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Effectt on pregnancy - Scleroderma

Unfortunately there is no reliable prospective statistical information  regarding the incidence or outcome for either the mother with scleroderma or her fetus, although this may become available with the establishment of a research registry for scleroderma [41]. The extent of diffuse skin disease and systemic involvement, particularly lung, cardiac, and renal, may be more important than the duration of the disease; limited disease carries a better prognosis for the mother and fetus [reviewed in ref. 42].

The enlarging uterus can have an adverse effect on the abdominal or chest skin and on pulmonary volume
already compromised by fibrosis; abdominal sclerosis is rare but chest involvement is more common. Other irritating symptoms may be an increase in reflux esophagitis, constipation, and the possibility of malabsorption due to small bowel dysfunction.

The third trimester has been considered the most dangerous period, the risks being sudden hypertension and renal failure. However, Steen et al. report that renal crisis developed in only 17% of 23 women (2 during pregnancy) with diffuse cutaneous scleroderma who had one or more pregnancies, which was not statistically different from 22% of 116 patients who were not pregnant during the course of disease [43]. These same authors found no increased  frequency of preeclampsia/eclampsia or hypertension in scleroderma pregnancies.

Although pregnancy is possible, there is information that fertility is decreased, the spontaneous abortion rate is increased, and full-term babies may have low birth weights.
An important, but to date unanswered, question is whether pregnancy is a risk factor for the development of scleroderma.

Advances in techniques for prenatal diagnosis have resulted in the unexpected finding that fetal cells can persist in the circulation of parous women and can result in false positive tests in a later pregnancy [44]. Fetal cells have been described in blood samples from women up to 27 years after pregnancy and have been identified as CD341CD381, representing hematopoietic stem cells capable of differentiation into lymphoid cells [45]. Given this fact and that scleroderma has been likened to graft-versus-host disease, which occurs in some patients after bone marrow transplantation or blood transfusion, it has recently been hypothesized that some cases of scleroderma

in women might be the result of graft-versus-host disease [46]. Accordingly, women in whom fetal CD341 stem cells or lymphocytes have entered the maternal circulation, and the paternal HLA genes are markedly similar or identical to the women’s HLA genes (such that fetal cells are not rejected), might be at increased risk for developing scleroderma [46]. In a recent abstract presented at the annual meeting of the American College of Rheumatology, Artlett et al. employed polymerase chain reaction to identify the presence of Y chromosome sequences in DNA extracts from active skin lesions in 19 women with scleroderma and in 68 normal female skin biopsies [47].

 Y chromosome sequences were identified in 58% of the former and in none of the latter group. Magnetically sorted
peripheral blood lymphocytes from two patients with male offspring and two nulliparous age-matched controls revealed the presence of Y sequences in CD141/CD451 and CD31 positively selected cells in the patients but not controls.

This scenario, extended microchimerism, would not apply to all cases of scleroderma because scleroderma has been described in nulligravid women and in men (although transfusion could also account for microchimerism).

REFERENCES

41. Mayes, M. D., Giannini, E. H., Pachman, L. M., Buyon, J. P., Fleckman, P. (1997) Connective tissue disease registries. Arthr. Rheumatol. 40, 1556– 1559.
42. Black, C. M. (1990) Systemic sclerosis and pregnancy. In Bailliere's Clinical Rheumatology (A. L. Parke, ed.), London: Bailliere Tindall, 105–121.
43. Steen, V. D, Conte, C., Day, N., Ramsey-Goldman, R., Medsger, T. A. (1989) Pregnancy in women with systemic sclerosis. Arthr. Rheumatol. 32, 151–157.
44. Simpson, J., Elias, S. (1993) Isolating fetal cells from maternal blood. J. Am. Med. Assoc. 270, 2357–2361.
45. Bianchi, D. (1994) Clinical trials and experience: Boston. Ann. NY Acad. Sci. 731, 147–153.
46. Nelson, J. L. (1996) Maternal-fetal immunology and autoimmune disease. Is some autoimmune disease auto-alloimmune or allo-autoimmune? Arthr. Rheumatol. 39, 191–194.
47. Artlett, C. M., Smith, J. B., Jiminez, S. A. (1997) Identification of fetal cells in the active lesions of skin biopsies of women with systemic sclerosis. Arthr. Rheumatol. 40 (Suppl.), S218.

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