Cases reported "Abortion, Spontaneous"

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1/11. zinc deficiency in malabsorption states: a cause of infertility?

    Thirteen patients with malabsorption, 7 women and 5 men, were investigated extensively. All showed low serum zinc concentrations irrespective of the duration of illness and degree of malabsorption. Eleven of the 13 had active coeliac disease. It was suspected that the low serum zinc concentrations reflected a state of zinc deficiency, and this theory was borne out by the fact that no inflammatory reaction, no clear-cut albumin deficiency, and no oestrogen or corticosteroid influence could be demonstrated. All 7 women suffered from infertility, in most of them of long standing. Two showed secondary infertility after pregnancy and abnormal labour resulting in infants with congenital malformations (one case of bilateral congenital dislocation of the hip and one of multiple cardiac anomalies). I have reported similar complications in pregnancies in which the serum zinc was low. One of the infertile women conceived after the institution of gluten-free diet and zinc therapy, but later aborted spontaneously. Investigations on zinc metabolism and intestinal absorption might well prove valuable in otherwise unexplained infertility and could open up a new therapeutic approach.
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2/11. Interchromosomal insertions. Identification of five cases and a review.

    In five families with questionable chromosome rearrangements, we identified an interchromosomal insertion by fluorescent in situ hybridization (FISH). In case 1 with a dir ins (5;11)(p14;q14q24) in three generations, the mentally retarded and microcephalic proband showed a 5p14-->pter deletion. In case 2, a duplication (13)(q21.31--> q31.2) combined with a deletion (11)(q14-->q22) segregated from a reciprocal ins(11;13)(q14q122)(q21.32q31.2), causing a mixed phenotype with psychomotor retardation, caput quadratum, choanal atresia, and pes equinovarus. In case 3, a dir ins (18;5)(q21.3;p13.1p14) was associated with spontaneous abortions, in case 4, the proband with mental retardation, microcephaly, and a heart defect showed a pure trisomy of (12)(q13-->q15), which had segregated from a carrier of an ins (18;12)(p11.3;q13q15). In case 5, a duplication of (10)(q26.3-->q25.2) segregated from an inv ins(5;10)(q15;q26.3q25.2), which was passed on directly from a mother to her son,with mental retardation. In all families the elucidation of the insertional translocation (IT) considerably increased the associated genetic risks of carriers. For the review, we collected data from 81 articles on 87 IT probands on ascertainment, origin, familial transmittance, progeny, and genetic risks of IT carriers. We also discussed the recombinant chromosomes and complex rearrangements associated with ITs, and listed chromosome regions occurring solely as deletions, or solely as duplications, or as both to facilitate genotype/phenotype correlations. We conclude that ITs are rare chromosomal rearrangements with an 1:80,000 incidence, of which nearly 80% were referred because of congenital abnormalities and mental retardation. A maternal origin was seen in 59.5%, a paternal origin in 26.6%, and 13.9% were de novo. No notable difference in fertility between male and female IT carriers was noticed. Bias of ascertainment was excluded in 15 familial cases and led to an estimate of the genetic risks for IT carriers of 32.0-36.0%. The mean size of the inserted regions occurring solely as duplications (n=39) measures 0.96% of the haploid autosomal length (HAL), and of regions solely occurring as deletions (n=14) 0.47% HAL. In the families where both aneusomies occurred, the size of the insertions ranged between 0.22 and 1.21% HAL. overall, the findings fit with the general idea that a surplus of genetic material is tolerated more easily than a deficiency.
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3/11. Internal jugular vein thrombosis following in-vitro fertilization in a woman with protein s deficiency and heterozygosity for the prothrombin 3' UTR mutation, despite anticoagulation with heparin.

    We report the case of a 31-year-old woman with protein s deficiency and heterozygosity for the prothrombin 3' UTR mutation who developed an internal jugular vein thrombosis despite therapeutic anticoagulation with a low molecular weight heparin, following in-vitro fertilization. This case indicates that the stimulus to thrombosis in such women is intense and can occur despite apparent therapeutic anticoagulation. Close attention should, therefore, be paid to any women with a personal or family history of thrombosis and the potential thrombotic risks associated with assisted conception must be discussed.
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4/11. Graves' disease associated with anticardiolipin antibody positivity and acquired protein s deficiency.

    A 33-year-old woman had experienced recurrent pregnancy loss. She had positive anticardiolipin antibody and protein s deficiency. Her pregnancy was managed with anticoagulant therapy and she delivered a healthy infant. Three years after delivery, she reported progressive sweating, tremor, tachycardia, and a 4-kg weight loss. She was diagnosed with Graves' disease. This is a rare case of combined anticardiolipin antibody positivity, acquired protein s deficiency, and Graves' disease.
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5/11. chorioamnionitis caused by serratia marcescens in a non-immunocompromised host.

    A 26 year old pregnant woman with antithrombin iii deficiency developed recurrent septicaemia with serratia marcescens. In spite of the administration of antibiotics, high grade fever persisted. She subsequently manifested lower abdominal pain, and spontaneous abortion occurred. After the abortion, she became completely afebrile. The amnion was turbid, and microscopic examination of the placenta showed haemorrhage and massive infiltration of neutrophils, suggestive of infectious chorioamnionitis. Pulsed field gel electrophoresis showed that isolates from the blood, urine, and vaginal discharge were genetically identical. Intravenous pyelography revealed that she had a bilateral completed double ureter. It was thought that a urinary tract anomaly caused infection with S marcescens, and the pathogen spread to the chorioamnion via the bloodstream. This is the first report of chorioamnionitis caused by S marcescens in a non-immunocompromised host. In addition, these findings indicate that the chorioamnion can serve as a site for persistent infection in normal pregnancies.
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6/11. factor xiii deficiency: a rare cause of repeated abortions.

    factor xiii deficiency is a rare cause of early abortion. The obstetrical outcome of four pregnancies in two women with factor xiii deficiency is reported. Both women were treated with substitution therapy using locally-prepared cryoprecipitate. The outcome in these two women demonstrated the need for substitution therapy in early pregnancy leading to an increased chance of obstetrical success.
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7/11. Successful pregnancy in a woman with congenital factor xiii deficiency treated with substitutive therapy. Report of a second case.

    A syndrome of marked fetal wastage is associated with congenital factor xiii deficiency in adult women. A previously unreported case of a woman with factor xiii deficiency is described, in which substitutive treatment with normal plasma or placental factor XIII concentrate permitted two normal pregnancies. Factor XIII activity was maintained above 1-2% with intermittent infusion of 300 ml to 450 ml of plasma every 14 days or of 500 units of concentrate every 21 days. This case confirms the only other case so far reported in which factor XIII substitutive therapy was able to permit a normal pregnancy in a woman with factor xiii deficiency and seems to suggest factor XIII to be involved in the process of annidation.
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8/11. The lupus inhibitor in thromboembolic disease and intrauterine death in the absence of systemic lupus.

    This study describes the use of a modified dilute thromboplastin assay for demonstration of the lupus coagulation inhibitor in plasma. A one-stage clotting inhibition assay is used in which the ability of the test plasma to prolong the clotting time of normal plasma is measured. The method is easy to perform and suitable for routine use. Clinical and laboratory data from five patients with the inhibitor but without systemic lupus erythematosus are presented. Thromboembolic manifestations were observed in three patients and obstetric complications possibly due to placenta thrombosis in two. One patient showed a bleeding tendency, associated with prothrombin deficiency. A number of pathological coagulation analyses and other laboratory data may be due to affinity of the lupus inhibitor for negatively charged phospholipids in vitro.
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9/11. Holoacardius: radiologic investigation.

    A case of holoacardius is presented from a monozygotic twin pregnancy of 20 weeks, in which the other twin was normal. The classification is reviewed. While the physiology and anatomy of these malformations are known, the etiology remains obscure. Theories of etiology may be divided in two groups: that the primary deficiency is a failure of the parts to develop; and the belief that the acardius is due to an abnormal vascular communication with secondary atrophy of the formed parts. The abnormal twin in the case studied was diagnosed by ultrasound prenatally and investigated radiologically post-mortem.
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10/11. Etiology of prune belly syndrome: evidence of megalocystic origin in an early fetus.

    BACKGROUND: prune belly syndrome is a rare and complicated condition affecting the genitourinary organs and abdominal wall. The etiology of abdominal musculature deficiency in prune belly syndrome is controversial. We present a case that should elucidate the etiology of this syndrome. CASE: A spontaneously aborted fetus at 12 weeks' gestation with an early stage of prune belly syndrome was investigated by necropsy and light and electron microscopy. Megalocystis resulting from urethral atresia was diagnosed. There was no hydroureter or hydronephrosis, and both light and electron microscopy demonstrated evidence of development of the abdominal musculature. Both testes were elevated as a result of the megalocystis. CONCLUSION: These findings suggest that hypoplasia of the abdominal musculature and cryptorchidism might develop secondary to the presence of chronic megalocystis in this syndrome.
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