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Therefore gastritis diet àâòîðèà proven 10mg rabeprazole, the use of specific antibodies enable the detection of pathogen-specific antigens and gastritis diet 3121 purchase rabeprazole on line, consequently gastritis diet 5 2 purchase rabeprazole pills in toronto, the direct detection of pathogens mild gastritis symptoms treatment order 10 mg rabeprazole otc. In the same respect, when pathogen-specific antigens are used, the pathogen can be detected based on the immune response specifically directed at it. On the other hand, individuals are considered non-reactive or seronegative when neither pathogen-specific antigens, nor a pathogen-specific immune response can be detected. The immune system of immunologically health individuals stores every significant incident of contact with immunologically relevant pathogen antigens in the organism’s immunological memory. Thus, contact with most pathogens can be detected months or even years later as evidenced by a specific immune response. Thus, contact with other, non detectable pathogens and pathogens that are difficult to cultivate or cannot be cultivated can be 13 detected. An organism’s antibody response functions as an amplifier after it has come into contact with even a tiny amount of pathogenic and non-pathogenic microorganism. At the same time, it becomes evident that serological testing for infectious diseases requires an immune system response in order to achieve diagnostic detection, at least when detecting pathogen specific antibodies. The specific immune response frequently correlates to the incubation period of the infection and the type of pathogen, however it also depends on the individual’s own immunology. Depending on the length of incubation time, diagnostic antibody reactions can also be negative in the early phase of an infection due to a delayed immune response. At the same time, a persisting immunological antibody response in the low reactive range, which can be diagnostically detected for months or even years after an acute infection, is not evidence per se of a current infection. On the one hand, it is not possible to make a diagnosis during the acute stage of an infection because there is a delayed immune response. On the other hand, no clear statement can be made as to whether the detected antibodies are a result of an acute infection or an infection that happened a while back since, in the case of many diseases, antibodies persist long after an infection occurs. The same holds true for pathogen-specific antigen detection in different bodily fluids. In this case the kinetics of the diagnostically useable antigens also crucially depends on the pathogen, the length of the infection and the type of testing material. As with pathogen-specific antibody detection, antigen detection in the early stage of an infection can be negative or can remain positive for days or weeks (in certain circumstances for months) following a healed or adequately treated infection. For a clinically sound and diagnostically accurate interpretation of pathogen-specific antigen or antibody detection there needs to be a fundamental understanding in everyday clinical practice of serological and immunological correlations and the varying pathogen-specific kinetics of humoral immunity. These usually include proteins, lipoproteins and polysaccharides, less commonly lipids or nucleic acids. In the case of whole-cell antigens, a distinction should be made with regard to so-called haptens. Haptens are unable to trigger a targeted immune response due to their low molecular size. Instead, they become immunologically effective after binding to the carrier substances, preferably proteins. The parts of the antigen that determine the specific immune response are called epitopes. They are responsible for binding to the specific antibodies directed against them in line with the lock and key principle. Epitopes are usually made up of segments of around 6 – 8 amino acids or polysaccharides. Synthesis occurs in plasma cells that are produced from clonally expanding B lymphocytes after antigen contact. Plasma cells are responsible for the monoclonal, class-specific and antigen-specific production of antibodies. Even when there is no longer any antigen stimulus, the production of specific antibodies can continue for months or even years thanks to memory cells which can be stimulated into producing an intensified immune response (secondary response) based on a renewed rapid clonal expansion after repeated contact with the antigen. All classes of antibodies (IgG, IgA, IgM, IgD and IgE) are made up of two identically heavy chains and two identically light chains. Light and heavy chains are individually present in two and five varieties respectively. At the molecular level, the variable region of the light and heavy chains are equipped with specific bonding sites for the immunologically recognized epitopes of the respective antigens. The molecular weights of the antibody classes fluctuate between 150 kD for IgG and 970 kD for the pentamer-shaped IgM (10% of the entire serum immunoglobulin). IgM is typically the carrier of the early immune response, while IgG is the carrier of the late immune response or the secondary response. The immunoglobulin classes IgD and IgE act as membrane receptors on B cells or mast cells, eosinophils and basophils. It is the main carrier of humoral immunity in mucosal secretions and bodily fluids. In the serum of healthy individuals, IgG constitutes 70 – 75% of the total amount of immunoglobulin. As the carrier of the secondary immune response, it is the most important antibody in terms of its protective function (Table 1). Though rarely relevant from a diagnostic perspective, IgG can be divided into various subclasses (IgG 1 – 4) that perform different tasks. In terms of the serological diagnosis of infectious diseases, these subclasses play a particular role with regard to complement activation and in terms of their proportional distribution pattern in serum. Accordingly, antibody deficiency syndrome or even IgG subclass defects can lead to a reduction in the informative value of diagnostic detection reactions. The same applies to potentially acquired, genetically determined defects at the B cell level. Usually the antibodies that have formed as part of a specific immune reaction to an antigen are polyclonal, i. Monoclonal antibodies, on the other hand, are antibodies that are produced from a clonally generated B cell line and are completely identical. These types of antibodies are mostly produced for industrial or research purposes and play a crucial role in serologically diagnosing infectious diseases and in treatment. IgG IgA IgM IgD IgE Heavy chains 1, 2, 3, 4 1, 2 µ Light chains,,,,, Molecular mass (kD) 150 150, 380 970 180 190 Serum concentration mg/100 mL 1300 350 150 3 0. Every clone develops specific receptors depending on the individual specificity of the recognized epitope. Prolonged antigen contact leads to consecutive clonal expansion of the initial cell as a result of continuous stimulation. The various stimulated B cell clones continuously compete for the antigens which are specific stimulants that further specialize and specify the antibody response. Once the antigen stimulus has been removed, the expansion process slows down, usually at a constant pace. These cells produce a much stronger secondary response when there is renewed exposure to the same antigen. After exposure to the antigen, antibodies increase in the serum within the first 10 days. This is called the primary response and is mainly borne by specific IgM antibodies. When the antigen stimulus persists, this development is followed by a rapid increase in specific IgG antibodies, whose numbers peak weeks or, under certain circumstances, even months after the primary contact with the antigen. At the same time, other classes of specific antibodies (IgA, IgD or IgE) may form depending on the antigen trigger. While IgD antibodies play no significant role diagnostically, antibodies from the subclasses IgA and IgE play a significant diagnostic role in certain instances. Once the antigen stimulus has been removed, the concentration of specific antibodies decreases continuously for months or even years. When the triggering antigen is reencountered, a rapid and sufficient secondary response is produced by the remaining memory cells in which the immunity is stored. Even though the kinetics of the specific antibody response exhibits a regular progression in principle, this can vary widely depending on the triggering epitope, the pathogen behind the infection, the length of incubation time, and the entry point of the infection. In principle, the immune response of virological infections proceeds in a relatively orderly fashion characterized by regular kinetics and a typical IgM/IgG switch as an expression of a new infection, or diminishing or a past infection. On the other hand, many bacterial, fungal and parasitic infectious agents are less regular in terms of the progression and kinetics of the antigen and antibody-related class-specific immune response. In these cases it can take a month for seroconversion to occur after an infection. This makes it more difficult to interpret the results of the serological test when the clinic is unaware of this fact. The same applies to the long-term excretion of specific antigens as part of a diminishing or treated infection.
It may be asymptomatic or it may present with urinary tract infection or occasion ally with bladder outow obstruction gastritis or appendicitis cheap 10 mg rabeprazole mastercard. It is managed by endoscopic incision or ureterocele excision with ureteric reimplantation gastritis cure order rabeprazole mastercard. Anomalies of bladder compartmentalization – duplication of bladder gastritis diet ãîî rabeprazole 10 mg low price, septate bladder sample gastritis diet cheap 20mg rabeprazole free shipping, hourglass bladder, and bladder diverticulae 3. Megacystis – congenital megacystis, megacystis-megaureter syndrome, and megacystis-microcolon-hypoperistalsis syndrome 4. Urachal abnormalities – patent urachus, urachal cyst, urachal sinus, and ura chal diverticulum 5. Clinical presentation ranges from a stillborn to urinary incontinence, hydronephrosis or renal dysplasia, urinary tract infections, and renal fail ure. Exposure of the bladder mucosa to air results in inammation and poly poid appearance. In epispadias the bladder is closed and the urethral plate remains open and anteriorly displaced. The urethral meatus in most patients with epispadias is at the penopubic junction. Vesicoureteral reux occurs because the ureters enter the bladder with almost no tunnel. Clinical Presentations Prenatal ultrasound ndings in bladder exstrophy are absence of bladder lling, low-set umbilicus, widened pubis rami, and diminutive genitalia. Anterior abdominal mass suggests bladder exstrophy, omphalocele, or gastroschisis. After birth – obvious exposed bladder with associated abnormalities in the abdo men and perineum, the urinary tract, the genitalia, and the bony pelvis. Immediate Management the umbilical cord is preferably tied with 2-0 silk close to the abdominal wall so that the umbilical clamp does not traumatize the delicate bladder mucosa. The blad der can be covered with a nonadherent lm of plastic wrap to prevent sticking of the bladder mucosa to diapers. The plastic wrap is regularly changed and the bladder surface is irrigated with saline. Management • Objectives: (1) secure abdominal wall closure, (2) urinary continence, (3) preserving renal function, and (4) creation of functionally and cosmetically acceptable external genitalia. Staged approach includes bladder and posterior urethral closure shortly after birth. Successful initial bladder closure is an important factor for achieving continence. Recent series have shown improved rates of renal preservation (80–87 %) compared to older series where intestinal augmentation or ureterosigmoidostomy was employed. Longitudinal evaluation that includes serial renal nuclear scans and ultrasounds, and renal functional studies are essential part of follow-up in bladder exstrophy patient. Infertility may be due to retrograde ejaculation or duct obstruction from scarring. Substantially higher fertility rates have been achieved in female following reconstruction after reconstruction than in males. The urethral meatus opens on the ventral (under) side of the penis proximal to the tip of the glans penis. Classi cation According to meatal location: (1) glandular – opening on the ventral aspect of the glans penis, (2) coronal – opening at the coronal sulcus, (3) penile shaft, (4) penos crotal, and (5) perineal About 70 % of all cases of hypospadias are distal penile or coronal. Clinical Findings • Hooded appearance of the penis, caused by decient or absent ventral foreskin. Hypospadias with bilaterally non-palpable testes needs urgent work-up to rule out masculinized female with congenital adrenal hyperplasia. Work-up includes abdominal and pelvis ultrasound, karyotyping, genitogram, urethroscopy, and cystoscopy. Management Newborns with hypospadias should not be circumcised, because the preputial skin may be useful for future reconstruction. Surgical repair is preferred between 6 and 18 months of age for psychological reasons. Surgical reconstruction aims at achieving a straight penis and creation of a normally located cosmetically acceptable urethral meatus. Prognosis After corrective surgery, most patients are able to void in the standing position as well as to deposit semen into the vagina. Findings – posterior urethral dilatation, trabeculated bladder, and vesicoureteric reux. An infant feeding tube is preferred over a Foley catheter (balloon can fall back into the dilated posterior urethra). The valves can be incised at the 12, 5, and 7 o’clock positions with either a cold knife or electrocautery. Options include percutaneous placement of a vesicoamniotic shunt, open fetal surgery, and fetal cystoscopic ablation. Signicant complications may occur, resulting in maternal or fetal morbidity as well as fetal loss. Rapid worsening of renal functions may occur at the time of puberty due to the increased meta bolic workload placed on the kidneys during that time. Beyond 1–2 years, there is female preponderance with male to female ratio of 1:10. However, existing challenges and priorities in regions with limited resources, such as easy access to medical care and advanced diagnostic technologies, make it difcult for clinicians in emerging countries to abide by western protocols. A needs based approach prevails taking into account the lack of follow-up, equipment and trained personnel as well as medical insurance. Hematogenous spread is common in newborns and infants in contrast to ascend ing infection in older children. The urine sample needs to be appropriately collected and evaluated for bacterial growth (Table 6. Yes bObtain urine for urinalysis and culture via age appropriate sample Treat with ampiric antibiotics according to local sensitivity patterns. Oral or Parenteral Are both urinalysis and cultutre No Discontinue antibiotics and positive The majority of recurrences will occur within the rst 12 months after the primary infection. Adequately powered, well-designed, placebo-con trolled trials of long-term antibiotics for the prevention of urinary tract infection in children are lacking. The wide-spread clinical practice of routine antimicro bial prophylaxis is now being questioned. Early diagnosis and prompt treatment of urinary tract infection and predisposing factors are likely to go a long way towards preventing long-term renal damage. Guidelines from the American Academy of Pediatrics, American Urological Association, and Swedish Medical Research Council rec ommend using long-term antibiotic prophylaxis (Table 6. Chemoprophylaxis in antenatal hydronephrosis: All infants diagnosed with (higher grade) antenatal hydronephrosis should receive antibiotic prophylaxis until they are further evaluated with imaging studies. Change of the prophhylactic antibiotic after breakthrough infection is not usually required. There is no role for “cyclic” therapy, where the antibiotic used for prophylaxis is changed every 6–8 weeks. Patients suffering breakthrough infections may benet from double prophylaxis with cotrimoxazole and nitrofurantoin. Children with renal scarring should receive continued care once or twice a year through adulthood. However, genetic factors, the social environment, deprivation, and lack of access to qualied renal care may be the more important determinants of adverse renal outcome. Look for a palpable bladder, kidneys, perineal sensations, urine stream, anal reex, gait, high-arched feet, hammer toes, limb length discrepancy, deep tendon reexes and tone of lower limbs, and hypertension. Physical examination A critical point to remember is that the level of the vertebral defect cannot be reliably used to predict the degree of neurological impairment Emphasis placed on tone and function of abdominal wall, lower extremities, and anal sphincter the presence or absence of the bulbocavernosus reex should be noted Abdominal exam to assess for bladder distension and renal size Attempt to characterize voiding pattern: Stream with dry intervals Continuous dribbling 2. Laboratory investigation Serum electrolytes Blood urea nitrogen and creatinine Creatinine reects that of the mother initially and should be repeated in a few days Urinalysis 3.
Less common than prostatitis or epididymitis and usually caused by a viral infection gastritis colitis diet order 20 mg rabeprazole fast delivery. Fever (temperature greater than 38°C) gastritis diet 4 idiots order genuine rabeprazole, chills gastritis buy rabeprazole no prescription, ank pain chronic gastritis outcome buy rabeprazole online now, costo vertebral-angle tenderness, and nausea or vomiting, with or without symptoms of cystitis (see Chapter 30 for details). The history should focus on the timing of events, risk factors, comorbid condi tions, medication allergies, and recent antimicrobial therapy. Urethritis may have indolent onset, occur intermittently, and may be most noticeable in the morning with rst micturition; however, cystitis generally has a more acute onset. Pyelonephritis tends to also have an acute onset but patients may or may not recall preceding lower urinary tract symptoms. Urethritis may demonstrate as vaginal discharge in women and a visible penile urethral discharge in men. An enlarged or slightly boggy prostate is nonspe cic; however, a swollen, rm, and exquisitely tender prostate is associated with acute prostatitis. Microscopic examination of urine showing at least 10 white blood cells per cubic millimeter is considered signicant pyuria. Hematuria (the presence of blood in the urine) is also commonly associated with cystitis. Positive culture result indicating signicant bacteriuria is tra ditionally dened as 105 colony-forming units per milliliter. Women with cys titis frequently have lower colony counts (102–104 colony-forming units per milliliter); therefore, in this clinical setting, urine culture generally does not add diagnostic accuracy but is helpful for the correct identication of the pathogen and determination of antimicrobial susceptibility. The vulva and glans penis should be cleaned by using three swabs with soap and sterile water. The rst 10 mL of urine should be collected in a separate container or discarded as this represents the urethral urine. The midstream sample should be collected in a sterile container and trans ported to the laboratory immediately. Storage of a urine sample at room temperature for more than 2 hours results in signicant increases in bacterial counts resulting in an unreliable sample. In the evaluation of prostatitis, quantitative cul tures of urine samples obtained before and after prostate massage can be helpful in isolating a particular pathogen. The glans penis should be cleaned by using three swabs with soap and sterile water. The rst 10 to 20 mL of urine should be collected in a separate container or discarded as this represents the urethral urine. Prostatitis is suggested by more than 15 white blood cells per high-power eld on microscopic examination. Useful to detect urinary calculi, calcication, soft tissue masses, and abnormal gas patterns. Allows characterization of size and contour of kidneys and bladder, identication of renal mass or abscess, visualization of certain calculi, and discernment of hydronephrosis. Offers ne anatomic detail and can evaluate focal nephritis, renal or perirenal abscesses, and masses as well as both radiopaque and radiolucent calculi; however, caution must be used because renal injury may be aggravated by intravenous contrast material. In randomized, controlled trials, placebo groups have spontaneous resolution of symptoms in 25% to 42% of women; therefore, antibiotic therapy is not mandatory but is generally prescribed to limit morbidity and speedy reso lution of symptoms. Ciprooxacin 250 mg twice daily (or 500 mg extended release once daily) for 3 days (only if other options cannot be used). Acute prostatitis can be treated with agents appropriate for cystitis, pending results from urine culture to guide therapy. Cases of chronic prostatis may require 4 to 6 weeks of oral uoroquinolones therapy. Symptomatic improvement should be seen in 3 days; however, if no response, reevaluation is indicated. Viral orchitis resolves within 2 weeks in most cases; however, antimi crobial treatment of bacterial orchitis should be based on culture results with the duration dictated by resolution of symptoms. In the case of empiric therapy failing in the setting of cystitis, midstream urine collection should be sent for culture and sensitivity testing to identify the appro priate organism. Negative routine cultures with recurrent or persistent cystitis symptoms should raise concern for mycobacterial infection, or noninfectious causes of cystitis, such as malignancy or interstitial cystitis. Women who have recurrent cystitis without evidence of the aforementioned complications (malignancy, mycobacterial infection, interstitial cystitis) may be candidates for prophylaxis, or self-treatment. With the exception of topical estrogen therapy in postmenopausal women, cranberry juice and D-mannose (bacterial adhesion blocker) have no proven role in reducing recurrent cystitis. Additionally, behavioral modications with liberal uid intake, immediate postcoital urination, elimination of douching and form-tting 29. In general, a 6-month trial is provided with daily bedtime dosing of the following agents: 1. Nitrofurantoin 50 to 100 mg (long-term continuous exposure with this agent can be associated with pulmonary hypersensitivity, hepatitis, and peripheral neuropathy) 2. International clinical practice guidelines for the treatment of acute uncomplicated cystitis and pyelonephritis in women: a 2010 update by the Infectious Diseases Society of America and the European Society for Microbiology and Infectious Diseases. An inammatory process of the upper urinary tract system, speci cally the renal parenchyma. Pyelonephritis can be classied according to the chronicity and/or complexity of clinical presentation. This is an acute inammatory process of the renal parenchyma most commonly as the result of a bacterial infection. Acute pyelonephritis can also be further classied by the complexity of the clinical presentation: a. This is typically dened as acute pyelonephritis involving a typical bacteria and a healthy immune-compe tent patient with normal renal function and urinary tract anatomy. This is typically dened as acute pyelonephritis involving a patient at the extremes of age (less than 5 years or greater than 65 years), an atypical bacterium. This condition would be considered as a complicated pyelonephritis and can be associated with renal scarring and systemic hypertension, most commonly in children. This is the most common mechanism and results from the migration of bacteria from lower urinary tract upward to the kidneys. Infection of the kidney resulting from seeding of circulating bacteremia, from a distant site of infection. While considered unusual, lymphatic connections between the ureters and kidneys may contribute to the development of increased bladder pressures and increased lymphatic ow directed to the kidney, which may lead to the development of ascending infections. Similar to cystitis, or lower urinary tract infection, risk factors (see Chapter 29, Urinary Tract Infections) include: 1. Sexual intercourse (homosexuality and anorectal intercourse are also a risk factor for men) 2. New sexual partner within the past year (vaginal colonization with typical pathogens) 3. Renal transplantation (most commonly occurs within 60 days after transplant as a result of immunosuppression and surgical vesicular–ureteral reux) 10. Consists mainly of Enterobacteriaceae bacteria with Escherichia coli as the most common infecting organism (80%); others include Klebsiella pneumoniae and Proteus mirabilis. Pseudomonas spp can rarely cause pyelonephritis but are commonly associated with urinary tract instrumentation or surgical procedures. May include Staphylococcus saprophyticus, Entero coccus faecalis, and Streptococcus agalactiae (group B streptococci). Most commonly results from dissemination from a primary site of infection such as the lung or gastrointestinal tract (see Chapter 14, Tuberculosis). Symptoms and signs of pyelone phritis can vary based on patient age and comorbid conditions, and the clinical presentation can range from a silent illness. Patients may already have an established diagnosis of acute cysti this with dysuria (burning or pain on urination), frequency (frequent voiding of small volumes), urgency (sudden urge to void), suprapubic or lower abdominal pain, and hematuria; however, patients with pyelonephritis may also experience the additional following symptoms: 1. Fever (temperature greater than 38°C): may be the most reliable nding to differentiate an upper urinary tract infection 2. A complete and chronologically accurate history should be obtained in all patients suspected of an upper urinary tract infection. Pyelonephritis should be included in the differential diagnosis of any patient who has a fever, especially when associated with symptoms of dysuria, frequency, urgency, and/or back or ank discomfort. The history should focus on the timing of events, risk factors, comorbid conditions, medication allergies, and recent antimicrobial therapy.
These studies suggest that multiple mechanisms or genetic factors may be involved in the disease process gastritis diet questionnaire rabeprazole 10 mg on-line. In support of this gastritis symptoms when pregnancy purchase rabeprazole 10mg mastercard, two studies using the National Academy of Sciences – National Research Council twin registry in the United States concluded that there was genetic predisposition to gastritis diet øàðèêè discount 10 mg rabeprazole with amex organ-specific complications of alcoholism based on the significant concordance rates in monozygotic twins (Hrubec & Omenn gastritis diet ppt discount 20mg rabeprazole otc, 1981; Reed et al. Gene polymorphisms encoding for the enzymes responsible for ethanol metabolism, oxidative stress, and proinflammatory/immune responses have been investi gated (Bataller et al. A genetic analysis of individuals participating in a study evaluating liver disease in northern Italy suggested that heavy drinkers with cirrhosis or alcoholic liver disease had a higher frequency (0. A study in alcoholic patients in Japan reported an increase in the frequency of individuals homozygous for the C1 allele in men with alcoholic cirrhosis (Yamauchi et al. In contrast, there was no difference in either C1 or C2 allelic distribution in an earlier study conducted in Caucasian men (Carr et al. Cytokine gene polymorphisms have also been suggested to play a role in the pathogenesis of alcoholic liver disease. The i511 146 Chemical/Physical Agents and Autoimmunity allele 2 was found at a higher frequency in patients with cirrhosis than in heavy drinkers without liver disease. Jarvelainen and colleagues (2001) demonstrated that in Finnish males, expression of one T allele was associated with both alcoholic hepatitis and cirrho sis. There is conflicting evidence as to whether variations in the genes encoding for manganese superoxide dismutase represent a risk factor for alcoholic liver disease (Degoul et al. The data on cytokine and metabolic enzyme gene polymorph isms in the human population as well as experimental studies with ethanol-fed rodents are indicative of the importance of inflamma tion, oxidative stress, and endotoxin in the pathogenesis of alcohol induced liver damage. Chronic ethanol exposure has been associ ated with the formation of alcohol-modified proteins, leading to autoantibody formation and immune-mediated damage to the liver. Circulating antibodies recognizing acetaldehyde–malondialdehyde adducts have been found in Wistar rats fed an ethanol-containing liquid diet (Xu et al. Immunization with acetaldehyde adducts in conjunction with ethanol feeding stimulated ex vivo lymphocyte proliferation in B6 mice, but not in several other strains (Shimada et al. The antibodies generated by these alcohol-modified proteins may also respond to unmodified self-proteins, leading to a breaking of tolerance and autoimmune pathology. Obese strain chickens spon taneously develop a disease very similar to Hashimoto thyroiditis. They were the first model that showed that exposure to iodine affects the course of disease. Depletion of iodine after hatching, achieved by injections of potassium chlorite, reduced thyroid infiltration. In contrast, the onset of spontaneous thyroiditis was hastened by adding sodium iodide to the diet. This effect, however, was reduced by administration of antioxidants, suggesting that reactive oxygen intermediates are one mechanism by which iodine contributes to cell injury. The Biobreeding/Worcester rat has been widely used as a model for studying spontaneous diabetes mellitus, but it also develops autoimmune thyroiditis. Administration of excess iodine accelerates the appearance of the lymphocytic infiltration of the thyroid and the production of thyroid-specific autoantibodies. The incidence of diabetes is very low, but many of the animals develop autoimmune thyroiditis. Iodinated thyroglobulin is more antigenic than the same molecule lacking iodine, suggesting another mechanism by which iodine enhances thyroiditis. Several studies have evaluated the effects of excessive iodine intake in humans, and antithyroid antibodies and iodine-induced hypo and hyperthyroidism have been reported following long-term iodine treatment for endemic goitre (Boyages et al. Although a few epidemiological analyses have been published, they are often confounded by the absence of a clear-cut diagnosis. Clinical outcomes can be the result of immunoallergic, pseudoallergic, or autoimmune-like mechanisms. However, a comprehensive review of adverse autoimmune responses and autoimmune diseases associated with therapeutic agents is beyond the scope of this monograph, and only a few examples will be discussed below. Table 13 provides an abbreviated list of therapeutic drugs that have reportedly been associated with autoimmune reactions. When considering drug-induced autoimmunity, it is important to differentiate two situations. On the other hand, one given agent is associated with only one given type of autoimmune disease. In the latter case, the disease can be organ specific and then closely mimic the spontaneous disease, except that cessation of the offending agent leads to the progressive recovery of clinical and then biological manifestations of the disease. The disease can also be systemic and consists of clinical manifestations and biological/immunological changes markedly different from those of spontaneous diseases. Interestingly, drug-induced systemic autoimmune-like reactions often resemble systemic hypersensitivity reactions, and this further illustrates overlapping mechanisms between immunoallergic and autoimmune-like reactions. Hydralazine inhibits the covalent 150 Chemical/Physical Agents and Autoimmunity binding reaction of the complement protein C4, and susceptibility to hydralazine-induced lupus, as in idiopathic systemic lupus erythema tosus, may depend partly upon genetically determined C4 levels (Sim & Law, 1985; Speirs et al. Adoptive transfer of T cells made autoreactive by treatment with either hydralazine or procainamide causes a lupus like disease (Yung et al. The possibility of a lupus-inducing effect of the drug on T cell development in the thymus has been suggested (Quddus et al. Studies of the specificities of B cells that respond to chroma tin-reactive T cells at the initiation of this autoimmune process demonstrated a rapid and robust expansion of anti-chromatin-secret ing B cells, thus indicating the presence of a normal immune reper toire that includes non-tolerant autoreactive B cells that respond to strong T cell drive and are readily manifested if Fas-mediated activation-induced cell death is inhibited (Ayer et al. Because of a high incidence of adverse events and the strong association with several autoimmune-like phenomena, including myasthenia, pemphigus, and Goodpasture disease, the clinical use is limited. The adverse effects of D-penicillamine in animals are similar to those observed in humans. A study on the effects of D-penicillamine in various strains of mice indicated that D-penicillamine facilitates the induction of autoantibodies in animals with an inherent suscep tibility to autoimmunity (Brik et al. Studies using the popliteal lymph node assay demonstrated that D-penicillamine is capable of inducing an antigen. In rats, particularly Brown Norway rats, D-penicillamine induces a disease characterized by dermatitis, vasculitis, production of antinuclear antibodies, formation of circulating immune com plexes, and IgG deposits along the glomerular basement membrane (Donker et al. Interestingly, low 152 Chemical/Physical Agents and Autoimmunity dose pretreatment of D-penicillamine-treated Brown Norway rats was found to induce complete tolerance to a subsequent pathogenic dose of the drug (Donker et al. The syndrome was preceded by influenza-like symp toms, such as fever, headache, muscle and joint pains, and myalgia, which generally started within 6–17 days after starting zimeldine treatment. The British Department of Health and Social Security reported that 400 out of 100 000 patients displayed similar adverse responses to zimeldine. A number of experiments performed thereafter were supportive for the immune-based etiology of zimeldine-induced adverse effects (Kristofferson & Nilsson, 1989). Three individuals occupationally exposed to zimeldine developed allergy to the compound and showed positive patch and skin prick tests and positive response to zimeldine in the lymphocyte transformation test. These findings indicate that zimeldine may be immunogenic; indeed, zimeldine has been shown to be positive in the popliteal lymph node assay, based on cell numbers and including germinal centre formation and production of IgM and IgG antibodies (Thomas et al. The most common adverse effects associated with gold therapy appeared in skin and mucous membranes (about 15% of all patients) and kidneys (about 5–10%), mostly as proteinuria. It is suggestive, moreover, that progressive interstitial lung fibrosis was found in gold therapy (Smith & Ball, 1980), possibly with an autoimmune pathogenesis. Gold therapy occasionally causes autoimmune haemolytic anaemia (Hunziker, 1978), autoimmune thrombocytopenia (Kotsy et al. Early studies showed that injections of gold thiomalate caused renal lesions, immune complex nephropathy, and proteinuria in Wistar rats (Nagi et al. The histology of these lesions can be characterized as either interstitial nephritis or glomerulonephritis, with specific diagnosis dependent on the presence of specific autoantibodies. Recent works using inbred animals have provided additional information on the pathogenesis of gold-induced renal autoimmunity. These findings indicate that gold compounds appear to cause polyclonal B cell activation to induce a variety of autoantibodies, but detailed mechanisms have not been established. The main difference between classical low molecular weight pharmaceuticals and biopharmaceuticals is that biopharmaceuticals are large molecules that can be recognized directly by the immune system, without the need of metabolism or haptenation. Indeed, it has become clear that nearly all biopharmaceuticals induce anti bodies, although many are of human origin and thus immunolog ically tolerated (Schellekens, 2003). The formed antibodies may have no effect at all or are neutralizing, but occasionally adverse reactions may occur. For instance, erythropoietin has been shown to induce autoimmune anaemia in macaques (Chenuaud et al. Treatments with recombinant therapeutic cytokines occasionally induce autoimmune phenomena.
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Differential Diagnosis Social and Physical Disability Radiculopathy of L2 or L3; upper lumbosacral plexus When severe gastritis diet ginger buy rabeprazole from india, may impede ambulation and physical ac lesion due to gastritis foods to eat list cheap rabeprazole american express infection or tumor; entrapment of superior tivity involving hip gastritis from ibuprofen discount rabeprazole 20mg amex. Page 198 Pathology Usual Course Obturator hernia; osteitis pubis gastritis nunca mas order discount rabeprazole on line, often secondary to lower Constant aching pain which persists unless cause is suc urinary tract infection or surgery; lateral pelvic neoplasm cessfully treated. Complications Essential Features Progressive sensory and motor loss in femoral nerve or Pain in groin and medial thigh; with time the develop its branches depending upon site of lesion. Social and Physical Disability Major gait disturbance if quadriceps femoris is paretic. Differential Diagnosis Tumor or inflammation involving L2-L4 roots, psoas Pathology muscle, pelvic side wall. X4a Neoplasm Differential Diagnosis Neoplasm or infection impinging upon femoral nerve, L2-L4 roots, psoas muscle, or pelvic sidewall. X6b Arthropathy Anterior surface of thigh, anteromedial surface of leg, medial aspect of foot to base of first toe. Definition Main Features Pain in the distribution of the sciatic nerve due to pa Constant aching pain in anterior thigh, knee, medial leg, thology of the nerve itself. The pain may involve only a portion of the sensory field due to pathology in only one branch of the Site nerve. There may be sensory loss in similar areas and Lower extremity; may vary from gluteal crease to toes weakness of the quadriceps femoris, sartorius, and asso depending upon level of nerve injury. If the disorder is secondary to femoral hernia, pain is increased by increase in intra-abdominal pressure. Main Features Trauma to the saphenous nerve may result in an isolated Continuous or lancinating pain or both, referred to the sensory deficit in the knee or leg with local pain. Hypoesthesia in anterior thigh, medial leg, and foot or portion thereof; weakness and atrophy in sartorius or Associated Symptoms quadriceps femoris muscles if lesion proximal to upper Weakness and sensory loss in muscles and other tissues thigh. There may be local tenderness at the site of nerve innervated by the damaged portion of the nerve; secon injury. Laboratory Tests None Usual Course If a progressing lesion is the cause of the pain, the pa Usual Course tient will have an increasing neurological deficit and Pain initially when walking, relieved by rest. If a static intraneural lesion is the sively severe and frequent lancinating pain in the toes cause of the pain, the neurological deficit is fixed and associated with constant metatarsal ache. Often associated with abnormal postures (narrow shoes or high Relief heels) or deformities of the foot and alleviated by treat Remove offending lesion impinging upon nerve. Complications Relief Progressive neurological deficit in the territory of the Orthotic devices to force plantar flexion, i. Pathology Pathology Compression of interdigital nerve by metatarsal heads Varying degrees of myelin and axonal damage within and transverse metatarsal ligament; development of in nerve. Essential Features Pain in region of metatarsal heads exacerbated by Essential Features weight-bearing. Differential Diagnosis Differential Diagnosis Myelopathy, radiculopathy, lumbosacral plexus lesion Sciatic or peroneal neuropathy, plantar fasciitis, metatar involving L4-S 1 segments. Aching myofascial pain arising from trigger points lo cated in one of the three gluteal muscles. Main Features Constant aching pain, often lancinating; often worse at Site night or during exercise; perceived in the region of the Gluteus maximus, medius, or minimus muscles. Page 200 System the sacroiliac joint or pain in the posterior leg and foot, Musculoskeletal system. Gluteus Maximus: Trigger points Site in this muscle may refer pain to any part of the buttock Buttock from sacrum to greater femoral trochanter with or coccyx areas. Gluteus Medius: Trigger points in this or without posterior thigh, leg, foot, groin, or perineum. Those in the or in which the piriformis prevents excessive medial posterior portion refer pain downward into the lower rotation by acting as a lateral rotator of the thigh during part of the buttock, the posterior part of the thigh, and twisting and bending movements. The knee joint is not aware of the injury until hours or days after the inci spared in this distribution. Symptoms are particularly aggravated by sitting to that of sciatica and also of other low back pain condi (which places pressure on the piriformis muscle) and by tions involving the gluteal musculature. Placing the hip in external rotation may de located in the anterior portion refer pain similarly except crease pain. Course: without appropriate intervention, that it is distributed along the lateral rather than posterior persistent pain. Aggravating Factors A foot with a long second and short first metatarsal Associated Symptoms bone. It can act as a perpetuating factor for all the gluteal Paresthesias in the same distribution as the pain; other muscles, especially the gluteus medius. Straight leg raising is usually dyspareunia, pain on passing constipated stool, impo restricted because of tightness in the hamstring and glu tence. Signs Pathology On external palpation through a relaxed gluteus maxi See myofascial pain syndromes. On Trigger points of the gluteal musculature very often internal palpation during rectal or vaginal examination: function as satellite trigger points of those located in the piriformis muscle tenderness and firmness (medial trig quadratus lumborum muscle. Reproduction of buttock Differential Diagnosis pain with stretching the piriformis muscle during hip Sacroiliac joint dysfunction, sciatic neuritis, piriformis flexion, abduction, and internal rotation while lying su syndrome. Painful hip abduction against resistance while sit Code ting (Pace Abduction Test). Pain in the buttock and posterior thigh due to myofascial Bone scan (Tc-99m methylene diphosphonate) is usually injury of the piriformis muscle itself or dysfunction of normal but has been reported to show increased piri Page 201 formis muscle uptake acutely. Selected nerve conduction studies Essential Features may demonstrate nerve entrapment. Buttock pain with or without thigh pain, which is aggra vated by sitting or activity. Posterolateral ten sponds well to appropriate interventions, particularly in derness and firmness on rectal or vaginal examination. Relief Correction of biomechanical factors (leg length discrep Differential Diagnosis ancy, hip abductor or lateral rotator weakness, etc. Pro Lumbosacral radiculopathy, lumbar plexopathy, proxi longed stretching of piriformis muscle using hip flexion, mal hamstring tendinitis, ischial bursitis, trochanteric abduction, and internal rotation. Facilitation of stretch bursitis, sacroiliitis, facet syndrome, spinal stenosis (if ing by: reciprocal inhibition and postisometric relaxation bilateral symptoms). May occur concurrently with lum techniques; massage; acupressure (ischemic compres bar spine, sacroiliac, and/or hip joint pathology. Xlf procaine/Xylocaine) to region of lateral attachment of piriformis on femoral greater trochanter (lateral trigger References point), or to tender areas medial to sciatic nerve near Travell, J. The lower extremities, piri sacrum (medial trigger point) with rectal/vaginal moni formis, and other short lateral rotators. If previous measures fail, surgical transection of & Wilkins, Baltimore, 1992, pp. Social and Physical Disabilities Difficulty sitting for prolonged periods and difficulty with physical activities such as prolonged walking, standing, bending, lifting, or twisting compromise both sedentary and physically demanding occupations. Main Features Metastases to the hip joint region produce continuous System aching or throbbing pain in the groin with radiation Nervous system. In some cases peripheral causes have through to the buttock and down the medial thigh to the been described; the spinal cord is probably also in knee. A me tastatic deposit to the femoral shaft produces local pain, Main Features which is also aggravated by weight-bearing. Sometimes re Pain at rest due to tumor infiltration of bone usually re lieved by activity, though it may be worse following sponds reasonably well to nonsteroidal anti exercise. Pain due to ments may be florid or almost imperceptible, and in the hip movement or weight-bearing responds poorly to latter case, the patient may never have noticed them. They consist of irregular, involuntary, and sometimes writhing movement of the toes, and they cannot be imi Signs and Laboratory Findings tated voluntarily. They can be suppressed for a minute or There may be tenderness in the groin and in the region two by voluntary effort and then return when the patient of the greater trochanter. There is not usually a relation between the formity unless a pathological fracture has occurred. Complications the major complication is a pathological fracture of the Relief femoral neck or the femoral shaft. Pathology Precise pathology unknown, but nerve root lesions have Summary of Essential Features and Diagnostic been described, and spinal cord damage. There is usually tenderness in the groin and increased pain on internal and external rota References tion. Differential Diagnosis the differential diagnosis includes upper lumbar plexo Nathan, P.