Lupus Holistic Treatment
The dog was the first domestic animal however, the beginning of its coexistence with humans is still unclear. The wolf (Canis lupus) is the progenitor of all domestic dog breeds and feral populations. Fifteen thousand years ago, the wolf lived in all of Eurasia, in north Africa, and in North and Central America. It evolved into many subspecies, which differ in size and color. The small Indian wolf (C. l. pallipes) and the larger Eurasian wolf (C. l. lupus) are the most likely dog ancestors.
Contact allergy to fragrances usually causes dermatitis of the hands, face, and or armpits 16-18 , the latter site being explained by contact allergy to deodorants and fragranced antiperspirants. In the face, the skin behind the ears and neck is exposed to high concentrations of fragrances in perfumes and aftershaves. Microtraumata from shaving facilitates (photo)contact allergy to aftershave fragrances. The sensitive skin of the eyelids is particularly susceptible to developing allergic contact dermatitis to fragrances in skincare products, decorative cosmetics, and cleansing preparations, as well as from fragrances spread through the air (airborne contact dermatitis) 19 . Most reactions are mild and are characterized by erythema (redness) only with some swelling of the eyelids. More acute lesions with papules, vesicles, and oozing may sometimes be observed. Dermatitis attributable to perfumes or toilet water tends to be ''streaky.'' In some cases, the eruption resembles other skin...
A few early studies have examined whether expression of the FcyRIIa-Arg His131 polymorphism influences susceptibility to infectious or autoimmune disease. In theory, the weaker binding of human IgG2 to the FcyRIIa-Arg131 variant suggests that this gene might be overrepresented among patients with recurrent infections characterized by certain microbes with polysaccharide coats (i.e., involving an IgG2 antibody response) and overrepresented in disease characterized by circulating immune complexes (because phagocytic cells bearing the FcgRIIa-His131 variant would clear these complexes more readily). Certainly, a skewed genotypic distribution favoring the FcyRIIa-Arg131 variant has been noted in patients with Haemophilus influenzae infections (Sanders et al., 1994) and meningococcal septic shock (Bredius et al., 1994b). Furthermore, there is also predominance of FcgRIIa-Arg131 in patients with elevated levels of immune complexes and glo-merulonephritis complicating systemic lupus...
Internuclear ophthalmoplegia (INO) results from a lesion in the medial longitudinal fasciculus (MLF) and may be demyelination, tumor, vascular disease, Wernicke's disease, systemic lupus, and others. Lesions at the anterior end of the MLF will have defective convergence. Posterior lesions have better medial rectus function on convergence than on gaze.
The diagnosis of this syndrome may be confused with infection, lymphoma, hypereosinophilic syndrome, and collagen vascular disease. Histological examination of skin lesions showed lymphocytic infiltration in the dermis and sometimes the epidermis (epitheliotropism). The infiltrate may resemble the infiltrate observed in the mycosis fungoides (cutaneous T-cell lymphoma) dense band-like infiltrate in the epidermis with atypical lymphocytes. Regarding this lymphocytic infiltration, the biological hematological abnormalities and the clinical lymphadenopathy, pseudolymphoma denomination was also alternatively used for the same patients. The case record of the Massachusetts general hospital reported in 1996 in the New England Journal of Medicine illustrated this discussion (Gorlin and Ferry, 1996). A 7-year-old child was admitted for the association of fever, lymph-adenopathy, hepatosplenomegaly, and eosinophilia. This boy had been receiving carbamazepine and phenytoin for 2 months after a...
Renal artery thrombosis is a rare complication in transplantation that is more common in kidneys with donor vascular disease or with multiple vessels requiring bench surgery before transplantation. It is also common in kidneys from paediatric en bloc donors. Other possible causes include persistent hypotension, dehydration, and procoagulant conditions (e.g., lupus anti-coagulant and diabetes). It can be an acute event postoperatively or up to a few months postoperatively. Reasons for early arterial thrombosis are usually technical. Fine vascular suture materials should be used for the anastomosis. We usually use 5 0 Prolene for the vein and 6 0 Prolene for the artery. If the allograft does not perfuse properly the vascular clamps are re-applied, the kidney flushed with cold perfusion solution, and the anastomosis redone. In delayed arterial thrombosis salvage is rarely possible. The patient may experience severe pain, swelling, or severe haema-turia. There may be cessation of urine...
Hypersplenism refers to a condition in which the blood cells are culled excessively within the spleen. It usually occurs when the haemopoietic cells are intrinsically abnormal - as in idiopathic thrombocytopenic purpura (ITP), congenital spherocytosis and acquired haemolytic anaemias (due to various leukaemias, Hodgkin's lymphoma, sarcoidosis, lupus erythematosus, etc.).
Contraindications myasthenia gravis, complete heart block, SLE, Torsades de pointes. Adverse effects hypotension, heart block, myocardial depression, ventricular dysrhythmias, lupus, fever, agranulocytosis, GI irritation, lupus-like syndrome, positive Coombs' test, confusion. Comments use caution in asymptomatic PVCs, digitalis intoxication, CHF, renal or hepatic impairment
Mation, such as inflammatory bowel diseases, alopecia areata, psoriasis, lichen sclerosus or lupus erythematosus, IL1RN*2 homozygosity increases the severity of the inflammation, suggesting that persons with this allele have a more prolonged and more severe proinflammatory immune response than do persons with other IL-1RA genotypes 73 . Interestingly, the frequency of the two-repeat allele of IL-1RN is increased among patients with acne conglobata but not among those with HS. In addition, IL1RN*2 homozygosity was detected only amongst patients with severe acne conglobata, suggesting that allele 2 of the IL-1RN gene may contribute to the development of acne conglo-bata but not HS 38 .
Mixed connective tissue disease is characterized by a combination of overlapping features of systemic lupus erythematous, scleroderma, and polymyositis. Typical presentation is with Raynaud's phenomenon, arthralgias, inflammatory myopathy, lymphadenitis, skin or mucosal lesions, and serositis. A key distinguishing factor of the disorder is a high titer of antibody to ribonucleoprotein, a finding absent in any of these three disorders (SLE, scleroderma, and polymyositis). Neurologic dysfunction is present in approximately 10 to 15 of cases, usually presenting with facial pain, facial paresthesias, or aseptic meningitis (96,97). Facial nerve involvement, although far less common than trigeminal nerve involvement, has been described and is felt to be an early manifestation of the disorder (98). Although CSF analysis has suggested an inflammatory involvement of
Activity of factors II, VII, IX and X. Common causes of prolonged PT are warfarin, liver disease, and vitamin K deficiency. The APTT detects disorders of the intrinsic pathway, such as, the haemophilias or von Willebrand disease (VWD) though may be normal in some cases of mild haemophilia or VWD. Common acquired causes of prolonged APTT include unfractionated heparin and the presence of a lupus anticoagulant. Unlike unfractionated heparin low molecular weight heparins do not reliably prolong the APTT, and anti-factor Xa assays are required if monitoring is necessary. The most common cause of prolongation of both PT and APTT is disseminated intravascular coagulation (DIC). In DIC, D-dimers are usually raised and, in later stages, fibrinogen levels are reduced. Anyone suspected of a bleeding disorder should be referred to a haematologist for assessment so that screening tests might be performed together with specialised investigations. These tests may include bleeding time and...
However, recent studies have shown that the autoimmunity may be severely aggravated also in the MRL-lpr lpr strain, provided that a lower dose of Hg is administered (Pollard et al., 2005). By use of the AKR strain, which is H-2 congenic with the MRL strains, aggravation of the autoimmune disease was linked to non-MHC genes (Pollard et al., 1999). Studies in the autoimmune-prone BXSB and the nonautoimmune C57BL 6 strains, which share the H-26 haplotype, showed that Hg triggers the Yaa-gene dependent lupus-like autoimmune disease in BXSB mice by aggravating lymphoid hyperplasia, anti-chromatin antibodies, and glomerulonephritis, whereas Hg had little effect on the MHC-congenic C57BL 6J strain, linking the genetic susceptibility for acceleration of autoimmunity by Hg to non-MHC genes also in this disease model (Pollard et al., 2001). Interestingly, a short course of Hg to BXSB mice was sufficient to cause a lifelong increase in the autoimmune response. Furthermore, a dose...
Two other etiologies have to be evaluated. Could this presentation be secondary to an inflammatory cause There was no history or clinical findings consistent with a collagen vascular disease such as systemic lupus erythematosus, which may be associated with coronary artery vasculitis. She was not in the age-range of patients affected by Kawasaki disease (mucocutaneous lymph node syndrome, which is exclusively a pediatric condition), or temporal arteritis (a disease of the elderly, which as a giant cell
Approximately 10 of patients with lupus inhibitors will have antibodies that react with prothrombin. The antibodies do not react with the active site but lead to increased consumption of the molecule. Rarely this may result in bleeding. Patients will have elevated aPTTs that behave like an inhibitor on the 50 50 mix. Factor levels show a low factor VIII. Sometimes testing is indeterminate between a specific factor VIII inhibitor and lupus inhibitor. Levels of factor VIII will increase with dilution of the test plasma in patients with a lupus inhibitor but not with true factor VIII inhibitors. Also, it is rare for patients with lupus inhibitors to have significant bleeding. The strength of the factor VIII inhibitor is reported in Bethesda Units. Due to the complex kinetics, these levels in acquired factor VIII inhibitors are often difficult to measure and interpret.
A pregnant woman with systemic lupus erythematosus who was treated with dalteparin developed HIT at week 25. Her platelet count dropped from 230 to 59 X 10 L, after which she was treated with lepirudin (15 mg sc twice daily), with aPTT and ECT used to monitor her dosage. Following delivery by cesarean section, she experienced no postpartum bleeding complications, and treatment with lepirudin was continued for several weeks thereafter (Huhle et al., 2000b). Another pregnant woman with lupus anticoagulant and HIT was successfully treated for 36 wk with lepirudin.
Totani and co-workers (2001) described an HHV-6-positive interstitial pneumonitis in a 47-year-old woman with Sjoegren's syndrome and Lupus ery-thematosus. Both autoimmune diseases were previously shown to be accompanied by higher incidences of HHV-6 reactivation (Krueger et al., 1991 De Clerck et al., 1992).
Multiple diseases can present with findings similar to those seen with Adamantiades-Behget's disease and should be considered when a patient presents with recurrent oral or genital ulcers, inflammatory eye disease, or other manifestations of vasculitis. Included in the differential diagnosis are systemic lupus erythematosus (Chapter 1), seronegative spondyloarthropathies, inflammatory bowel disease (Crohn's or ulcerative colitis) (Chapter 20), herpes or other viral infections (Chapter 10), other forms of vasculitis (Chapter 8), and inflammatory skin diseases such as pemphigus vulgaris or pemphigoid lesions (Chapter 37). All patients presenting with oral and genital ulcerations should undergo testing for herpes simplex virus using culture or polymerase chain reaction methods, to ensure that viral infection is not present. aFindings applicable only in the absence of other clinical explanations (systemic lupus erythematosus, inflammatory bowel disease, seronegative spondyloarthropathies,...
Immunofluorescence immunofluorescent examinations are required for the diagnosis of chronic blistering diseases and are useful in connective tissue diseases. The site of biopsy is important for immunofluorescence, particularly in the blistering disorders. In dermatitis herpetiformis a biopsy for immunofluorescence should be taken from clinically normal skin away from the area of blistering. In the other blistering disorders, perilesional skin is submitted. The skin should have an intact epidermal dermal junction. In most of the connective tissue disorders lesional skin is submitted for immunofluorescence except for the lupus band test, where normal non-sun-exposed skin is used. Most patients having skin submitted for immunofluorescence should
Acute pericarditis due to infection caused by viruses or bacteria. Viruses include coxsackie B, echoviruses, influenza, mumps and Epstein-Barr virus. Bacterial pericarditis may be due to Staphylococcus aureus, Streptococci or Haemophilus influenza. Tuberculous pericarditis usually becomes chronic. Acute pericarditis can also be secondary to acute rheumatic fever, myocardial infarction, connective tissue disorders such as systemic lupus erythematosus and rheumatoid disease, uraemia, renal transplantation, irradiation or following cardiac trauma.
The indications for screening patients, who present with a first episode of venous thrombosis to identify underlying thrombophilia, are controversial. From a practical viewpoint, screening would be indicated if the results influenced the duration of anti-coagulant therapy or the need for family counseling. The duration of anti-coagulant therapy is influenced by finding deficiencies in anti-thrombin, protein C, or protein S, homozygous factor V Leiden, homozygous prothrombin gene mutation double heterozygosity, and persistently elevated anti-phospholipid antibodies. Family counselling is particularly important for female carriers who are contemplating oestrogen use. Based on these considerations, we think that it is reasonable to perform screening for thrombophilia in the following groups first episode of idiopathic thrombosis at age 50 or younger history of two or more episodes of recurrent thrombosis, especially if the events were unprovoked thrombosis in an unusual site (e.g.,...
Patients with APLA (almost always those with lupus inhibitors) may have an elevated prothrombin time (PT) for two reasons. The APLA may be present in such high titers that they will also interfere with the PT test. Alternatively, 10 of patients with lupus inhibitors will develop non-neutralizing antibodies to prothrombin. This leads to increased clearance of prothrombin from
As reviewed extensively in chapter two, there is unfortunately no one screening test for APLA (Table 19.4) One must perform the entire diagnostic panel on patients suspected of having APLA. A good screen is to perform 1) Anticardiolipin antibodies, 2) dRVVT 3) Lupus Inhibitor Screen (different aPTT reagents). One caveat in testing is that levels of APLA may fall during thrombotic events. Patients with an isolated thrombosis and only low titers of APLA should have the APLA retested in six weeks to ensure these were not transient APLA related to infection. Patients with persistent lupus inhibitors and thrombosis are at very high risk of recurrent events. In general, APLA are significant if they are of medium or high titer
Venous thrombosis was the first described manifestation of APLA and is the one most clinically predominant. Overall, retrospective studies show that 31 of patient with APLA have venous thrombosis. Patients with lupus and APLA have a thrombosis rate of 42 patients with infectious or drug-induced APLA have a thrombosis rate of less than five percent. Patients with APLA are over-represented in young patients with deep vein thrombosis. Prospective studies have demonstrated a relative risk for venous thrombosis of 5.3 for patients with IgG anticardiolipin antibodies. Patients with APLA-associated venous thrombosis may be difficult to treat. These patients have high rates of recurrent thrombosis (20-50 year) if anticoagulation is stopped. Occasional patients may be refractory to warfarin and will need to be on long-term heparin therapy.
HEENT Cornea, sclera, iris lesions, oral ulcers (lupus) jugulovenous distention (cardiac tamponade). Skin Malar rash (butterfly rash), discoid rash (lupus). Differential Diagnosis Idiopathic pericarditis, infectious pericarditis (viral, bacterial, mycoplasmal, mycobacterial), Lyme disease, uremia, neoplasm, connective tissue disease, lupus, rheumatic fever, polymyositis, myxedema, sarcoidosis, post myocardial infarction pericarditis (Dressler's syndrome), drugs (penicillin, isoniazid, procainamide, hydralazine).
1-like domains), which is responsible for cleaving ultralarge vWF multimers released from endothelium. Thus, the pathogenesis of idiopathic (primary) TTP likely reflects the formation of arteriolar-occluding complexes of ultralarge vWF multimers and platelets, thereby explaining both the thrombocytopenia and the tissue ischemia. Secondary TTP has been reported to occur in association with pregnancy, certain drugs (e.g., ticlopidine, clopidogrel, quinine, cyclosporine, mitomycin), autoimmune disorders (systemic lupus erythematosus), organ transplantation, and infections (human immunodeficiency virus, bacterial endocarditis). TTP clinically resembles a nephrotropic microangiopathic hemolytic anemia known as hemolytic uremic syndrome (HUS) however, there are certain unique triggers of HUS (especially, preceding infection with E. coli H0157) and anti-ADAMTS13 autoantibodies are not detected in HUS.
Persistent HHV-6 may cause functional disturbances of the immune system as indicated by elevated antibody titers against HHV-6 in allergies, drug-induced hypersensitivity reactions and in systemic lupus erythematosus, Sjogren's syndrome and progressive systemic sclerosis (Krueger et al., 1991, 1994b De Clerck et al., 1992 Klueppelberg, 1994 Lasch et al., 1996 Descamps et al., 1997, 2001 Toh-yama et al., 1998 Conilleau et al., 1999). Virus persistence may constitute a risk factor for additional immune dysregulation and for increasing the severity of adverse reactions (Suzuki et al., 1998).
Once HSP appear on the cell surface, they are accessible to the immune surveillance system. HSP expressed on cell surfaces can elicit strong immune responses, as these molecules contain several highly conserved epitope sequences with strong immunogenic properties (Kaufmann and Schoel, 1994 Shinnick, 1991 Zugel and Kaufmann, 1999). On the other hand, an overzealous immune response to HSP can have several undesirable effects. Due to high degree of phylogenic conservation, HSP species of microbial origin and HSP molecules produced by stressed host cells have similar immunogenic properties (Zugel and Kaufmann, 1999). Moreover, abundantly expressed HSP undergo processing by antigen presenting cells, and cells expressing HSP alone or presenting them in the context of MHC molecules are recognized by immune cells as potential targets of self-reactive antibodies or lymphocytes with specificity for HSP (Kaufmann and Schoel, 1994 Zugel and Kaufmann, 1999). In a number of autoimmune disorders in...
No benefit has been demonstrated for umbilical artery velocimetry for conditions other than suspected intrauterine growth restriction, such as postterm gestation, diabetes mellitus, systemic lupus erythematosus, or antiphospholipid syndrome. Doppler ultrasonography has not been shown to be of value as a screening test for detecting fetal compromise in the general obstetric population.
The connective tissue disorders or diseases comprise three distinct conditions, namely systemic lupus erythematosus, systemic sclerosis and polymyositis dermatomyositis (Fig 28.1). 1 Mixed connective tissue disorder is that disease which includes features of all three disorders and is sometimes referred to as 'overlap' syndrome. Common features include
This is an acquired condition, sometimes associated with systemic lupus erythematosus or other autoimmune diseases in its secondary form. Lupus anti-coagulant and anti-cardiolipin antibodies together form the anti-phospholipid antibody family.41 The prevalence of anti-phospholipid antibodies in patients with VTE ranges from 5 to 15 , while the prevalence in the general population is not well established.42,43 Clinically, individuals with this acquired throm-bophilic state may develop venous or arterial thrombosis and recurrent foetal loss. Placental insufficiency is thought to be the cause of the obstetric complications.42,43 It has been shown that the thrombotic risk in individuals with this abnormality is increased 9-fold, and the probability of recurrence may be higher.44
There is evidence that the immune response induced by protein-drug conjugates can lead to autoimmunity against the native proteins. Drug-induced (e.g., hydralazine, qui-nidine, or isoniazid) systemic lupus erythematosus is associated with the development of auto-antibodies, particularly antinuclear antibody (24). As a result, the manifestations of the disease can continue even after withdrawal of the offending drug.
Positive antiphospholipid antibody test or lupus inhibitor test that is persistent when tested at least 6 weeks apart with at least one clinical feature Lupus anticoagulant and lupus inhibitor are terms which are interchangeable. Lupus inhibitor is an APLA in which the antibody is detected by a coagulation test.
Pathogenesis of the hypercoagulable state in nephrotic syndrome is urinary loss of natural anticoagulants. Low levels of both antithrombin and protein S are commonly seen. The presence of concurrent autoimmune diseases such as lupus may add associated antiphospholipid antibodies to the mix. The hypercoagulable state seen in other renal disease is less well defined. Plasma homocysteine levels are markedly elevated in renal failure and this may play a causative role in the thrombosis.
Isolated elevations of the PT are indicative of an isolated factor VII deficiency. Isolated elevations of the aPTT are typically due to heparin contamination, lupus inhibitors, isolated defects ofVIII, IX, XI, or the contact pathway. Mixing studies can provide information to narrow the list of possible diagnoses. Prolongation of both the PT and aPTT suggests multiple defects or deficiency of factors II, V, or X. Marked prolongation of the PT and aPTT can also be seen with low levels of fibrinogen ( 50 mg dl).
Factor VIII, IX, XI deficiencies are associated with an increased aPTT and bleeding. Factor VIII and IX deficiency will present as classic hemophilia. Factor XI deficiency has more variable bleeding tendencies and often is associated with post-surgical bleeding. Acquired factor inhibitors will present often with a sudden onset of bleeding. Factor XII and contact protein deficiencies do not have associated bleeding. Patients with lupus inhibitors rarely bleed. Some patients with APLA will have bleeding if they have associated prothrombin deficiency. The laboratory clue is that they will also have an elevated PT-INR. The rare factors X, V and II deficiencies have both an elevated PT-INR and aPTT. More common etiologies are multiple deficiencies due to liver disease, vitamin K deficiency or disseminated intravascular coagulation. Lupus inhibitors with associated anti-prothrombin antibodies can also present with both tests elevated. Not bleeding Lupus inhibitor, factor XII deficiency...
The most well-studied autoimmune-prone model examining the impact of CR on immune function is the autoimmune-prone (NZBxNZW)F1 (B W) mouse. This model is especially valuable since multiple organs have been examined, such as spleen, kidney, mesenteric lymph nodes, peripheral blood, and submandibular glands. The B W mouse is a good model to study the human disease Systemic Lupus Erythematosis. As in humans, autoantibodies can be found in young adult B W mice prior to the detection of clinical disease. The B W mice die from autoimmune renal disease (i.e., nephritis), which can be monitored by measuring proteinurea, at approximately 10 to 12 months of age. Feeding the B W mouse a 40 CR diet beginning at six weeks of age delayed autoimmune kidney disease by 30 (Jolly, 2004). The life span of the B W mice could be doubled when the corn oil (CO) based CR diet was substituted with fish oil (FO) (Jolly et al., 2001). It is equally important to note that CR typically does not impact T cell...
In an alternative and intriguing test of the GRP94 cross-presentation hypothesis, the Li laboratory created a transgenic mouse expressing a cell surface form of GRP94 (Liu et al., 2003). These mice were shown to display lupus-like, systemic inflammatory symptoms that correlated with the constitutive activation of dendritic cell function. Interestingly, if dendritic cells from the cell surface GRP94-transgenic mice were adoptively transferred to a mouse of the parent strain, they then display symptoms of chronic systemic inflammation. However, when such dendritic cells were adoptively transferred to MyD88 knock-out mice, no response was seen. Conversely, when MyD88- - dendritic cells were adoptively transferred to the cell surface GRP94-transgenic mice, autoimmune symptoms were observed to resolve (Liu et al., 2003). These data favor the argument that GRP94 is acting principally as an immunological adjuvant, rather than as a cross-presentation antigen and implicate potential signaling...
Known mechanisms can involve antibody responses to cell surface or matrix components, for example in Goodpasture's syndrome, where the autoantigen is part of the basement membrane. This disease is organ-specific. In other cases, such as systemic lupus erythematosus (SLE), the disease is systemic and multiple tissues and organs may be affected. Immune complexes are thought to play a major role in the pathology of systemic autoimmune disease. A third group of diseases is characterized by T cell destruction of tissues and associated activated cells. This type includes T1D and RA. The classification of autoimmune diseases as organ specific or systemic reflects the underlying etiology. In some families with organ-specific disease several family members may be affected but with different organs involved. Similarly, systemic autoimmunity can affect multiple individuals in a family or a single individual can have more than one systemic condition, such as SLE together with Sjogren's syndrome.
EC-reactive antibodies have been found in patients suffering from disorders characterized by vasculitis or thrombosis (for review see Praprotnik et al., 2001a Meroni et al., 2005). The best-studied example is allograft rejection, a setting in which there is extensive evidence for AECA, in part directed at carbohydrate antigens that regulate procoagulant activity in vitro (Saadi and Platt, 1995 Diujvestijn et al., 2000). AECA have also been identified in patients with hyper-acute and acute graft rejection, systemic lupus erythematosus (Constans et al., 2003), antiphospholipid antibody syndrome (Cesarman-Maus et al., 2006), and thrombotic thrombocytopenic purpura (Praprotnik et al., 2001b). What is curious is the extraordinary diversity of the clinical syndromes associated with AECA. Also of interest, the target cells used in most assays (i.e., ECs derived from human umbilical vein HUVEC ), are not known to be affected by immune vascular injury in the clinical setting. This suggests...
Approximately 30-50 of patients with SLE will have APLA. The antibodies can also be found in patients with other autoimmune diseases. Patients without lupus or other autoimmune disease can have symptomatic APLA ( Primary APLA Syndrome ). Children will often develop transient non-thrombotic APLA after viral infections. This laboratory finding often comes to attention during pre-operative evaluation for tonsillectomy. Up to 30 of patients with HIV infection will also develop APLA. The infection-associated APLA are not associated with thrombosis and are usually Anti-p2GP negative. Medication may also induce APLA. Chlorpro-mazine is the most common cause, but APLA has also been associated with use of procainamide, dilantin and quinidine. In screening studies of blood donors and normal controls, up to 10-20 of asymptomatic people have APLA. However, the APLA in these people are usually low-titer and most often occurs in young women.
The existence of autoimmune diseases, however, perhaps weakens this idea to some extent. Human examples of autoimmunity include many life-threatening diseases type 1 (juvenile) diabetes mellitus in which the host destroys its own pancreas, the nerve demyelination disease multiple sclerosis, systemic lupus erythe-matosus, which attacks a variety of organs, and many others. However, these may not simply reflect aberrant anti-self attack, because there is some evidence that they occur with various epidemic patterns in populations, including after the host has experienced an infection. An idea has been that some infections can closely mimic self antigens and the similarity triggers an autoimmune reaction as a consequence of an attack on the infectious agent. In any case, the mechanism by which purging of self-recognition molecules is controlled, once thought to be known, seems now not to be so well understood.
Children with Evans syndrome often have complex immunodeficiencies. In adults, Evans syndrome most often complicates other autoimmune diseases such as lupus. There are increasing reports of Evans sydrome occurring as a complication of T-cell lymphomas. Often the autoimmune disease can predate the lymphoma diagnosis by months or even years.
Patients with lupus inhibitors who require heparin are difficult to monitor since their aPTTs are already prolonged. One option is to use LMW heparin due to its predictable dosing. The other choice is to directly assay for heparin by measuring its ability to inhibit factor Xa. This assay is insensitive to lupus inhibitors. Therapeutic range for standard heparin is 0.35 - 0.7 anti-Xa units. Heparin assays are also valuable in patients where an acute-phase inflammatory process may lead to nonspecific heparin binding to inflammatory proteins, resulting in the aPTT not reflecting he-parin levels. This can be seen in patients on cyclosporin. In pregnant women the acute rise in factor VIII may also lead to a misleading aPTT thus, one should use heparin levels to guide therapy in those patients even with prophylactic doses of standard heparin.
The definition of leukoplakia, according to the WHO, is the following A predominantly white lesion of the oral mucosa that cannot be characterized as any other definable lesion 11 . As such, leukoplakia is a descriptive, clinical term and a diagnosis of exclusion, not a pathological term. This appearance reflects changes in the thickness and or composition of the epithelium (such as increased keratiniza-tion and parakeratosis) and or in the lamina propria (such as fibrosis), altering its translucence. Lesions as heterogeneous as candidiasis, discoid lupus, carcinoma in situ, and invasive squamous cell carcinoma may all appear clinically as a white patch (Table 4.4). Thus, leukoplakia is a clinical diagnosis, whose true nature can only be unveiled by histological examination. The distinguishing feature of those leukoplakias that are truly preneoplastic, which is but a small subset of all clinically diagnosed leukoplakias, is the occurrence of dysplasia 11 . Discoid lupus
Canis lupus Canis lupus Linnaeus, 1758, Sweden. Twenty-six races are recognized. The largest races live exclusively on large ungulates while the smallest are from the desert regions. Two genetically distinct stocks appear to occur in North America, with wolves in the western part of the continent perhaps representing a separate colonization from Eurasia. Canis lupus H Canis simensis H Chrysocyon brachyurus
Heparin-induced thrombocytopenia (HIT) is caused by heparin-dependent antibodies that usually recognize multimolecular complexes of platelet factor 4-heparin (PF4-H). HIT can be viewed as a clinicopathologic syndrome (Warkentin et al., 1998). Thus, a diagnosis of HIT should be based on two criteria (1) clinically evident abnormalities, most commonly thrombocytopenia with or without thrombosis (see Chapter 2), and (2) detection of HIT antibodies. In some ways, HIT resembles another clinicopathologic disorder, the antiphospholipid (lupus anticoagulant) syndrome (Table 1).
Conditions such as systemic lupus erythematosus, systemic sclerosis, and insulin autoimmune syndrome (Ito et al., 1993 Crow et al., 1994 Kuwana et al., 1995a). In both lupus and scleroderma, T-helper cells mediate antigen-specific autoanti-body production by B cells (Adams et al., 1991 Mohan et al., 1993 Kuwana et al., 1995b).
This 20 year old Caucasian woman, diagnosed at 8 years of age with systemic lupus erythematosus (SLE), presented to the hospital with a one month history of non-traumatic low back pain. She was significantly incapacitated and required crutches for ambulation. The pain had a sudden onset and woke her up from her sleep. There was no history of recent changes in her urinary or gastrointestinal functions. Prior to admission, she had been seen by a physician who prescribed ibuprofen (400 mg q6h), but with no relief. Other medications at the time of admission were prednisolone (60 mg day) and furosemide (20 mg QD). She had increased her steroid dose on her own because of worsening arthralgias. She had not visited her rheumatologist for a considerable period of time and admitted poor compliance regarding scheduled medical appointments. Her knowledge of her medical condition was limited. The initial presentation during childhood was that of epistaxis secondary to thrombocytopenia. She had...
Precipitating Factors Alcohol, gallstones, trauma, postoperative pancreatitis, retrograde cholangiopancreatography, hypertriglyceridemia, hypercalcemia, renal failure, Coxsackie virus or mumps infection, mycoplasma infection. Lupus, vasculitis, penetration of peptic ulcer, scorpion stings, tumor.
F1 hybrids have one great advantage over pure inbred strains they are much more robust. They tend to live longer, have fewer of the idiosyncrasies of the parental strains, and are less sensitive to adverse environmental conditions than inbred strains. They are particularly valuable as foster mothers in the production of transgenic strains. However, they should be used with caution in experiments involving breeding, as their offspring will be genetically segregating for the gene loci, which differ in the parental strains. Sometimes, they also have useful characteristics not normally found in the parental strains. For example, the NZBNZWF1 is widely studied as a model of autoimmune systemic lupus erythematosus, which is not found in the parental strains.39 They can be of some value in immunological studies, as they will accept tissue, organ, tumor, or cell grafts from either of the parental strains without immuno-logical rejection. One possible disadvantage of F1 hybrids is that they...
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