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One of the two common mutations causing factor XI deficiency in Ashkenazi Jews (type II) is also prevalent in Iraqi Jews, who represent the ancient gene pool of Jews.

In recent years four mutations causing factor XI deficiency have been identified in Jews of Ashkenazi (European) origin. Two of them, type II (a nonsense mutation) and type III (a missense mutation), were found to prevail among 125 unrelated Ashkenazi Jews with severe factor XI deficiency. A finding of type II mutation in four unrelated Iraqi-Jewish families raised the possibility that this mutation is also common in Iraqi Jews, who represent the ancient gene pool of the Jews. A molecular-based analysis performed in 1,040 consecutively hospitalized patients disclosed the following results: Among 531 Ashkenazi-Jewish patients, the type II allele frequency was 0.0217 and among 509 Iraqi-Jewish patients, 0.0167 (P = .50). The type III allele frequency in the Ashkenazi-Jewish patients was 0.0254, whereas none of 502 Iraqi-Jewish patients examined had this mutation. These data suggest that the type II mutation was present in Jews already 2.5 millenia ago. The data also indicate that the estimated risk for severe factor XI deficiency in Ashkenazi Jews (due to either genotype) is 0.22% and in Iraqi Jews, 0.03%, and that the estimated risk of heterozygosity in Ashkenazi Jews is 9.0% and in Iraqi Jews, 3.3%. As patients with severe factor XI deficiency are prone to bleeding after injury and patients with partial deficiency may have similar bleeding complications when an additional hemostatic derangement is present, the observed high frequencies should be borne in mind when surgery is planned for individuals belonging to these populations.

Aged↗

Familial empirical risks for inflammatory bowel disease: differences between Jews and non-Jews.

The Jewish population has an increased frequency of inflammatory bowel disease compared with their non-Jewish neighbours. Genetic factors have been implicated in the aetiology of this disorder and may contribute to ethnic differences. This study determined the familial empirical risks for inflammatory bowel disease in the first degree relatives of inflammatory bowel disease probands (for both Jews and non-Jews) for the purpose of accurate genetic counselling and genetic analysis. A total of 527 inflammatory bowel disease patients from Southern California (291 Jews and 236 non-Jews) were questioned about inflammatory bowel disease in their first degree relatives (a total of 2493 individuals). Since inflammatory bowel disease has a variable and late age of onset, age specific incidence data were used to estimate the life time risks and to make valid comparisons between the different groups. In the first degree relatives of non-Jewish probands, the life time risks for inflammatory bowel disease were 5.2% and 1.6% when probands had Crohn's disease and ulcerative colitis respectively. These values were consistently lower than the corresponding risks for relatives of Jewish patients -7.8% and 4.5% for Crohn's disease and ulcerative colitis probands respectively (p value for comparison between Jews and non-Jews: 0.028; between ulcerative colitis and Crohn's disease: 0.005). These data provide the requisite basis for genetic counselling for these disorders in the white American population. In addition, these different empirical risks for relatives of Jewish and non-Jewish probands allow rejection of single Mendelian gene models for inflammatory bowel disease, but are consistent with several alternative genetic models.

Adolescent↗

Gc subtypes in some population groups from Israel. Comparison between world population groups and between Jews and non-Jews of the same areas.

Results of Gc subtyping on 1,222 Israelis, Arabs and Jews, are summarized and their gene frequencies are analyzed in comparison with available data on Gc subtypes in non-Jews. A discriminant and a cluster analysis demonstrated that in their Gc subtype frequencies European and non-European Jews resemble the populations of the areas where they lived before immigrating to Israel. A possible explanation for this resemblance, which is seen in some and not seen in other genetic markers in Jews, is suggested here to be connected with the function of Gc as a vitamin D-binding protein.

Ethnicity↗

Kaposi's sarcoma-associated herpesvirus infection in elderly Jews and non-Jews from New York City.

BACKGROUND: Worldwide, Kaposi's sarcoma (KS) occurs in immunocompetent elderly adults, especially men. Elderly Jews have relatively high KS risk, but it is unclear whether this indicates heightened prevalence of KS-associated herpesvirus (KSHV), the KS agent. We studied Jewish and non-Jewish patients at a New York City geriatrics clinic. METHODS: We measured plasma antibodies against K8.1 (a KSHV glycoprotein) by enzyme immunoassay and against viral latency antigens by immunofluorescence assay. Individuals positive by either were considered KSHV-seropositive. Titres were performed for positive subjects. We used polymerase chain reaction to quantify circulating KSHV DNA. RESULTS: Of 467 subjects (median age 80 years), 40 were KSHV-seropositive (8.6%). Seroprevalence was 8.8% among Jews (18 of 204), similar to other religious groups, and did not differ by sex or region of birth. However, K8.1 antibody titres were higher in men than women (geometric mean titre 177 versus 35, P = 0.03) and increased with age (P = 0.02). The K8.1 titres were higher in three people from Central/Eastern Europe (1,280, 1,280, 320), all of whom were Jewish, than in others (geometric mean titre 39, P = 0.006). The single person with detectable circulating KSHV (457 copies/million cells) had the highest titre (5,120). CONCLUSIONS: The KSHV seroprevalence was not elevated among elderly Jews, despite their known high risk for KS. However, among KSHV-seropositive individuals, K8.1 titres were highest in subgroups at greatest risk for KS (men, older individuals, people from Central/Eastern Europe) and may identify individuals with poor immune control of KSHV replication during asymptomatic infection.

Age Distribution↗

The lower incidence of myotonic dystrophy in Ashkenazic Jews compared to North African Jews is associated with a significantly lower number of CTG trinucleotide repeats.

Myotonic dystrophy (DM) is associated with an increased number of CTG repeats in the 3' untranslated region of the myotonin gene. Because DM has been observed more frequently in North African Jews than in Ashkenazic Jews in Israel, a study of the CTG repeat polymorphism was undertaken in these 2 groups. Alleles from 70 unrelated North African subjects and 70 unrelated Ashkenazic subjects were studied by PCR analysis of the trinucleotide repeat in the DM gene to determine the ethnic distribution of the number of CTG repeats. The alleles ranged in length from 5 to 26 repeats in the North Africans and 5 to 23 in the Ashkenazim. As has been seen in other populations, none of the chromosomes had a 9-repeat length. North African Jews were found to have significantly more repeats in the normal range than Ashkenazim (for over 14 repeats: 34/140 compared to 7/140; p < 0.0001). It is suggested that this more frequent occurrence of a large number of CTG repeats in the normal range may represent a greater predisposition to DM.

Africa, Northern↗

Mutations in human 11 beta-hydroxylase genes: 11 beta-hydroxylase deficiency in Jews of Morocco and corticosterone methyl-oxidase II deficiency in Jews of Iran.

Steroid 11 beta-hydroxylase is encoded by two homologous genes, CYP11B1 and CYP11B2, located on chromosome 8q21-22. CYP11B1 encodes a specific cytochrome P-450 (P-450c11) necessary for cortisol biosynthesis, with predominantly 11 beta-hydroxylase and moderate 18-hydroxylase activity, whereas CYP11B2 encodes another isozyme (P-450cmo) necessary for aldosterone biosynthesis, with 11 beta-hydroxylase, 18-hydroxylase and 18-oxidase activities (the latter two termed corticosterone methyl-oxidase I and II; CMO-I and II, respectively). Two steroid biosynthetic defects, both relatively frequent in Israel, are caused by specific mutations in each of these genes. 11 beta-Hydroxylase deficiency is frequent among Jews from Morocco (1 in 5000 to 7000 births), and is characterized by virilization, hypertension, impaired cortisol biosynthesis, and increased deoxycorticosterone and androgens. Affected individuals have a single base substitution in exon 8 of CYP11B1, codon 448, from CGC (arginine) to CAC (histidine). This sequence, normally absent in CYP11B2, constitutes a true point mutation within the heme binding domain of CYP11B1 that results in marked impairment of enzymatic activity. The clinical expression is characterized by a wide range of variability in the signs of both androgen and mineralocorticoid excess, even though an identical mutation was found in all but one of the affected alleles examined. CMO-II deficiency is frequent among Jews from Iran (1 in 4000 births), and is characterized by a typical salt-wasting syndrome, increased 18-hydroxycorticosterone, impaired aldosterone biosynthesis, and a high ratio of these steroids. No mutation was found in CYP11B1, but all individuals affected were homozygous for two missense mutations in CYP11B2. The first, in exon 3, codon 181, from CGG (arginine) to TGG (tryptophane) is a mutation that completely abolishes both CMO-I and II activities, whereas the second, in exon 7, codon 386, from GTG (valine) to GCG (alanine) is a more conservative substitution that produces only a minimal reduction in CMO-I activity. Individuals homozygous for either one of these mutations are asymptomatic.

Adrenal Hyperplasia, Congenital↗

Orosomucoid (ORM1) polymorphism in Arabs and Jews of Israel: more evidence for a middle eastern origin of the Jews.

A study of 8 Israeli population groups for the ORM1 polymorphism included 1242 serum samples: 156 samples from Arab Moslems, 139 from Arab Druzes, and 947 from 6 Jewish groups. The two most frequent alleles in Europeans and Asians, ORM1*F1 (ORM1*1) and ORM1*S (ORM1*2) were found in Jews and Arabs at frequencies similar to those in Europe. Unique to Arab and Jewish populations were polymorphic frequencies of two ORM1 slow electrophoretic variants, designated ORM1*S1 and ORM1*S2. These were formerly observed only in Europe, where two individuals with *S1 and two with *S2 have been observed so far. The Chueta community of converted Majorcan Jews is the only previously studied group that, like the other studied Jewish groups, has polymorphic frequencies of both ORM1*S1 and ORM1*S2. In this study we associate the Chuetas with the Israeli groups, as a population of Middle Eastern origin. Published data on ORM1 in Europe and East Asia together with the present data, making a total of 47 populations, were subjected to a discriminant analysis that resulted in a correct classification of 93.6% of the populations. Results of this analysis suggest that ORM1 is a useful polymorphic marker for anthropological studies.

Arabs↗

Genetic polymorphisms among Bukharan and Georgian Jews in Israel.

Bukharan and Georgian Jews have lived in central Asia for many centuries. Approximately 30,000 Bukharan and 37,000 Georgian Jews lived in their respective countries within the USSR between 1920 and 1960. Genetic markers of blood--blood groups, isoenzymes, HLA antigens, and gamma and kappa chain allotypes--were tested in blood samples from 113 Bukharan and 134 Georgian Jews living in Israel. Estimates of inbreeding were low: alpha = 0.0088 for Bukharan and alpha = 0.0011 for Georgian Jews. G6PD deficiency was relatively rare in Bukharan (2.2%) and in Georgian Jews (6.0%), when compared to other Jews in the area. Both populations showed frequencies of some markers similar to that of other Jewish populations, but frequencies of several markers were extremely high or low. Bukharan Jews showed very high frequencies of B(0.243), cDe (0.122), JkA (0.705), HLA-A29 (0.167), A30 (0.116) and B7 (0.124), and AcPA (0.451) and very low ones of O(0.518), CDe(0.422), AcPB (0.513) and GLO1 (0.140). Very high frequencies in Georgian Jews were observed for cDE (0.189), HLA-A3 (0.194), Bw35 (0.300) and GLO1 (0.367). Yet the greatest difference between both populations was in African characters. While in Bukharan Jews Fy was very frequent (0.146) and cDe was the highest observed among Jews (0.122), neither of these markers was detected among the Georgian Jews tested. Yet, another African character, the Gm1,5,10,11,13,14,17,26 haplotype, occurred in both populations (0.028 and 0.042 in Bukharan and Georgian Jews, respectively). Distance measures for Bukharan, Georgian, Iranian, Cochin, and Libyan Jews based on 13 polymorphic loci showed the greatest distance between Cochin Jews and the other populations and the smallest distance between the Georgian and Iranian Jews.

Blood Group Antigens↗

Increased prevalence of HCV antibodies in dialyzed Ashkenazi Jews--a possible ethnic predisposition.

BACKGROUND: The prevalence of hepatitis C (HCV) antibodies in dialysis patients is considerably higher than that found among healthy blood donors. This increased seroprevalence has been correlated to increased duration of dialysis, mode of dialysis and to the number of blood transfusions administered. However, factors other than nosocomial ones also seem to play a part in disease transmission. The role of the patient's ethnic origin, possibly reflecting on his/her genetic makeup has received scant attention. In this study, HCV seroprevalence in our dialysis population, which consists of three major ethnic subgroups (Ashkenazi Jews, Sephardi Jews and Arabs), was examined. METHODS AND RESULTS: Altogether HCV seropositivity was determined in 120 dialysed patients--65 males/55 females (76 hemodialysis, 44 CAPD), using second generation ELISA confirmed by RIBA-2. Mean age was 59.7 +/- 15.7 (range 16-86 years). Patients had to have been on dialysis for a minimum of 3 months (mean duration 45.2 +/- 44.5 months). Patients whose end-stage renal disease was due to diabetic nephropathy (DN) or those who had previously been transplanted (TP) were considered as separate groups and compared to the group as a whole. Of the 120 patients, there were 49 Ashkenazi Jews (40.8%), 57 Sephardi Jews (47.5%) and 14 Arabs (11.7%). Overall HCV prevalence was 21.7% (26/120) with a significantly greater prevalence in HD compared to CAPD (30.3 vs. 6.8%, P < 0.01). Respective values for Ashkenazi Jews, Sephardi Jews and Arabs were 30.6, 15.8, and 14.3% (P < 0.01, Ashkenazi Jews vs. Sephardi Jews and Arabs). DN had a lower 3.7% while TP had a higher 46.1% prevalence compared to the group as a whole (P < 0.01). In general, the increased frequency of anti HCV antibodies was significantly correlated to the duration of dialysis and the number of blood transfusions administered. This, however, was not the case in the greater prevalence of HCV found in Ashkenazi Jews compared to Sephardi Jews and Arabs which was independent of the above factors and the mode of dialysis. CONCLUSION: Our results showing increased HCV seropositivity in Ashkenazi Jews compared to Sephardi Jews and Arabs, suggest that ethnic factors might predispose to HCV transmission and infectivity.

Adolescent↗

Maternal, perinatal and infant health in Bedouin and Jews in southern Israel.

A study has been made of 3,745 Bedouin and 9,422 Jewish babies born in 1972-73 to residents of the Beersheba district of southern Israel (the Negev). Newborn infants weighing less than 1 kg were excluded. Thirty-seven percent of the Bedouin babies were born at home; their mothers tended to be older and of higher parity than those choosing to deliver in hospital. Less than 6% of Bedouin mothers had been to school, compared with 90% of the Jews; 30% were aged under 20 or over 34 years, compared with 18% of the Jews, and 23% were having their seventh or later baby, compared with 12% of the Jews. Mean birth weight of babies born in hospital was about 200 g lower in Bedouin than in Jews, and 11.4% of Bedouin and 6.5% of Jewish infants weighed less than 2.5 kg. There was little variation in complications of labor between the 1,959 Bedouin and 8,877 Jewish women delivered in Beersheba's Soroka Medical Center. The cesarean section rate was 1.8% in Bedouin and 4.3% in Jews, while in 0.3% of Bedouin and 1.4% of Jews labor was induced. Monozygous twinning rates were similar in the two ethnic groups (4.8 and 4.5 sets/1,000 deliveries, respectively) but dizygous twinning was twice as common among the Bedouin as among the Jews (13.0 vs 6.0 sets/ 1,000). Male births accounted for 0.526 and 0.512 of the total in Bedouin and Jews, respectively. Perinatal mortality rates for hospital births were 31.1 and 18.3/1,000 in Bedouin and Jews, respectively. Infant deaths among Bedouin (31.0/1,000) were underreported; the rate was 16.8/1,000 for Jewish infants. Although rates of all specific causes of death were higher in Bedouin than in Jews, patterns of mortality in subgroups based on birth weight, sex, twinning and maternal age were quite similar in the two ethnic groups. There were six reported deaths from tetanus among Bedouin babies. For the cohort of babies born in 1972, admissions to the Soroka Medical Center pediatric wards were recorded in 366 (195.5/1,000) Bedouin and 787 (174.3/1,000) Jewish babies younger than the age of one year. Bedouin admission rates were higher than those of Jews for gastroenteritis (119.1 and 64.5/1,000 respectively), infectious and parasitic diseases (29.4 and 21.9), malnutrition (25.6 and 8.0) and external causes (10.1 and 4.4). Admission rates for bronchitis and pneumonia were, however, lower among Bedouin than Jews in the first six months of life.

Birth Order↗