavirin on the platelet count. The...

Renal Biopsy

182 KashgarianM 1994 Lupus nephritis lessons from the path lab. Kidney Int 45 928-938 194 WernickRM, SmithDL, HoghtonDC, PhillipsDS, Booth JL,, Runckel DN 1993 Reliability of his-tologic scoring for lupus nephritis a community-based evaluation. Annals Intern Med 119 805-811

Tissue Factor

The presence of tissue factor in the circulation initiates the coagulation cascade. Tissue factor is also produced in circulating monocytes and is involved in the patho-biology of atherothrombosis and several inflammatory disorders, such as systemic lupus erythematosus (54,55).


Algorithm approach to the patient with acute glomerulonephritis. ANA antinuclear antibody ANCA antineutrophil cytoplasmic antibody ASO antistreptolysin-O c-ANCA cytoplasmic antineutrophil cytoplasmic antibody GBM glomerular basement membrane HSP Henoch-Schonlein purpura MPGN membranoproliferative glomerulonephritis PAN periarteritis nodosa p-ANCA perinuclear antineutrophil cytoplasmic antibody SLE systemic lupus erythematosus. C. Systemic lupus erythematosus

Disease Variants

Biclonal gammopathies The simultaneous presence of more than one type of M-protein can be seen in as many as 5 of patients with monoclonal gammopathies. This likely represents the proliferation of two separates clones of plasma cells, producing M-proteins of different immunoglobulin classes. Patients with three different types of M-proteins also have been reported. Most of these were associated with malignant lymphoproliferative disorders, though a few were of undetermined significance. Kyle et al. reported on 57 patients with biclonal gammopathy, of whom 37 had a biclonal gammopathy of undetermined significance.92 These patients had clinical features indistinguishable from those with monoclonal gammopathies. The remaining patients with a biclonal gammopathy had myeloma, macroglobulinemia, or another lymphoproliferative disorder. Nilsson et al. found 20 patients (2 ) from among 1034 patients with monoclonal gammopathy, who had two distinct monoclonal spikes 3 were associated with...


Improvement in the survival rate of female NZBAV F1 mice. It also caused a retardation of development of lupus nephritis and decreased the numbers of anti-DNA reproducing cells. The suppression of anti-DNA antibody synthesis was specific and Id-mediated. These results indicate that the use of a limited number of anti-Id antibodies in combination with a cytotoxic agent may be applicable therapeutically to autoimmune diseases. Saporin is one of the most widely used toxin compounds for immunotoxin preparation. We have recently demonstrated the suppression of experimental systemic lupus erythematosus (SLE) with specific anti-idiotypic antibody-saporin conjugate 12 . The anti-Id treatment was specifically shown to reduce anti-DNA antibodies by a specific hybridoma cell line 12 , The immunotoxin (saporin) had a significantly superior result compared with the anti-Id itself. Yet, although impressive, the effect of the saporin in reducing anti-DNA antibody production and abrogation of SLE...

Immunomodulation Of

In the same vein, strategies that might specifically block or inactivate helper T cells necessary for the sustained production of anti-DNA pathogenic antibodies may provide specific suppression of disease progression. As discussed earlier, Hahn and her colleagues have raised CD4+ T-cell clones specific for Id GN2. Their program includes innoculating low doses of anti-Id GN2 to NZB W F1 mice, harvesting T cells by draining lymph nodes, and obtaining T cells from the spleens of lupus mice with active nephritis. Stimulating these clones with rat concanavalin A supernatant, DNA antigen soluble Id GN2, or hybridoma B cells expressing Id GN2 on their surface, yields T-cell clones which significantly increase the production of Id GN2 IgG anti-DNA in a culture using B cells from the spleens of 16-week-old lupus mice.


Accuracy of genotyping and exclusion of Mendel errors are important for success, but so is the careful definition of affection status. This may not always be easy for diseases like asthma, schizophrenia or systematic lupus erythematosus (SLE). Even with diabetes, the definition is based upon artificial cut-offs of plasma glucose. Dichotomising variables may result in loss of power. One alternative is therefore to search for linkage to a qualitative trait, e.g. blood glucose, blood pressure or body mass index, instead of diabetes, hypertension and obesity. Heritability (h2) is often used as a measure of the genetic component of a quantitative trait. The higher the heritability, the more likely it is a genetic cause of a trait will be found. Several statistical programmes have been developed to support genome-wide scans of quantitative trait loci (QTL), such as the variance component models SOLAR and Merlin Linkage will only identify relatively large chromosomal regions (often > 20...

BXSB Animals

Like NZ animals, disease in BXSB consists predominantly of anti-DNA antibodies and glomerulonephritis antierythrocyte antibodies have been described, but are not well characterized. Unlike other lupus models, however, BXSB develops a male-predominant disease because of the Y-linked autoimmune accelerator (Yaa see refs. 158 and 159), inherited from the SB Le parental strain (160), which is solely responsible for conferring disease to susceptible strains (161,162). 1.3.3. Use in the Study of Lupus Pathogenesis Although less well studied than NZ or MRL mice, BXSB animals have also been used in studies of lupus genetics (163-166), and for studies of the T-cell-dependent development of pathogenic anti-DNA antibodies (105,167,168). The roles of some cell lineages, cytokines, and costimulatory molecules have been investigated (169-172), and some transgenic studies have implicated the impor tance of abnormalities of antigen presentation (45,173). Like other lupus models, BXSB animals are...


A careful history is the most effective way to determine the presence and significance of a bleeding disorder. Abnormal hemostasis may result from liver disease, uremia, malignancy, or systemic lupus erythematous. The history should include medications, including over-the-counter products (aspirin), family history of abnormal bleeding, epistaxis, menorrhagia, excessive prolonged bleeding from minor cuts, bruising, prolonged or profuse bleeding after dental extraction, excessive bleeding after major surgery or obstetric delivery, and trauma followed by bleeding considered excessive relative to the injury. The timing and type of bleeding have diagnostic significance. For example, if bleeding following dental extraction is immediate and lasts > 24 hours, a problem with primary hemostatic plug formation may be present. Therefore, this may suggest a platelet disorder. If initial hemostasis seemed normal but prolonged bleeding developed 2-3 days later, a problem in the coagulation phase...

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