Effective Home Remedy to Cure Lupus

Proven Lupus Treatment

Dr. Gary Levin is helping lupus patients with a step-by-step system that rehabilitates your immune system and boosts the bodys natural supporting systems to begin eliminating all lupus symptoms. The step-by-step treatment involves Directed Nutrition and a vitamin regime, helps the patient to lose weight, get rid of hair loss and it reduces the constant aches and pain, numbness and tiredness. This Natural Lupus Treatment is addressed first to those who want to learn more about Lupus, and those who are familiar with this area and have a fairly comprehensive knowledge base. More here...

Proven Lupus Treatment By Dr Gary Levin Overview


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This is one of the best e-books I have read on this field. The writing style was simple and engaging. Content included was worth reading spending my precious time.

As a whole, this book contains everything you need to know about this subject. I would recommend it as a guide for beginners as well as experts and everyone in between.

Aberrant T Cell DNA Methylation Gene Expression and Cellular Function in Idiopathic Lupus

Initial studies compared total genomic dmC content in T cells from patients with inactive and active lupus with controls using reverse-phase HPLC. These studies demonstrated that T cells from patients with active lupus have decreased genomic dmC levels as well as decreased levels of DNA methyltransferase activity. Intracellular pools of SAM and S-adenosylhomocysteine, both regulators of transmethylation reactions, were normal (Richardson et al., 1990). Subsequent studies demonstrated decreased Dnmt1 mRNA levels, implicating decreased maintenance DNA methylation in the DNA hypomethylation (Richardson et al., 1990 Deng et al., 2001). Dnmt3a, but not Dnmt3b, transcripts were also decreased in lupus T cells (C. Deng and B. Richardson, unpublished data). Mechanisms contributing to the decreased DNA methyltransferase expression and consequent DNA hypomethylation were sought. Others have reported that signaling is abnormal in lupus T cells (Kammer et al., 2002), and our group reported that...

Autoimmune disorders Systemic lupus erythematosus

Systemic lupus erythematosus is characterized by the production of autoantibodies that injure tissue in several organ systems, most frequently the skin, central nervous system, kidney, and lungs. In addition, non-specific symptoms occur in a large majority of patients, including fatigue, fever, weight loss, arthralgias, and myalgias.(74) The most common presenting symptoms are fever, arthralgias, butterfly rash, photosensitivity, Raynaud's phenomenon, and mucous ulcers. The laboratory diagnostic hallmark of systemic lupus erythematosus is the production of high-titre autoantibodies directed against a variety of cell nucleus components (antinuclear antibodies). Systemic lupus erythematosus has no known cure, so treatment is based on symptom relief, suppression of inflammation, and preventing future pathology. The most common psychiatric presentations of active systemic lupus erythematosus are psychosis, delirium, primary generalized seizures, complex partial seizures, and global...

T Cell in Human Lupus

Sion of an extracellular signal that can trigger cell activation, proliferation, secretion of soluble mediators, phenotypic changes, acquisition of effector functions, anergy, and programmed cell death (Lanzavecchia et al., 1999 Germain, 2001 Yablonski and Weiss, 2001). The TCR stimulation outcome can vary considerably depending on the degree and extent of integration of other membrane receptor-initiated specific accessory signals. In particular, CD28-CD80 86 and CD40-CD40 ligand interactions are important for complete T cell and B cell activation, respectively. Because TCR-mediated signaling events direct these diverse but equally important outcomes, it is likely that the diverse cellular aberrations described in lupus patients reflect signaling defect(s) responsible for the disease pathogenesis. Such defects might be due to expression of a signaling molecule(s) stemming from either a defective gene(s) or defective gene expression regulation. Tsokos et al. studied TCR CD3-mediated...

Systemic lupus erythematosis SLE

Lupus pleurisy and pericarditis Patients typically have a prolonged activated partial thromboplastin time due to circulating lupus anticoagulant. but are more prone to thrombotic episodes. Lupus anticoagulant is associated with anticardiolipin antibodies and a false positive VDRL. Recurrent pulmonary emboli may be associated with chronic pulmonary hypertension. Treatment is long term anticoagulation.

Systemic Lupus Erythematosus

Diagnosis Systemic Lupus Erythematosus then prednisone 50 mg PO qd. -Betamethasone dipropionate (Diprolene) 0.05 ointment applied bid. 1G. Extras CXR PA, LAT, ECG. Rheumatology consult. 11. Labs CBC, platelets, SMA 7& 12, INR PTT, ESR, complement CH-50, C3, C4, C-reactive protein, LE prep, Coombs test, VDRL, rheumatoid factor, ANA, DNA binding, lupus anticoagulant, anticardiolipin, antinuclear cytoplasmic antibody. UA.

Estrogen and Lupus Human and Animal Studies

It is beyond the scope of this chapter to discuss the role of estrogens in all autoimmune diseases. Therefore, we focus primarily on estrogen effects on lupus, since the effects of this hormone have been noted in humans and in murine models of lupus. SLE patients have autoantibodies against many self-antigens including double-stranded DNA (dsDNA), red blood cells, platelets, leukocytes, and clotting factors, which leads to the formation of immune complexes. The deposi tion of these immune complexes triggers inflammation, culminating in widespread tissue damage (Abdou et al., 1981). Gender is a strong risk factor for SLE since this disease primarily affects women in the reproductive years and the female-to-male susceptibility ratio can be as high as 13 1 (Rider and Abdou, 2001). SLE has been associated with situations where levels of gonadal hormones are changing such as during pregnancy, postpartum period, menopause, and during estrogen administration. The first onset of the disease...

Lupus Erythematosus

Lupus erythematosus is an autoimmune disease of unknown origin. The two main forms that affect the mouth are discoid lupus erythematosus (DLE chronic cutaneous lupus erythematosus) and systemic lupus er-ythematosus (SLE). Oral lesions are present in over 20 of patients with SLE. Fig. 3.10. Discoid lupus erythematosus showing irregular focal epithelial hyperplasia and follicular plugging Fig. 3.10. Discoid lupus erythematosus showing irregular focal epithelial hyperplasia and follicular plugging underlying corium. This feature is sometimes so florid that it produces a pseudoepitheliomatous appearance. The slender downgrowths can also show a tendency to fuse with each other producing an appearance simulating an embedding artefact. Dyskeratotic cells are an occasional feature. There is apoptosis and liquefaction degeneration of the basal cells, sometimes with Civatte body formation. The BMZ may become hyalin-ised and thickened and this is sometimes a notable feature. There is a band-like...

Lupus Nephritis

Systemic lupus (SLE) is an autoimmune disease characterized by several autoantibodies directed against intracellular antigens. Kidney involvement is frequent and indeed constitutes one of the primary causes of morbidity and mortality. It is generally agreed that antibodies are the principal agents at work in lupus nephritis, forming immune deposits by different mechanisms, more than one of which may be involved. Their central role in causing renal damage has been convincingly demonstrated in a genetically manipulated autoimmune mouse strain. MRL lpr-lpr mice lacking Ig heavy chain Jh genes, and therefore lacking B cells and autoantibodies, do not develop glomerular, tubular, or interstitial damage, even in the presence of the lpr mutation (Shlomchik et al, 1994). While not excluding the contribution of T cells, soluble mediators, and B cell functions other than antibody formation (Chan et al., 1999 Tipping and Holdsworth, 2003), antibodies have been demonstrated to be a key factor in...

Lupus anticoagulant

The paradoxically named lupus anticoagulant (LA) is arguably the commonest coagulation abnormality predisposing to thrombosis. It is something of a misnomer as it increases the risk of thrombosis not bleeding. It is an IgG IgM autoantibody and prolongs phospholipid dependent coagulation tests (hence the use of the term anticoagulant) bleeding is very rare despite the prolonged APTT. The LA and other antiphospholipid antibodies (APL) are found in association with arterial or venous thrombosis and or recurrent fetal loss, the 'antiphospholipid syndrome', first described by Hughes in 1988.

Lupus pneumonitis

Lupus pneumonitis may present as either an acute or a chronic illness. Lupus pneumonitis is rarer than pulmonary hemorrhage, with an incidence ranging from 1.5 to 9 per cent. In several reported cases, lupus pneumonitis has been the first manifestation of the disease. The pathophysiology of both acute and chronic lupus pneumonitis involves deposition of immune complexes in the blood vessels and alveolar walls with or without associated vasculitis. Acute lupus pneumonitis is reported to occur more frequently during the immediate postpartum period in women who have SLE. It is usually accompanied by other manifestations of SLE. It mimics acute lung infection so that an infectious etiology for respiratory illness should be excluded. Acute lupus pneumonitis is characterized by the acute onset of dyspnea, high fever, and cough, with occasional hemoptysis. Physical findings are minimal unless hypoxia is severe enough to cause cyanosis. A slightly elevated leukocyte count, increased...

Cell Receptor Mediated Signaling Checkpoints

Throughout B cell development, lymphocyte survival and selection are determined by the specificity of the hetero-oligomeric BcR, a module that interacts with coreceptors, protein tyrosine kinases (PTKs) and phosphatases (PTPs), adapters, and other proteins to propagate signaling cascades (Reth and Wienands, 1997 Benschop and Cambier, 1999). Since the BcR is responsible for Ag recognition, the transduction events that occur after its ligation mediate interpretation of the magnitude and duration of BcR signaling. In addition to orchestrating the efficient development and subsequent activation of B lymphocytes at several discrete stages during B lineage differentiation, the BcR plays a central role in self-tolerance. During B lymphocyte development, potentially aggressive autore-active B cells must be tolerized at various checkpoints. While studies over the past few years have provided a wealth of new information regarding the selection processes, systemic autoimmune disease is often...

Critical Regulators of B Cell Receptor Signaling

The key role of Lyn in establishing and maintaining peripheral tolerance also comes from studies of the consequences of sustained activation of Lyn in vivo using a targeted gain-of-function mutation (Hibbs et al., 2002). The mice, designated Lynup up, carry a single point mutation (Y508) in a sequence that negatively regulates Lyn activity and express a constitutively activated form of Lyn, allowing study of the consequences of constitutive engagement of both stimulatory and inhibitory signaling pathways. The mutant mice have reduced numbers of conventional B-2 lymphocytes, downregulated surface IgM and costimulatory molecules, and elevated numbers of B-1a cells. In vitro, there is a heightened Ca2+ flux in response to BcR stimulation and exaggerated positive signaling. While there is a constitutive phosphorylation of negative regulators of BcR signaling (SHP-1 and SHIP-1), Syk and phospholipase Cy2 are constitutively phosphorylated. Surprisingly, Lynup up mice developed circulating...

Protein Kinase A Function

Moreover, a series of experiments indicate that the P isoform of the R-sub-unit (RIIB) of PKA-II isoenzyme could mediate impaired cAMP-initiated responses in the nucleus of lupus T cells (Kammer, 2002). In the nucleus, tran-scriptional regulation by cAMP is mediated by a family of cAMP-responsive nuclear factors, which bind to and regulate the expression of genes containing the cAMP-responsive element (CRE) consensus in their promoters. Phosphorylation of these CRE-binding proteins (CREBs) by the C subunit of PKA that translocates into the nucleus following activation by cAMP modulates their activity (Skalhegg and Tasken, 2000). In SLE T cells, deficient PKA-II activity is characterized by spontaneous dissociation of the cytosolic RIIP2C2 holoenzyme, aberrant RIIP translocation to the nucleus from the cytosol, and retention of RIIP in the nucleus. Experiments addressing a possible interplay with extracellular stimuli in the lupus microenvironment showed that RII disorder was primary...

Regulation of Transcription Determines Interleukin 2 Deficiency in Sle T Cells

Interleukin-2 (IL-2) represents a crucial cytokine in the activation of lymphocytes. IL-2 exerts multiple functions, which serve both the promotion and the suppression of the immune response (Nelson, 2004). Fine-tuning of the production of this cytokine is the result of numerous interrelated events, which make its study a complex but intriguing task. Reduction in IL-2 production in SLE T cells upon stimulation was first documented in the 1980s, when PHA-primed cells from lupus patients produced less IL-2 compared to normal T cells (Linker-Israeli et al., 1983), and it was later on associated with the decreased immune responses to infectious agents encountered in patients with SLE.

Understanding the Side Effects of TNFa Inhibitors

The induction of antinuclear antibodies is common, but rarely associated with clinical manifestations of lupus (Shakoor et al., 2002). A positive connection between TNFa and lupus has been established in lupus mice where the inhibition of TNFa increases incidence and mortality from renal disease (Kontoyiannis and Kollias, 2000). Conversely, administration of TNFa has a protective effect on mouse lupus. The anti-inflammatory cytokine IL-10 is directly involved in the production of autoantibodies and IgG (Llorente et al., 1995). These properties indicate a mutual inhibition between TNFa and IL-10 actions. Furthermore, the inhibition of TNFa favors the production of IL-10, leading to the production of

Humoral Immunity in Atherosclerosis

Patients with systemic lupus erythematosus (SLE) or antiphospholipid antibody syndrome (APS) are prone to develop arterial complications including arterial thrombosis and atherosclerosis (Roubey, 1996 Haviv, 2000 Hughes, 2000 Urowitz and Gladman, 2000). This fact has attracted attention on the possible role of the autoimmune process in atherosclerosis development. Antibodies to oxLDLs are frequently detected in SLE patients, and several reports have suggested that they also cross-react with phospholipids, suggesting the existence of a significant over

Vaccination or Immunoglobulin Administration in Atherosclerosis

In addition to active immunization, passive administration of antiphospho-lipid antibodies can also improve disease in atherosclerosis-prone mice (Nicolo et al., 2003). We obtained a panel of antiphospholipid IgG monoclonal antibodies from (NZW x BXSB) F1 mice, a cross that spontaneously develops systemic autoimmunity reminiscent of lupus and APS (Monestier et al., 1996). We observed that biweekly administration of one such monoclonal antibody, FB1, prevents plaque formation in LDLR- - mice when compared to PBS- or control antibody-treated animals (Nicolo et al., 2003).

Deficiencies of C4A or C4B in Human SLE

It has been known for over half a century that SLE patients manifest reduced complement hemolytic activity (CH50) (Vaughan et al., 1951 Elliot and Mathieson, 1953). Reduced serum or plasma levels of complement C1q, C4, and C3 have been consistently observed in lupus patients, particularly those with lupus nephritis (Lewis et al., 1971 Cameron et al., 1976 Hebert et al., 1991). Serial analysis of serologic factors in SLE revealed that in many patients lower C4 levels occurred before the depression of other complement components. After the induction of remission, C4 had a tendency to return to normal levels more slowly than C3 (Gewurz et al., 1968 Kohler and Ten Bensel, 1969). The persistence of low C4 levels in many lupus nephritis patients before relapses and after remissions suggests the presence of a genetic factor as a cause for low C4 protein levels. The French probably have the lowest frequencies of C4AQ0 in both patient and control groups. However, the allelic frequency of C4AQ0...

Disrupted B Cell Signaling Pathways in Human Autoimmunity

As discussed above, experimentally induced modification of receptor expression or alteration of signaling pathways may have a significant impact on B cell tolerance to self. In humans too, there are indications that abnormal B cell signaling may contribute to autoimmune disease. In lupus, stimulation of circulating B cells through their sIgM produced significantly higher Ca2+ fluxes compared with similarly induced responses of B cells from patients with other systemic rheumatic diseases (Liossis et al., 1996). The overall level of sIgM-initiated protein tyrosyl phosphorylation also was significantly enhanced, and correlated with the augmented BcR-mediated free Ca2+ responses. This aberrant BcR-mediated signaling process was not associated with disease activity, medications used, or specific clinical manifestations. It was disease-specific, suggesting a possible intrinsic SLE B cell defect that may have pathogenic implications. In further studies, the content of lupus B cells in Lyn,...

IFNg in SLE and Other Autoimmune Diseases

Several lines of evidence implicate IFNy in inflammatory autoimmune disease (Billiau, 1996 Schwarting et al., 1998). First, signaling through the IFNy receptor is essential for the initiation and progression of lupus nephritis in lupus-prone, MRL-lprfas mice (Schwarting et al., 1998). Second, the IFNy-related transcription factor T-bet has been shown to regulate IgG2a class switching and induction of pathogenic autoantibodies in murine lupus (Peng et al., 2002). Third, during the course of SLE, the increased level and the expression of IFNy was accompanied by an increase in IgG2a and IgG3 levels (Reininger et al., 1996). Fourth, in the absence of IFNy gene, the levels of anti-dsDNA and ss-DNA autoantibodies, and immune complex-mediated glomerulonephritis are decreased in murine models of SLE (Carvalho-Pinto et al., 2002). Fifth, blocking IFNy by the administration of plasmids with cDNA encoding the IFNy-receptor Fc into MRL-lpr mice (at preclinical or advanced stages of lupus)...

Concluding Remarks and Perspectives

Complete deficiencies of C4A and C4B are among the strongest genetic risk factors associated with SLE or lupus-like diseases, across all HLA haplo-types and racial backgrounds. However, the age of disease onset and the disease severity vary substantially among the C4-deficient subjects, which underscores the importance of other genetic and environmental factors contributing to disease pathogenesis and progression. In contrast to the rarity of complete C4A and C4B deficiencies, partial and homozygous deficiencies of C4A are present in 32-55 of SLE patients from all races studied except Spanish, Mexican, and Australian Aborigines who had increased frequencies of C4B deficiency instead of C4A deficiency. This phenomenon underscores the relevance of C4A and C4B proteins in the fine control of autoimmunity. Different racial genetic backgrounds could change the thresholds and the requirement of C4A or C4B protein levels in immune tolerance and immune regulation. An important unanswered...

The Critical Role of B Cells in Autoimmunity

The main immunological event in the pathogenesis of SLE is B cell hyperactivity, and several lines of evidence demonstrate that B cells are essential for development of autoimmunity and disease expression (Lu and Cyster, 2002 Zouali, 2005). Transfer of cultured pre-B cells derived from (NZB x NZW) F1 fetal liver into SCID mice is sufficient to generate a lupus-like syndrome (Reininger et al., 1992). Since T cells do not develop from these donor cells, it appears that B-lineage-intrinsic defects play a primary role in the pathogenesis of the autoimmune disorder. It is also clear that, before disease development, (NZB x NZW) F1 mice have large numbers of B cells spontaneously producing low-affinity, IgM anti-DNA antibodies (Steward and Hay, 1976). In human lupus, the number of B cells that secrete Igs spontaneously is dramatically increased (Zouali et al., 1991). Characterization of autoantibody genes shows that pathogenic, high-affinity IgG anti-DNA antibody (Ab) result from an...

T Cell Signaling Abnormalities in Systemic Autoimmune Disease

Recently, the role of pattern recognition receptors (PRRs) serving as links between APCs and adaptive immune cells has shed new light on our understanding of the interplay between innate and adaptive responses, a subject fundamental to the pathogenesis of autoimmune disease. Defective expression or altered molecular configuration of toll-like receptors (TLRs), a highly conserved family of 10 PRRs expressed in innate and adaptive immune cells, may foster sustained responses to self-antigens. For example, the expression of TLR2 by antigen-activated T cells (Komai-Koma et al., 2004) may render them susceptible to activation by bacterial lipopeptide, a ligand for TLR2, and partly explain the triggering of autoimmune disease or its reactivation in the presence of bacterial infection. Another example is the breaking of tolerance to proteolipid protein in mice naturally resistant to experimental encephalomyelitis, when T cells are stimulated in the presence of APCs that have been activated...

Defective Clearance of Self Antigens in SLE

Aberrant rates of apoptosis and increased levels of free-circulating chromatin have been reported in human lupus (Amoura et al., 1997), and humans with DNASE1 and C1q gene mutations develop SLE (Kirschfink et al., 1993 Yasutomo et al., 2001), suggesting that efficient removal of chromatin or chromatin-protein complex is crucial to prevent SLE. For example, serum amyloid P component (SAP)-deficient mice develop an SLE-like syndrome (Bickerstaff et al., 1999). Two models are likely to explain the connection between SAP deficiency and SLE. First, SAP participates in dissolution of chromatin, activates complement components, C1-C4, and potentiates hepatic clearance through complement receptors. Thus, Boes et al. (2000) established mutant mice that cannot secrete IgM but that are able to express surface IgM and IgD, and to secrete other classes of immunoglobulins (Boes et al, 2000). They crossed these mutant mice with lupus-prone lymphoproliferative (lpr) mice and observed elevated levels...

Do Data from BLyD Support the Trojan Horse Concept

Protein and RhF levels are almost linear in many RA patients. In SLE, the drop in anti-DNA antibodies mirrors renal disease most closely (Leandro et al., 2002a). In other conditions antibodies are more difficult to quantify. In contrast, levels of antimicrobial antibodies, to pneumococcal capsular polysaccharide (PCP) and tetanus toxoid, in most patients with RA and lupus did not decrease significantly, even after several cycles of treatment (Cambridge et al., 2003). There is also a suggestion that marginal zone B cells in the spleen, which secrete antibodies to T cell-independent, often carbohydrate, antigens, may be relatively resistant to rituximab. This could explain preservation of levels of antibodies to PCP seen in RA and lupus (Cambridge et al., 2003 G. Cambridge, M. J. Leandro, J. C. W. Edwards, manuscript in preparation). In fact there is sometimes a transient rise in such levels after B cell depletion, suggesting that marginal zone-derived plasma cells may take over space...

Pharmacogenetics Of Drugmetabolizing Enzymes

It was later discovered that this polymorphism existed in the N-acetyltransferase-2 gene and thus the NAT-2 enzyme. More important, it has become clear that slow acetylators (about 50 of the caucasian population) are more prone to adverse effects following administration of certain drugs than fast acetylators. For example, it is well established that slow acetylators receiving the antiarrhythmic drug procainamide are much more likely to develop the systemic lupus erythemato-sus-like syndrome that has been described as a characteristic and therapy-limiting event associated with this drug. In fact, this adverse event is rare in fast acetylators. Fortunately, the number of drugs that depend on NAT-2 for their primary metabolic fate is small, so this polymorphism is clinically relevant only in certain situations.

Carbohydrates and Lipids

There seems to be no reason in principle why the immune system should not see the more hydrophilic portions of lipid-containing molecules, such as hydroxyl, phosphate or carbohydrate groups (Bendelac, 1995 Sieling et al., 1995). The extent to which the more hydrophobic portions of such amphi-pathic molecules are seen by the immune system is currently rather unclear. Antibodies to phospholipids such as cardiolipin are commonly said to be found in patients with systemic lupus erythematosus, but their specificity may be directed to protein lipid complexes rather than the lipids in isolation (Roubey, 1994 Harris et al., 1995 and references therein).

The concept of core depression

Hypopituitarism hypoglycaemia glandular fever, syphilis, AIDS, encephalitis stroke, Parkinson's disease, multiple sclerosis, brain tumours (classically meningioma), trauma, cerebral lupus common non-metastatic manifestation, especially pancreatic carcinoma, which may otherwise remain occult, and lung carcinoma

Variants And Related Syndromes

Heterogeneity is common, with some patients following a relaps-ing-remitting course and some experiencing a monophasic illness. Some patients with the syndrome undoubtedly have a form of MS, whereas others may have one of a variety of autoimmune or granulomatous disorders, such as systemic lupus erythematosus (SLE) and sarcoidosis. The term Devic disease is probably best reserved for patients with no evidence of disease outside the optic nerves and spinal cord, and who have had other potentially responsible disorders excluded.

Epilepsy And Pregnancy

The frequency of seizures may decrease in pregnancy. The patient may present with the first seizure during pregnancy (when investigation is limited) or during the puerperium. Tumours and arteriovenous malformations can enlarge in pregnancy and produce such seizures however, these causes are rare and most attacks are idiopathic. Cortical venous thrombosis and systemic lupus erythematosus should be considered as alternative explanations. Care must be taken when prescribing treatment in pregnancy although a change or withdrawal of medication is rarely necessary. The role of drugs in teratogenesis is complex genetic mechanisms in epilepsy account for an increased incidence of birth defects. Over 90 of pregnant women with epilepsy will deliver a normal child.

Oral Lichen Planus

A number of reports of malignant transformation of OLP exist (83). Malignant transformation of OLP is still controversial and the reported rates of malignant transformation range from 0 to 5.6 (83-85). A lack of consensus as to the exact criteria used in the clinical and histopathologic diagnosis of OLP has confounded the matter. The diagnosis of OLP may be complicated by some overlap with other entities such as chronic discoid lupus erythematous and leukoplakia. Aggressive use of steroids for treatment of OLP has been proposed as a possible reason why OLP patients may be vulnerable to malignant transformation (86). Clinicians should have a high index of suspicion of patients with OLP developing an oral malignancy. The clinical variants most often associated with the transformation are the erosive and atrophic forms. In one study based on the outcome of 832 patients, investigators found a transformation rate of 0.8 and recommended a follow-up of at least six years for patients with...

Immunologic Screening Tests

In addition to those conditions in which paraproteins may conceal true antibody deficiencies within normal total IgG levels, several diseases may be associated with nonspecific polyclonal B-cell activation that may cause the total IgG or IgM level to be within the normal range or even elevated, whereas specific antibodies may actually be deficient. This occurs most often in systemic lupus erythematosus, Epstein-Barr virus infection, and HIV infection ( 43,44). Finding low or absent serum IgA together with low-normal or borderline levels of one or more IgG subclasses, particularly subclass 2, should also raise suspicion of more severe defects in specific antibody production than would be suggested by the total IgG concentration itself, and such patients should also be investigated further ( 45). Elevated serum IgE and IgA concentrations may be found coexisting with deficiency of antibodies to polysaccharides in Wiskott-Aldrich syndrome, and extremely high IgE levels may suggest, but...

Other Hypersensitivity States

In type III, or immune complex, disease, IgG and IgM antigen-antibody complexes of a critical size are not cleared from the circulation and fix in small capillaries throughout the body. These complexes activate the complement system, which leads to the influx of inflammatory white blood cells, resulting in tissue damage. Clinical examples include serum sickness (after foreign proteins or drugs), lupus erythematosus, and glomerulonephritis after common infections.

Acute Transverse Myelitis

ATM may occur only once or may appear in a relapsing, recurrent form. When it occurs as an isolated event without an apparent reason it is called idiopathic ATM. It may, however, occur within the context of a systemic disease (lupus, Sjogren's syndrome, antiphospholipid syndrome) in which multiple body systems are affected, following an

Diseases Of The Blood

These IgB or IgM antibodies prolong prothrombin time and appear to be associated with thrombotic stroke. There remains uncertainty as to whether they are caused or represent a transient non-specific 'acute phase' reaction to illness. Such antibodies can be found in patients with systemic lupus erythematosus.

Differential diagnosis Physical disorders

A few hypochondriacal patients suffer from undetected physical disease. Consequently, it is important to exclude medical conditions that, in their early stages, may cause vague symptoms with few definite signs or laboratory abnormalities. These might include neurological conditions such as multiple sclerosis or myasthenia gravis, endocrine conditions such as thyroid or parathyroid disease, diseases that affect multiple body systems such as systemic lupus erythematosus, or occult

Use Of Corticosteroids In Clinical Practice

The beneficial results of high-dose pulse IV MP therapy in systemic conditions like lupus nephritis, glomerulonephritis, and acute transplant rejections prompted the use of high-dose IV MP in the acute relapse of MS. Using double-blind controlled studies, highdose IV MP has been demonstrated to show significant improvement when compared to placebo in patients with MS relapse.

Epidemiology Of Fatigue

Fatigue is associated with worse physical and mental health27,33,34 and often adds morbidity to common medical disorders such as diabetes,35 chronic renal failure,36 and cancer.37 It is a diagnostic symptom of mood disorders such as depression and generalized anxiety disorders38 and occurs in many psychiatric illnesses.39 Fatigue is consistently associated with several neurological disorders6-40-44 and affects 80 to 100 of patients with systemic lupus erythematosis.45-47 In one study, fatigue was deemed the most bothersome symptom in more than

Impact And Nature Of Fatigue In Pd

Although some authorities argue that better definitions and rating instruments are needed,88 it is likely only that different rating instruments will be developed that are disease specific. It is unlikely, for example, that the fatigue of myasthenia gravis will be measured sensitively by an instrument aimed at multiple sclerosis or lupus, where effects of medications or polysystem diseases are important.

Topical Glucocorticosteroids

Topical corticosteroids are most useful in inflammatory dermatoses, such as eczematous dermatitis and psoriasis they may also be helpful in other skin diseases that have a prominent inflammatory component, such as autoimmune blistering diseases (e.g., bullous pemphigoid and pemphigus vulgaris) and lupus erythematosus.

Making Decisions About Endomyocardial Biopsy In Myocarditis

Immunosuppressive therapy is not recommended in patients with acute infectious or postinfectious myocarditis, but a small subset of patients with noninfectious myocarditis due to giant cell myocarditis, scleroderma, lupus erythematosus, polymyositis, or sarcoidosis may benefit from immunosuppressive therapy.

The Strongyloides hyperinfection syndrome

Risk factors for disseminated strongyloidiasis are systemic corticosteroid therapy, human T-cell lymphotropic virus I infection, HIV infection, anticancer chemotherapy, leukemia, lymphoma, lepromatous leprosy, visceral leishmaniasis, systemic lupus erythematosus, and malnutrition.

Treatment and prognosis

Pleural effusion responds favorably to systemic corticosteroid therapy, with an occasional large effusion being refractory. Lupus pneumonitis and alveolar hemorrhage syndrome may respond to high-dose corticosteroid therapy. Cytotoxic agents have been used in patients refractory to corticosteroid therapy, but there is little evidence to suggest improved efficacy of the latter. Sepsis and progressive renal dysfunction are the most frequent causes of mortality in patients with SLE, but acute pulmonary alveolar hemorrhage is also important. Dramatic response can be expected in some patients with lupus pneumonitis following systemic corticosteroid therapy.

Studies of TPMT in Rheumatology

Naughton et al. (67) found in a cohort of 135 patients, mostly with systemic lupus erythematosus, that although the single patient homozygous for mutant alleles experienced bone marrow toxicity, only one of the eleven others with drug-induced neutropenia had a polymorphism detected. Clearly, additional unknown polymorphisms may account for some of these patients. Therefore, genotyping may detect the small number of patients who are homozygous for TPMT polymorphisms who are clearly at risk of significant toxicity. In this group, an alternative agent can be used. In heterozygous patients, avoidance of the drug may not be necessary, although a lower dose may be needed to avoid bone marrow or GI toxicity. Taking all the current data into consideration, it appears that genotyping alone is insufficient to identify all patients who are at risk of developing AZA tox-icity, and, therefore, regular monitoring is still necessary even when no TPMT polymorphisms are detected.

Class Ia drugs quinidine procainamide disopyramide

Procainamide has a similar mode of action to quinidine but prolongs the QT interval less. Long-term administration may result in a lupus syndrome. It is generally safe and well tolerated. Torsade de pointes is less common. It is useful in the treatment of sustained monomorphic ventricular tachycardia where it has been shown to be

Does patient have any previously documented urinalysis

Any history of constitutional symptoms or signs (intermittent fever, rash, abdominal pain, mouth sores, lymphade-nomegaly, joint symptoms, weight gain or loss) These symptoms and signs could be features of significant underlying disease causing proteinuria (eg, systemic lupus erythematosus, hemolytic uremic syndrome, Henoch-Schonlein purpura, among others).

Other demyelinating diseases

This is a demyelinative disease occurring in association with systemic illness in which cell-mediated and occasionally humoral immunity is depressed, e.g. AIDS (4 of cases), lymphoma, sarcoidosis, systemic lupus erythematosus. The disorder is due to reactivation of previous papavirus (SV40 or JC virus) infection. Clinical picture Features of diffuse process personality change, hcmiparcsis, cortical visual loss, seizures, etc. Duration of illness 3-6 months. Non-remitting and fatal.

Associated antiphospholipid antibodies

CRAO is also associated with elevated levels of antiphospholipid antibodies (APA).34-39 Among patients with systemic lupus erythematosus, persistently positive tests for APA, especially lupus anticoagulant and anticardiolipid antibody (aCL), characterise a subset of patients with thrombotic tendency.38 In particular, the presence of aCL has been found to be an independent risk factor for ischaemic stroke, especially among young patients,39 and an association between transient monocular blindness and elevated levels of APA, especially aCL, has been suggested (for review see Donders et al.40).

Ischemic Stroke Subtypes

Despite complete diagnostic evaluation, the cause of cerebral ischemia cannot be identified in as many as 40 of ischemic strokes. Patients with these cryptogenic strokes usually have no prior TIAs, no bruits on physical examination and, usually, normal angiography. CT scanning or MRI may be normal or may show an infarct limited to a surface brain territory. Some of these infarcts have been attributed to conditions such as sickle cell disease, hyperco-agulable states or protein C and protein S deficiencies, lupus anticoagulant or anticardiolipin antibodies.

Platelet clumping due to activation during collection

AIDS acquired immunodeficiency syndrome HIV human immunodeficiency syndrome HUS hemolytic uremic syndrome ITP idiopathic thrombocytopenic purpura SLE systemic lupus erythematosus TAR thrombocytopenia with absent radii. AIDS acquired immunodeficiency syndrome HIV human immunodeficiency syndrome HUS hemolytic uremic syndrome ITP idiopathic thrombocytopenic purpura SLE systemic lupus erythematosus TAR thrombocytopenia with absent radii. b. Autoimmune diseases with thrombocytopenia as a manifestation. Immune thrombocytopenia associated with cancer, systemic lupus erythematosus (SLE), Evans syndrome, antiphospholipid antibody syndrome, cyclic thrombocytopenia (variant of chronic ITP), autoimmune lym-phoproliferative syndrome.

Personality change due to a general medical condition JLC

In most cases this disorder is associated with structural damage to the brain. Head trauma, cerebral neoplasms, vascular accidents, multiple sclerosis, Huntington's disease, and complex partial epilepsy may all cause personality change, especially when affecting frontal and temporal lobes. Systemic diseases involving the central nervous system, including endocrine disorders, AIDS, lupus erythematosus and chronic metal poisoning, may have the same effect.

Postmarketing Experience 19831986

Reports of other severe untoward events that could have had an immunological basis also appeared in the literature in 1984-1985 thrombocytopenia (Green et at., 1984), hepatitis (Vaz et at., 1984), alveolitis (Hamm et at., 1985) and a systemic lupus erythematosus (SLE)-like reaction (Garcia-Morteo and Maldonado-Cocco, 1983 Schonhofer and Groticke, 1985). Those appearing in the British medical literature could possibly have contributed

Contraindications and Drug Interactions

Gold compounds are contraindicated for use in patients with systemic lupus erythematosus, Sjogren's syndrome, severe debilitation, or uncontrolled congestive heart failure or hypertension. Caution must be used in administering gold compounds to individuals who have conditions that might increase their susceptibility to gold toxicity blood dyscrasias, immunosuppression, renal disease, hepatic disease, skin diseases, or inflammatory bowel disease. Animal studies have shown adverse effects on reproduction gold compounds may distribute to breast milk and are therefore contraindicated for women who are breast-feeding.

Catastrophic antiphospholipid syndrome

Patients with this rare condition often present critically ill with multiple vascular occlusions death, usually from cardiopulmonary arrest, frequently results ( Asherson, , 1992). There is widespread organ damage with renal dysfunction, hypertension, and respiratory distress with chest radiograph appearances typical of adult respiratory distress syndrome. Thrombotic skin manifestations are common (digital gangrene or ulceration, acrocyanosis, and livido reticularis), as are central nervous system symptoms and signs. Small- and large-vessel thrombosis is a hallmark of the disease, both arterial and venous. There may be a history of systemic lupus erythematosus or primary antiphospholipid syndrome. Laboratory features in addition to the presence of antiphospholipid antibodies include thrombocytopenia, leukocytosis, and an elevated erythrocyte sedimentation rate. Creatinine is often elevated and liver function tests may be abnormal. Treatment must be started early, although it is often...

Physical Exam Key Points

Observe for facial swelling and for pitting edema of legs and sacral area if patient is nonambulatory. Look for vasculitic rash and sores on the buccal mucosa. If lupus is suspected, check lymph nodes. 5. Joints. Thorough exam of joints is necessary if lupus or HSP is suspected. 2. CBC. Anemia alone may indicate glomerulonephritis. Anemia with schistocytes and thrombocytopenia is expected in HUS. Leukopenia, usually with anemia and sometimes with thrombocytopenia, is frequent finding in lupus. HSP does not have characteristic findings on CBC. 4. Serum serology. Low C3 is expected in lupus, APIGN, and MPGN. Moderately elevated ANA (1 80-1 160) is frequently seen without vasculitis, but higher titers should raise the suspicion of lupus.

Pulmonary thromboembolism

Thrombophlebitis involving the veins of the lower extremities occurs in 5 to 12 per cent of patients with SLE. Predisposing factors include chronic low-grade disseminated intravascular coagulation, angiitis of small vessels, prolonged bed rest, and increased thromboplastin generation. Among the etiologies for thromboembolic phenomenon in patients with SLE is the antiphospholipid antibody syndrome, which refers to a spectrum of autoantibodies, including lupus anticoagulant antibodies and anticardiolipin antibodies, that bind to negatively charged phospholipids. The antiphospholipid antibody syndrome plays a major role in causing the thromboembolic phenomenon in the extremities and the pulmonary vasculature. The syndrome is characterized by a prolonged activated partial thromboplastin time in association with otherwise normal clotting and platelet counts, the presence of anticardiolipin antibody, and a false-positive VDRL test. Recurrent thromboembolism and pulmonary emboli complicated...

Clinical Assessment of Complement Activation

Measured but in whom hemodilution is rarely considered. Finally, complement activation reactions that consume more than 5 to 10 percent of available serum C3 would be truly massive. Assessments of the functional capability of the complement lytic system using the CH50 assay have been employed as a repetitive measure with which to monitor the activity of a chronic systemic inflammatory disorder, such as systemic lupus erythematosus. However, the CH50 is a highly contrived assay designed to measure differences in red cell hemolysis at limiting dilutions of complement proteins (typically several hundredfold). Whether undiluted serum can ever acquire a complement lytic functional deficiency is doubtful. Thus, the mainstay of assessments for complement activation is the measurement of complement activation-derived cleavage products such as C3a desArg. However, assuming that complement activation has occurred simultaneously with measured elevations of C3a desArg could be misleading, as the...

Causes Pathophysiology

Systemic diseases of the skin (e.g., psoriasis, lupus erythematosus, scleroderma) can affect the ear canal and eventually cause external canal obstruction. One important feature of psoriasis is that mild trauma to surrounding skin induces lesions localized to the area of injury.9 Therefore, patients with psoriasis in or near the ear canal should be asked to avoid manipulation of the lesions, so as to prevent stenosis. Cutaneous (contact dermatitis) reactions to shampoos, medications, and foreign material in the ear canal can be severe and may require rapid medical attention to prevent scarring and stenosis of the soft tissue of the canal.

Genetic Variability In Drug Metabolizing Enzymes

AMany of these associations have only been shown in single studies and or may not have been replicated. Abbreviation SLE, systemic lupus erythematosus. aMany of these associations have only been shown in single studies and or may not have been replicated. Abbreviation SLE, systemic lupus erythematosus.

Diagnosis of pleural effusions

Low pleural fluid glucose (below 60 mg dl) or a pleural fluid to serum glucose ratio below 0.5 is typical of infectious effusions, particularly empyema. Tuberculous effusions may have a low glucose value. Rheumatoid effusions also have a characteristic low glucose level. Systemic lupus erythematosus, esophageal rupture, and 15 per cent of malignant effusions have low glucose levels. Low glucose levels are the result of increased glucose metabolism by bacteria and leukocytes which exceeds the rate of glucose transport into the pleural space.

Prolapse Syndromes

Include rectal prolapse, failure of puborectalis relaxation, increased anorectal angle, abnormal perineal descent, and decreased anorectal sensitivity to balloon inflation.19 Abnormal perineal descent has been seen in patients with SRUS, and behaviors such as digitization have been related. Other disorders such as defecation disorders, constipation, fecal impaction, erythema nodosum, and lupus have also been associated with SRUS.20

Drug Transporters

Blood and tissue concentrations of most drugs are influenced by interindividual variation in the structure and function of the metabolizing enzyme and transporter genes. Transporters are genes that control drug uptake, distribution, and elimination. The multidrug resistance gene (MDR1) encodes for a P-glycoprotein (PgP), which belongs to the large adenosine triphosphate (ATP)-binding cassette (ABC) protein. The MDR1 gene was originally discovered as the protein causing cross-resistance of tumors to many different cyto-toxic agents (16). Multiple substrates are transported by PgP, including the chemotherapeutics tamoxifen and mitoxantrone, the antibiotics cefotetan and cefazolin, the immunosuppressant cyclosporin A, the antiarrytmic drug quindine, the cardiac stimulants digoxin, and such opioid drugs as morphine, to name a few (17). Many cancers are known to overexpress the PgP protein, and this has been correlated with poor prognosis, particularly in patients with leukemia (18)....

Vital signs

May be due to pain or an underlying medical condition related to chest pain (eg, systemic lupus erythematosus). Serious associated medical problems (eg, diabetes mellitus, asthma, Marfan syndrome, Kawasaki disease, sickle cell anemia, systemic lupus erythematosus) Use of drugs (cocaine, oral contraceptives) Associated complaints (syncope dizziness, palpitations) Significant trauma Foreign body ingestion or aspiration Fever

DOGS Unknown

The Dog family (Canidae) arose from primitive carnivores in the Eocene, about 35 million years ago, in North America. Common characteristics include elongated jaws, long legs relative to body size, five toes on the front feet and four toes on the hind feet, nonretractile claws, and an omnivorous diet. Most species are uniform in coloration, with special markings usually confined to the head and the tip of the tail. In size, canids range from the Fennec fox (Fennecus zeerda) that weighs about 3 pounds to the Gray wolf (Canis lupus) that weighs up to 175 pounds.


Autoimmune responses may arise when antigens that have been normally sequestered from the immune system (e.g., in immunologically privileged sites) are exposed as a result of trauma. Having never been detected previously by the immune system as it developed its sense of self versus nonself, such antigens are now seen as foreign. Second, the interaction of self molecules with small reactive chemicals (e.g., haptens) or with infectious agents may produce alterations in self molecules (altered antigens or neoantigens), resulting in their detection as nonself. Third, immune responses against determinants on infectious agents may generate clones of lymphocytes with receptors capable of cross-reacting with self antigens (cross-reactive antigens). A classic example is rheumatic fever, which results from immune responses against streptococcal antigens that are cross-reactive with molecules found on cardiac tissue. Finally, some autoimmune responses, especially those that tend to develop in...

Veneer Theory

If we are indeed Hobbesian competitors who don't care one bit about the feelings of others (Homo homini lupus, or Man is wolf to man), how did we decide to transform ourselves into model citizens Can people for generations maintain behavior that is out of character, like a shoal of piranhas that decide to become vegetarians How deep does such a change go

Retinal Findings

Filtrates, retinal vasculitis, optic disk edema) may occur in patients with intraorbital inflammatory (e.g., scleritis, systemic lupus erythematosus, Wegener's granulomatosis), infectious (e.g., endophthalmitis with extrascleral extension), or neoplastic (e.g., orbital lymphoma) conditions.


The list shown in Box 4.4 is a guideline of suggested first-and second-line investigations for identifying the physical agent(s) responsible for delirium in an individual patient. The choice of investigations ordered will obviously be dictated by the findings on history taking and examination. For instance, a cranial computed tomography (CT) scan or magnetic resonance imaging (MRI) is a first-line investigation if neurological signs are present or the history or examination suggests head trauma.74 If, after initial investigation, no cause can be found for the delirium, it may then be appropriate to run a full test screen, given the serious nature of the untreated condition. In so doing one may detect uncommon presentations of relatively common diseases, such as systemic lupus erythematosus. Even after thorough investigation, some patients remain without an identified cause for their disorder. In such cases, it may be necessary to reconsider the diagnosis.

Historical Overview

Beans can be harmful to some, but not all, individuals, leading to red cell hemolysis. This was also described with primaquine, an antimalarial drug, in 1956, and related to a deficiency of glucose-6-phosphate dehydrogenase (13). Another classic example reported in the 1950s was the occurrence of prolonged apnea after treatment with suxamethonium in patients with a deficiency of butyrylcholinesterase (14,15). In the 1960s, the occurrence of peripheral neuropathy associated with the intake of isoniazid was related to a deficiency of N-acetylation of the drug in the so-called slow acetylators (16). The first ADR with a P450 polymorphism, the occurrence of hypotension with debrisoquine (17), led to the discovery of CYP2D6 (at that time called debrisoquine hydroxylase). The same genetic defect was later associated with the development of hepatotoxicity and peripheral neuropathy in patients taking the antianginal perhexilene (18,19). Since then, the majority of pharmacogenetic studies of...

Available Assays

In most circumstances, a functional assay of plasma APC resistance is the preferred initial test. In the original assay, aPTT was measured before and after addition of a standardized amount of APC that was sufficient to prolong the aPTT about 2-fold. The result was usually expressed as the APC-R ratio (defined as the ratio of the aPTT clotting times in the presence and absence of APC). An APC-R ratio of less than 2.0 was indicative of APC-R. About 95 of patients with APC-R were carriers for Factor V Leiden. Although specific, the original APC-R assay was relatively insensitive. Factor V Leiden carriers can have an APC-R ratio as high as 2.9, and the assay did not reliably distinguish heterozygotes from homozygotes. Moreover, the original assay was uninterpretable if the baseline aPTT was prolonged due to warfarin or heparin anticoagulation, factor deficiency, or a lupus anticoagulant or other specific factor inhibitor. A modified (second-generation) APC-R functional assay that...

Medical conditions

Only a limited number of general medical conditions present vague, non-specific, and multiple somatic symptoms (e.g. hyperparathyroidism, hyperthyroidism, acute intermittent porphyria, myasthenia gravis, AIDS, multiple sclerosis, systemic lupus erythematosus, Lyme disease, and connective tissues disease). In most of these medical conditions there will be positive paraclinical findings.


In most patients with thrombosis, trigger factors will be identified in the history. APL is a relatively common acquired thrombophilic defect detected by lupus anticoagulant activity or elevated anticardiolipin titres. 395 Should be considered in patients with VTE and young patient with arterial thrombosis or those without evidence of atherosclerosis. Testing for inherited thrombophilia is complex, more expensive and only worthwhile in familial thrombosis. A strong family history of VTE will increase the chance of identifying such defects.

Alopecia Areata

Differential diagnosis Tinea capitis, trichotillomania, secondary syphilis, and lupus erythematosus. F. A VDRL or RPR test for syphilis should be obtained. A CBC, SMAC, sedimentary rate, thyroid function tests, antinuclear antibody should be done to screen for pernicious anemia, chronic active hepatitis, thyroid disease, lupus erythematosus, and Addison's disease.

Quinone Imines

A further example of the design of drugs to remove aromatic amine functionalities even when present as a amide, is illustrated by the Na+ channel class of antiarrhythmic drugs 16 . Lidocaine is very rapidly metabolized (Figure 8.16) and so is only useful as a short-term intravenous agent. Oral forms include procainamide, tocainide and flecainide (Figure 8.16). Procainamide causes fatal bone marrow aplasis in 0.2 of patients and lupus syndrome in 25-50 . Tocainide also causes bone marrow aplasis and pulmonary fibrosis. In contrast, flecainide, whose structure contains no aromatic amine, masked or otherwise, has adverse effects related directly to its pharmacology. Interestingly, the lupus syndrome seen with procainamide is largely absent when N-acetyl procainamide is substituted.


Dapsone is approved for the treatment of an autoimmune blistering skin disease, dermatitis herpeti-formis. This intensely pruritic eruption is characterized histologically by a dense dermal infiltration of neu-trophils and subepidermal blisters. Other skin diseases in which dapsone is helpful are linear immunoglobulin A (IgA) dermatosis, subcorneal pustular dermatosis, leukocytoclastic vasculitis, and a variety of rarer eruptions in which neutrophils predominate, including some forms of cutaneous lupus erythematosus.

Antimalarial Drugs

Hydroxychloroquine is approved for the treatment of both systemic and cutaneous lupus erythematosus. Both chloroquine and quinacrine (Atabrine) are also effective in this skin disease. Low-dose chloroquine is used for the therapy of porphyria cutanea tarda in patients in whom phlebotomy has failed or is contraindi-cated. Other skin diseases in which the drugs are useful (after sunscreens and avoidance of sun exposure) include polymorphous light eruption and solar urticaria.

Pulmonary hemorrhage

Pulmonary hemorrhage, characterized by diffuse intra-alveolar bleeding, is an uncommon but life-threatening manifestation of SLE. It is likely that clinically insignificant or undetectable intra-alveolar hemorrhage occurs in many patients. One retrospective study of 76 autopsy cases of SLE collected over a period of 20 years observed that, even though pulmonary hemorrhage was clinically suspected or noted in less than 2 per cent of patients, it was the primary cause of death in 14 per cent. In another series of 57 patients pulmonary bleeding was the cause of death in 10.5 per cent. The mechanism of pulmonary hemorrhage is unclear, although pulmonary vasculitis and capillaritis are probably responsible. Other mechanisms include the activation of the complement system leading to deposition of immune-complex deposits in the capillary basement membrane of the lungs. The end result is a break in the integrity of the alveolar-capillary basement membranes. The presence of uremia, hemorrhagic...

Pleural involvement

Pleurisy is the most common and often the presenting manifestation of SLE, and is found in up to 83 per cent of patients at necropsy. Pleural effusions are seen more frequently in older patients and in drug-induced SLE. Non-specific pathological changes in the pleura include infiltration by lymphocytes, mononuclear cells, and plasma cells, together with various degrees of fibrosis. Painful pleurisy occurs in 41 to 51 per cent of patients, and pleuritic pain may be the first symptom in many. Young females who present with new-onset pleurisy or pleural effusion should be evaluated for SLE. An important differential diagnosis is pulmonary embolism, since SLE patients are at higher risk of thromboembolic phenomena. Pleuritic pain may be unilateral or bilateral and is usually located at the costophrenic margins. Pleural effusions are usually small to moderate, bilateral in nearly 50 per cent, occasionally associated with a small pericardial effusion, and frequently accompanied by dyspnea,...


Figure 24.5 Crusted scabies while in otherwise healthy persons the infestation usually means only 10-20 mites, an immuno-compromised patient (HIV, tumor diseases, etc.), might develop quite another clinical disease with widespread hyperkeratotic lesions crusted scabies or 'Norwegian scabies'. This patient suffered from systemic lupus erythematosus and was on high doses of cortisone since a long time. (See Colour Plate VII.) Figure 24.5 Crusted scabies while in otherwise healthy persons the infestation usually means only 10-20 mites, an immuno-compromised patient (HIV, tumor diseases, etc.), might develop quite another clinical disease with widespread hyperkeratotic lesions crusted scabies or 'Norwegian scabies'. This patient suffered from systemic lupus erythematosus and was on high doses of cortisone since a long time. (See Colour Plate VII.)

Clotting disorders

Uncommon as a secondary event in critically ill patients as they tend to be auto-anticoagulated. The risk of major venous thrombosis increases with long term immobility and paralysis, and in specific pro-thrombotic conditions such as pregnancy, thrombotic thrombocytopenic purpura, SLE (lupus anticoagulant), sickle cell crisis, hyperosmolar diabetic coma.


Studies to date have focused on the effect of acetylator status and side effects. Kitas et al. (39) found no effect of acetylator status on toxicity or efficacy. Pullar et al. (40) found that there was an increased risk of nausea and vomiting in slow acetylators but no difference in the rates of serious toxicity. Several studies have examined the effect of the N-acetyltrans-ferase 2 (NAT2) polymorphism on treatment outcome. To date, at least 19 SNPs have been identified within the coding region of NAT2 (41). Tanaka et al. (42) studied a Japanese RA cohort and found that patients without the NAT2*4 haplotype, which is associated with rapid acetylation status, had a significantly higher number of adverse events than patients with the NAT2*4 haplotype (62.5 vs. 8.1 OR 7.73). Sabbagh et al. (43) also found a higher rate of side effects with sulfasalazine in slow acetylators with chronic discoid lupus. However, a study by Ricart et al. (44) in ulcerative colitis patients found no...


Other drug-induced dermatitis includes discoid lupus erythematosus (DLE) and exfoliative dermatitis. Hydralazine hydrochloride (Apresoline), isoniazid (INH), phenothiazines, anticonvulsants, and antidysrhythmics such as procainamide (Pronestyl) may cause lupus-like symptoms. If lupus-like symptoms occur, the drug should be discontinued.

Phantom Wolf

Coleman and four others watched a large, wild dog, 3 feet high at the shoulder and with a long, thin tail, in a field on the north side of Elgin, Illinois. Possible explanations (1) The Gray wolf (Canis lupus) usually hunts in packs for large prey. Its average length is 5 feet from head to tail, and its coat varies from white to black, with many shades in between. Wolf predation on cattle and sheep in the United States is negligible. The U.S. Fish and Wildlife Service gives the following numbers for verified wolf kills from 1991 through May 1998 in Minnesota, a state with an estimated wolf population of 2,400 585 cattle, 200 sheep, 10 horses, 3 pigs, 5 goats, 4,889 turkeys, 30 chickens, 7 geese, 2 ducks, and 84 dogs. Pawprints are not reliable indicators of a wolf kill, since wolf prints can be

Hungarian Reedwolf

Scientific names Canis lupus minor, given by M. Mojsisovics in 1887 Canis aureus hungari-cus, renamed by Gyula fihik in 1938. Variant name Rohrwolf (German). Physical description Like a small wolf. Distribution Hungary eastern Austria. Present status Apparently became extinct in the early twentieth century. Some museum specimens exist. (1) A diminutive subspecies of Gray wolf (Canis lupus), first suggested by M. Mojsisovics and now the generally accepted identification. ungarische Rohrwolf (Canis lupus) war kein Schakal (Canis aureus), S ugetierkundliche Mitteilungen 4 (1956) 165-167 Janos Szunyoghy, Systematische Revision des ungarl ndischen Schakals, gleichzeitig eine Bemerkung ber das Rohrwolf-Problem, Annales Historico-Naturales, Musei Nationalis Hungarici, new ser. 8 (1957) 425-433 Eduard-Paul Tratz, Ein Betrag zum Kapitel 'Rohrwolf Canis lupus minor Mojsisovics, 1887, S ugetierkundliche Mitteilungen 6 (1958) 160-162.


(1) The Gray wolf (Canis lupus) was one of the first wild animals to be domesticated. The process of adopting young wolves by hunter-gatherer groups as companions in the hunt and as guard animals probably occurred in several places as early as 10,000 B.C. Close bonding and mutual dependence with an animal undoubtedly had great magical significance, and those individuals who took on the attributes of a wolf would be seen as skilled hunters and shamans. The earliest shape-shifting myths may well have Neolithic roots.


A history of hypercoagulable abnormalities should be ascertained, such as activated protein C resistance (factor V, Leiden) prothrombin variant 20210A antiphospholipid antibodies (lupus anticoagulant and anticardiolipin antibody) deficiency or dysfunction of antithrombin, protein C, protein S, or heparin cofactor II dysfibrinogenemia decreased levels of plasminogen and plasminogen activators heparin-induced thrombocytopenia or hyperhomocystinemia.55

Case 3

A 53-year-old woman developed subacute tetraplegia. Brain and spinal MRI was normal and CSF acellular. She made a partial recovery over 6 months after intravenous high-dose corticosteroids. Eighteen months later, she developed severe bilateral sequential optic neuritis and a left hemiplegia. Limb weakness partially improved, and her vision remained poor despite a further course of corticosteroids. Repeat MRI showed two infratentorial white matter lesions. MRI cervical cord showed an extensive cervical cord lesion extending over three levels. VEPs were delayed asymmetrically. She had unmatched CSF oligoclonal bands in addition to matched bands in the serum and CSF. She had a past history of two first-trimester miscarriages, an unprovoked ileofemoral deep vein thrombosis (DVT) for which she was on long-term warfarin, migraine, and one positive antiphospholipid antibody result. Her antineu-trophil antibody (ANA) was raised without more specific lupus autoantibodies. Three months on, she...


Iproniazid Medicine

Adduct formation, in that reaction with a second drug radical could form a closed shell species. Thus the mechanism by which radicals may form a covalent adduct to proteins is likely to be a two step process, (in contrast to electrophiles). Perhaps for this reason covalent binding of radicals to proteins with subsequent toxico-logical significance has been significantly less well demonstrated than for electrophiles. Among the few examples are ethanol, halogenated hydrocarbons, and possibly hydrazines. a Hydroxyl ethyl radicals have been shown to be formed during microsomal incubations with ethanol, and to subsequently covalently bind to proteins. These adducts have also been shown to be immunogenic, and therefore provide an alternative mechanism from acetaldehyde covalent binding, for ethanol induced immune mediated hepatitis (Moncada et al. 1994). In addition to the oxidative pathways discussed earlier, low molecular weight halocarbons can undergo reductive metabolism to form carbon...

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