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FMF: PAST, PRESENT AND FUTURE Mordechai Pras It is customary to start with history, but I shall concentrate on the present and the future. Number of FMF patients in the world First I will try to approximate the number of FMF patients in the world today. In Israel, where we have the best information regarding the number of FMF patients, there are about 7000 FMF patients recorded in clinics who are getting treatment. This is in a population of 6 million people. The prevalence is over 1: 1000. In Armenia, where the prevalence of FMF is similar, or even greater than that in Israel, there are about 4000 patients. Turkey, with its 80 million inhabitants, has a prevalence of FMF that is one half of that in Israel reaching a figure of about 40, 000. We can expect a similar prevalence among Arabs, which will add another 60, 000 patients in Arab countries of the Middle East and North Africa. Another 1000 patients in Greece and Cyprus, another 3000 among Europeans, and about 2000 patients in North and South America brings the total number to around 117, 000. Many patients are not diagnosed and thus, of course, are not getting treatment. As you know, the number of heterozygous carriers in the Middle East of MEFV gene mutations is very high in all nations that were tested, and the total number might reach over ten million only in the Middle East and Armenia. I shall not speak about the implications of these numbers - this will probably come up during the conference. Diagnosis You are all familiar with the Tel Hashomer Criteria for FMF. You know the more complex criteria of Avi Livneh, in which he checked the specificity and sensitivity of the criteria that he used. I would like to suggest a simple and reliable criteria for the diagnosis of FMF based on only two criteria: I. RECURRENT SHORT INFLAMMATORY ATTACKS II. A FAVORABLE RESPONSE TO COLCHICINE TREATMENT. I sure that the specificity and the sensitivity of these two criteria will exceed 90%, because 95% of the compliant FMF patients respond to colchicine treatment. These criteria will simplify the diagnosis of FMF and will, more importantly, enhance the early treatment with colchicine of FMF patients, especially small children, and may prevent the complications of the disease, especially the development of amyloidosis. The Present Help of Molecular Biology What is the role of molecular biology tests in the diagnosis of FMF? I would like to state that: at present, the diagnosis of FMF is clinical. On the one hand, we know people who are homozygotes, or compound heterozygotes, but they are healthy and do not suffer from any symptom of the disease. On the other hand, we know that in the 50-70 percent of our patients who respond to colchicne treatment, we are able to find one mutation only, or we do not succeed in demo nstrating even one mutation in the MEFV gene. The demonstration of mutations can establish a definite diagnosis in suspected patients, and this is especially helpful for physicians with little experience in treating FMF patients. The type of mutation establishes the severity of the disease. The mutations located within the mutational hotspots in codons 680 and 694 are associated with severe disease with early onset, high frequency of attacks, the necessity of a high dose of colchicine to control attacks and high frequent occurrence of amyloidosis in untreated patients. It is interesting that in Turkey, no prevalence of mutations in codon 694 was found among FMF patients who had suffered from amyloidosis in contrast to all other ethnic groups, including Armenians, Jews.

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This restriction adds a degree of asymmetry to the molecule. In 1933, Kuhn designated this type of stereoisomerism as atropisomerism from Greek "a" meaning not; "tropos" meaning turn ; [74]. The designation of this asymmetry is "aS or aR, " according to the rules of molecular asymmetry, in which the "a" stands for axial chirality [75]. In colchicine, the C-C bond between the A and C rings is the chiral axis Fig. 5 ; . In light of this molecular asymmetry, colchicine has four stereoisomers, as shown in Fig. 5. Each pair has either the R or S configuration at C-7. - ; - aS, 7S ; -Colchicine, the natural isomer, can interconvert between the two conformational isomers aR and aS, given enough energy. The energy barrier of rotation in colchicine, approximately 22-24 kcal mol [73], is large enough to allow the synthesis and isolation of the conformations as stereoisomers. The research of many medicinal chemists, in particular Arnold Brossi, has led to the conclusion that the counterclockwise aS conformation is that of the naturally occuring alkaloid [72, 73, 76-79]. Shown in Fig. 6 are energy-minimized models of the atropisomers of 7S ; -colchicine Constructed using Sybyl 6.4, Tripos, Inc ; . Note the very different arrangement of the acetamide group in the two conformations.

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Protect the liver: u Avoid alcohol consumption. u Discuss new medications with doctor providing HCV treatment; discuss both prescription and over-the-counter medications. Prevent transmission. Pept-1-mediated transport of Gly-Sar without any change in the Km. The short-term EGF treatment did not alter either the Pept-1 mRNA level or the intracellular pH 38 ; . However, the actual mechanism of increased Pept-1 functional expression remained unclear. Leptin Leptin secreted by the stomach may reach the lumen of the small intestine and, therefore, may be a regulator of intestinal functions such as absorption. Indeed, studies in rat intestine showed the presence of leptin receptors with preponderance in the jejunum 12 ; . Furthermore, in vivo perfusion studies in the rat jejunum showed that introduction of leptin into the perfusate specifically increased peptide absorption without any effect on fluxes of water, electrolytes, or glucose 12 ; . Because studies in Caco-2 cells revealed the presence of leptin receptors, these cells were used to investigate the mechanism of leptin stimulation of peptide absorption 12 ; . Within 30 min, leptin increased the transport of Gly-Sar and cephalexin a peptidelike antibiotic ; by Caco-2 cells. This increase in transport was observed when leptin was added to the apical side but not to the basolateral side of these cells. The kinetic analysis of this increased transport showed a 51% increase in the Vmax without any change in the Km, thus eliminating the modification of intrinsic activity of Pept-1 as a mechanism. Further investigation of the mechanism of leptin action showed a 60% increase in the membrane Pept-1 protein and a 50% decrease in the intracellular Pept-1 protein when this hormone was added for 30 min to the apical compartment of Caco-2 cells. These alterations were not accompanied by any change in the cellular Pept-1 mRNA level. To investigate the mechanism of leptin effect on Pept-1 protein, Caco-2 cells were pretreated with brefeldin and colchicine. The rationale for these studies has already been described in the section on insulin. It was found that the leptin stimulation of Gly-Sar transport was not prevented by brefeldin pretreatment, but it was abolished with colchicine pretreatment. Therefore, it appears that insulin and leptin share a common mechanism for stimulating dipeptide transport in Caco-2 cells, namely by increasing the trafficking of Pept-1 from intracellular pool to the apical membrane. Thyroid Hormone The above hormones initiate their action by binding with their respective receptors on the cell membrane, but there are hormones, such as triiodothyronine T3 ; , that enter the cell for initiating their action. Recently, it was reported 6 ; that pretreatment of Caco-2 cells with 100 nM T3 for 4 days resulted in significant inhibition of Gly-Sar uptake. The effect appeared to be specific, because no inhibition of transport of any other nutrients was observed. The studies of the mechanism of inhibition showed the following 6 ; : the kinetic analysis of the Gly-Sar uptake showed no change in the Km, but a near twofold decrease in the Vmax, suggesting a and erythromycin. 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Ellen M. Maathuis, Gerhard H. Visser, Joleen H. Blok Dept. of Clinical Neurophysiology, Erasmus MC Rotterdam, The Netherlands Introduction: Recordings of the maximum CMAP require sufficiently strong stimuli. To achieve this in clinical practice, the lowest stimulus intensity SI ; that produces a maximal CMAP on visual inspection is usually increased by a varying amount between 20 and 50% of the determined SI ; for final recordings.4-6 The aim of this study was to determine how large this surplus SI should be. The use of a supramaximal SI is motivated by the probabilistic response of axons to applied stimuli1-3 over an "activation range" of SI values range over which the firing probability increases from 0 to 100% ; . Starting from the SI at which the maximum CMAP can first be obtained SImax ; , SI should therefore be increased by an amount identical to the activation range of a MU certain of maximal CMAPs on every subsequent stimulus. For that reason, we aimed to determine the width of this activation range as percentage of SImax. Methods: We used stimulated single fiber EMG SFEMG ; of the first dorsal interosseus muscle in 5 healthy subjects. The ulnar nerve was stimulated percutaneously at the wrist. When visual inspection indicated that a stable single fiber potential was obtained, the number of times the MU was activated in response to 50 stimuli of constant SI was determined for a range of SI. This number was expressed as percentage of the 50 applied stimuli to obtain the firing probability of the MU. If another potential could be obtained by slight manipulation of the needle or by adjusting SI beyond the range of the first, stimulus-reponse curves were recorded for this second fiber. After two or three MU curves were obtained, the needle was shifted to a significantly different position within the muscle and the procedure was repeated. Each recording of a MU curve was followed by a registration of the so-called scan of the muscle CMAP vs. SI ; , to determine the lowest SI at which the maximum CMAP could be recorded SImax ; . The widths of the activation ranges of the recorded MUs and SImax were determined using curve-fitting procedures implemented in Matlab. Finally, for each MU activation curve the supramaximal percentage SMP ; value was determined by dividing its range width into SImax. Results: Between 4 and 7 different MU activation curves were obtained per subject total 27 ; . These curvewere mostly obtained for low to intermediate SIs SIs that generated CMAPs of 0-35% of the maximum CMAP ; . The corresponding SMP values ranged between 2.0% and 9.0%; their mean value was 4.5%. There was no statistically significant correlation between SMP and SI Spearman correlation; p 0.43 ; . Discussion & Conclusions: An important result of this study is that we have been able to isolate the contributions of single fibers in stimulated single fiber EMG of a distal muscle even at higher stimulus intensities. As far as we know, this possibility has not been reported previously. Because our results showed no systematic bias towards larger or smaller SMP with increasing SI, we consider them sufficiently representative for the highest threshold MUs. Adding 10% to SImax suffices to obtain maximal CMAPs consistently in healthy subjects. Because accurate determination of SImax may be difficult and because results in patients may be different, we recommend use of an additional safety margin of 10%. We conclude that stimulation at 120% 1.2SImax ; suffices to obtain maximal CMAPs. References : 1. Bergmans J 1970 ; . The physiology of single human nerve fibres. Vander. 2. Brown WF, Milner Brown HS 1973 ; . J Neurol Neurosurg Psychiatry. 1976 Mar; 39 3 ; : 249-57. 3. Hales JP, Lin CS, Bostock H. J Physiol. 2004 Sep 15; 559 Pt 3 ; : 953-64. 4. Kimura J. Electrodiagnosis in diseases of nerve and muscle. New York: Oxford University Press, 2001. 5. Meulstee J. Stimulatietechniek. In: Van Dijk J.G. Ed. ; EMG voor de algemeen neuroloog. Leiden: Boerhaave Cie, 2001. 6. Oh SJ. Clinical Electromyography.Baltimore: Williams & Wilkins, 1993 and exelon.
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Were not shared by the microtubule-inactive and `y-lumicolchicine. The present data and floxin. For example, embryos from a healthy 23 year old that are placed in a 45 year old will retain the pregnancy rate of the younger female. The death percentage would be even higher, but for the high doses of drugs that the calves are fed and fluoxetine!

These attacks are self-limited, last between 1 to 4 days. The patients recover fully at the end of an attack and are totally normal in between these bouts. Some of the attacks may be so painful that the patient or the family seeks for medical help. Especially severe abdominal attacks may mimic acute appendicitis and therefore some patients may undergo unnecessary abdominal surgery, such as appendicitis. However some of the attacks, even in the same patient, may be mild enough to be confused with abdominal distress. This is one of the reasons why it is hard to recognize these patients. During abdominal pain, the child usually is constipated, but as the pain gets better, short lived soft stools appear. The child can have very high fever during one attack, or a mild increase in temperature, in another. The chest pain is generally unilateral. It may be so severe that the patient can not breathe deep enough. It resolves within days without residue. Usually one joint is affected at a time monoarthritis ; . It is commonly an ankle or a knee. It may be so swollen and painful that the child can not walk. In about a third of these patients there is an erythematous rash over the involved joint. Joint attacks may last somewhat longer than the other forms of attacks. It can take from 4 days to 2 weeks before it resolves completely. In some children, the sole finding of the disease may be recurrent joint pain and swelling which is misdiagnosed as acute rheumatic fever, or juvenile rheumatoid arthritis. About in 5-10% of the cases joint involvement may become chronic and cause irreversible changes. There is a characteristic rash of FMF called erysipelas-like erythema, usually observed over the lower extremities and joints. Some children may complain of leg pains which may be disturbing. Among the rarest forms of attacks are recurrent pericarditis inflammation of the outer layer of the heart ; , myositis muscle inflammation ; , meningitis and orchitis testicular inflammation ; . Some diseases characterized by vessel inflammation vasculitis ; are seen more frequently among children with FMF, such as Henoch-Schnlein's purpura and polyarteritis nodosa. The most important complication of FMF, in untreated cases is the development of amyloidosis. Amyloid is a special protein that deposits in certain organs like kidneys, gut, skin, heart and causes gradual loss of function, especially of the kidneys. It is not specific for FMF it may complicate other chronic, inflammatory diseases that are not properly treated, such as rheumatoid arthritis, juvenile chronic arthritis, or tuberculosis. Finding amyloid in the gut or kidney maybe a clue to diagnosis. Children who are receiving proper dose of colchicines see drug therapy ; are safe from the risk of developing this life-threatening complication. Is the disease the same in every child? It is not the same in every child. Moreover, the type, duration and the severity of the attacks may be different even in the same child. Is the disease in children different from the disease in adults? In general FMF in children resembles that seen in adults. However some features of the disease like arthritis joint inflammation ; and myositis are more common in childhood and their frequency decrease as the patient gets older. Orchitis is detected especially in young boys rather than adult males. The age of onset of FMF is also important. The risk of amyloidosis is higher among untreated patients with early disease onset. How is it diagnosed? There is no specific tool for the diagnosis of FMF. Generally the following approach is followed: a ; Clinical suspicion: It is possible to consider FMF only after the child experience a minimum of 3 attacks. A detailed history of the ethnic back-ground should be considered as well as relatives with similar complaints, or renal insufficiency . Also the parents should be asked to give a detailed description of the previous attacks.
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