Fetal and Placental Causes of Elevated Serum Alpha-Fetoprotein Levels in Pregnant Women.

The most common association related to alpha-fetoprotein (AFP) is fetal neural tube defect (NTD), and indeed, this is where the international career of this protein began. In times when ultrasonography was not yet technically advanced, the detection of high levels of AFP in maternal serum (MS-AFP) and amniotic fluid was the basis for suspecting neural tube defects. In cases where there was no confirmation of NTD, other causes were sought. It has been established that high titers of MS-AFP could originate in other defects or diseases, such as (1) increased proteinuria in severe fetal kidney diseases; (2) pathological overproduction in liver diseases; (3) penetration through the membranes of gastrointestinal organs exposed to amniotic fluid; (4) passage through the walls of skin vessels; and as a side effect of (5) hepatic hematopoiesis and increased transfer through the edematous placenta in fetal anemia. This article provides a review of the current literature on congenital defects and genetic diseases in the fetus where an elevated level of MS-AFP may serve as the initial diagnostic clue for their detection.

Role of Alpha-Fetoprotein (AFP) in Diagnosing Childhood Cancers and Genetic-Related Chronic Diseases.

Alpha-fetoprotein (AFP) is a protein commonly found during fetal development, but its role extends beyond birth. Throughout the first year of life, AFP levels can remain high, which can potentially mask various conditions from the neurological, metabolic, hematological, endocrine, and early childhood cancer groups. Although AFP reference values and clinical utility have been established in adults, evaluating AFP levels in children during the diagnostic process, treatment, and post-treatment surveillance is still associated with numerous diagnostic pitfalls. These challenges arise from the presence of physiologically elevated AFP levels, inconsistent data obtained from different laboratory tests, and the limited population of children with oncologic diseases that have been studied. To address these issues, it is essential to establish updated reference ranges for AFP in this specific age group. A population-based study involving a statistically representative group of patients could serve as a valuable solution for this purpose.

SARS CoV-2 infection as a risk factor of preeclampsia and pre-term birth. An interplay between viral infection, pregnancy-specific immune shift and endothelial dysfunction may lead to negative pregnancy outcomes.

BACKGROUND: Since SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) was first identified as the cause of Coronavirus disease 19 (COVID-19) it has caused over 649,147,421 infections and over 6,730,382 deaths worldwide. SARS-CoV-2 presents higher infectivity than other coronaviridae (MERS-CoV and SARS-CoV). Pregnant patients, according to previous studies are at high risk of severe COVID-19 course and negative pregnancy outcomes (pre-term birth, low birth weight, preeclampsia, operative delivery and ICU admission with need for mechanical ventilation). METHODS: In this review we focus on the pathophysiology of subcellular changes in COVID-19 and try bring to light the aspects that occur in physiological pregnancy that may cause higher risk of SARS-CoV-2 infection and severe COVID-19 course. RESULTS: Knowledge of potential interplay between viral infection and physiological changes in pregnancy may point us in the direction of future prophylaxis and treatment in this special population.Key MessagesSARS-CoV-2 having affinity to ACE-2 and causing it's downregulation receptor may cause endothelial injury leading to compliment activation and formation of NETs, together with RAS dysregulation this may cause preeclampsia to develop in pregnant patients.PTB may occur in patients as an effect of SARS-CoV-2 infection in first or second trimester as an effect of TLR4 pathway dysregulation with lower levels of IFNß.

Pregnancy as a Risk Factor of Severe COVID-19.

Since first being identified in December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) as an etiological agent behind Coronavirus disease 19 (COVID-19), has caused three waves of a global pandemic, with a fourth in progress. Despite its high percentage of asymptomatic and low-symptomatic courses of illness, the SARS-CoV-2 pandemic has claimed a higher death toll than the SARS-CoV and MERS-CoV epidemics because of its high infectivity when compared to the other coronaviruses. High COVID-19 mortality is associated with age and other coexisting morbidities, as well as healthcare quality. According to several studies, pregnant women are at a higher risk of severe COVID-19 infection and adverse pregnancy outcomes (caesarean delivery, pre-term birth, low birth weight, preeclampsia, ICU admission, and need for mechanical ventilation). In our review of recent literature, we focused on the effects of COVID-19 in pregnant women, emphasizing the subcellular pathophysiology of SARS-CoV-2. In this paper, we concentrate on the pathophysiology of sub-cellular changes in COVID-19 and endeavor to highlight the aspects that manifest in physiological pregnancy and potentially create a higher risk of SARS-CoV-2 infection and acute COVID-19 symptoms. Understanding how pregnancy-associated changes can cause a synergistic effect with COVID-19 may point us in the right direction for future prophylaxis and treatment for women undergoing COVID-19 during pregnancy.

The Role of Inflammation in the Pathogenesis of Preeclampsia.

Preeclampsia (PE) affects 5-8% of pregnant women, and it is the major cause of perinatal morbidity and mortality. It is defined as arterial hypertension in women after 20 weeks of gestation which cooccurs with proteinuria (300 mg/d) or as arterial hypertension which is accompanied by one of the following: renal failure, liver dysfunction, hematological or neurological abnormalities, intrauterine growth restriction, or uteroplacental insufficiency. Currently, pathophysiology of preeclampsia poses a considerable challenge for perinatology. Preeclampsia is characterized by excessive and progressive activation of the immune system along with an increase in proinflammatory cytokines and antiangiogenic factors in fetoplacental unit as well as in vascular endothelium in pregnant women. A single, major underlying mechanism of preeclampsia is yet to be identified. This paper discusses the current understanding of the mechanisms which underlie the development of the condition. Some significant factors responsible for PE development include oxidative stress, abnormal concentration and activity in mononuclear phagocytic system, altered levels of angiogenic and antiangiogenic factors, and impaired inflammatory response triggered by inflammasomes. Detailed understanding of pathophysiology of inflammatory process in PE can largely contribute to new, targeted anti-inflammatory therapies that may improve perinatal outcomes in PE patients.

Perspectives in HPV Secondary Screening and Personalized Therapy Basing on Our Understanding of HPV-Related Carcinogenesis Pathways.

As cervical cancer is one of the most common malignancies in women worldwide even with present screening methods, the incidence in most developed countries is not decreasing for the last 15-20 years. A shift has been observed in the age of diagnosis in favour of younger women, and treatment of already developed cervical cancer is a challenge for surgeons. It is imperative to find new diagnostic methods for accurately pointing out patients at high risk of developing malignant disease and developing personalized treatment. Since cervical cancer is almost exclusively associated with HPV infection, understanding changes happening in an infected cell may prove invaluable for search of such methods, but it may also prove helpful in the diagnosis and treatment of other anogenital and nasopharyngeal region cancers. This review follows HPV-related changes in infected cell biology to point what potential markers and targets for therapy are in option when dealing with HPV-related diseases.

Do the physiological aging of the placenta and the changes in angiogenesis marker sFlt-1 and PlGF concentrations predispose patients to late-onset preeclampsia?

OBJECTIVE: Aging of the placenta is associated with natural processes that impair its functions. The processes are related to both oxidative stress exacerbation and the occurrence of higher concentrations of disordered angiogenesis markers. Both these types of processes are known to play roles in the development of preeclampsia. We attempted to show that natural ageing of the placenta can be one of the cofactors contributing to the development of late-onset preeclampsia. PATIENTS, MATERIALS AND METHODS: 159 pregnant patients were divided into four groups: Two of preeclampsia patients and two of patients with physiological pregnancies, depending on the gestational age. For each group, disordered angiogenesis markers sFlt-1 and PlGF before and after 34 weeks of gestation and in particular stages of gestation were analyzed. RESULTS: Lower PlGF and sFlt-1/PlGF ratio values were found in cases of late-onset preeclampsia. In physiological pregnancies, sFlt-1 values were observed to increase and PlGF values to decrease with gestational age. An association was shown to exist between disordered angiogenesis markers and gestational age both in preeclampsia and physiological pregnancies. CONCLUSIONS: (1) Analyses of disordered angiogenesis markers in early- and late-onset preeclampsia patients and patients with physiological pregnancies allow for a suggestion that natural "ageing of the placenta" and placental hypoperfusion lesions exacerbating with the advancing gestational age are some of the causes of late-onset preeclampsia. (2) Cases of early-onset preeclampsia are associated with more severe changes of disordered angiogenesis marker concentrations, which may be indicative of a more considerable impairment of placental perfusion in such patients. (3) In the course of the physiological pregnancy, there is a gradual increase in sFlt-1 and decrease in PlGF, which implies an elevated angiogenesis disorder that progresses with the gestational age.

sFlt-1/PlGF and Doppler ultrasound parameters in SGA pregnancies with confirmed neonatal birth weight below 10th percentile.

We explored whether there was a relationship between the sFlt-1/PlGF ratio in early-late and late-onset SGA patients and whether it is associated with neonatal birth weight. MATERIAL/METHODS: 110 patients who were diagnosed with a fetal weight below the 10th percentile for gestational age and who at the same time delivered neonates with a birth weight below the 10th percentile for gestational age. For each of the patients sFlt-1, PlGF and the sFlt-1/PlGF ratio were studied and uterine artery (UtA) and umbilical artery (UA) Doppler were performed. RESULTS: sFlt-1/PlGF ratios and neonatal birth weight which showed significant negative correlation across the entire population studied (R = -0.46, p < 0.001). In late-onset SGA patients this negative correlation was observed, as well (R = -0.54, p < 0.001) In the group of patients with pregnancies older than 34 weeks and an sFlt-1/PlGF ratio ≥38, we observed a significantly lower neonatal birth weight when compared to the same gestational age group with an sFlt-1/PlGF ratio <38 (2045 g vs 2405 g, p < 0.001). CONCLUSION: Late-onset SGA syndromes are characterized by lower sFlt-1/PlGF ratios, which indicates a lower degree of placental function impairment. The sFlt-1/PlGF ratio can be a predictor of more significant growth disorders and a lower neonatal birth weight. The sFlt-1/PlGF ratio can be helpful in distinguishing between disordered angiogenesis-dependent and other causes of late-onset SGA cases.

Maternal endothelial damage as a disorder shared by early preeclampsia, late preeclampsia and intrauterine growth restriction.

INTRODUCTION: Preeclampsia (PE) and intrauterine growth restriction (IUGR) are separate disease entities that have frequently been reported as sharing the same pathogenesis. In both of them, angiogenesis disorders and generalized endothelial damage with an accompanying inflammation are the dominant symptoms. In this study, we attempted to prove that both these processes demonstrate the same profile in early PE, late PE and IUGR patients, while the only difference is in the degree of exacerbation of the lesions. PATIENTS, MATERIALS AND METHODS: In 167 patients divided into four groups, three of those with early PE, late PE and IUGR and one control group, fms-like tyrosine kinase-1 (sFlt-1), placental growth factor (PlGF), high sensitive c-reactive protein (hsCRP) and fibronectin were determined. The behavior of these parameters in each of the groups was studied, and correlations between them were sought for. RESULTS: Higher concentrations of sFlt-1, hsCRP and fibronectin and a lower concentration of PlGF were found in the study groups compared to the control group. Significant correlations were observed between the factors concerned. CONCLUSIONS: The higher values of disordered angiogenesis markers, endothelial damage markers and inflammatory markers both in the PE and the intrauterine growth restriction (IUGR) groups suggest the existence of shared disorders in the development of these pathologies. The correlations between disordered angiogenesis markers and endothelial damage markers argue in favor of a mutual relationship between these two processes in the development of pathologies evolving as secondary to placental ischemia. The results obtained confirm that the lesion profiles are the same in both PE and IUGR patients, which can be utilized in developing common diagnostic criteria.

A Common Profile of Disordered Angiogenic Factor Production and the Exacerbation of Inflammation in Early Preeclampsia, Late Preeclampsia, and Intrauterine Growth Restriction.

Preeclampsia and intrauterine growth restriction are two separate disease entities that, according to numerous reports, share the same pathogenesis. In both, angiogenesis disorders and generalized inflammation are the dominant symptoms. In this study, we hypothesized that both diseases demonstrate the same profile in early preeclampsia, late preeclampsia, and intrauterine growth restriction patients, with the only difference being the degree of exacerbation of lesions. One hundred sixty-seven patients were enrolled in the study and divided into four groups: early preeclampsia, late preeclampsia, and intrauterine growth restriction groups, and one control group. Concentrations of the angiogenesis and inflammatory markers soluble fms-like tyrosine kinase receptor 1, placental growth factor, high-sensitivity C-reactive protein, and interleukin-6 were determined, and the behavior of these markers and correlations among them were studied. Higher concentrations of soluble fms-like tyrosine kinase receptor 1, high-sensitivity C-reactive protein, and interleukin-6 and a lower concentration of placental growth factor were observed in the study groups compared with the control group. No differences in concentrations of the studied markers were found among the study groups but significant correlations were observed. The higher values for the angiogenesis and inflammatory markers both in preeclampsia patients and patients with intrauterine growth restriction of placental origin compared with the control group suggest the existence of the same underlying disorders in the development of these pathologies. The observed mutual correlations for disordered angiogenesis and inflammatory markers are suggestive of a mutual relationship between these processes in the development of pathologies evolving secondary to placental ischemia. The same lesion profile was observed for both preeclampsia and 'placental' intrauterine growth restriction patients, which could be used in developing common diagnostic criteria for pregnant patients.

Expansion of medical vocabularies using distributional semantics on Japanese patient blogs.

BACKGROUND: Research on medical vocabulary expansion from large corpora has primarily been conducted using text written in English or similar languages, due to a limited availability of large biomedical corpora in most languages. Medical vocabularies are, however, essential also for text mining from corpora written in other languages than English and belonging to a variety of medical genres. The aim of this study was therefore to evaluate medical vocabulary expansion using a corpus very different from those previously used, in terms of grammar and orthographics, as well as in terms of text genre. This was carried out by applying a method based on distributional semantics to the task of extracting medical vocabulary terms from a large corpus of Japanese patient blogs. METHODS: Distributional properties of terms were modelled with random indexing, followed by agglomerative hierarchical clustering of 3 ×100 seed terms from existing vocabularies, belonging to three semantic categories: Medical Finding, Pharmaceutical Drug and Body Part. By automatically extracting unknown terms close to the centroids of the created clusters, candidates for new terms to include in the vocabulary were suggested. The method was evaluated for its ability to retrieve the remaining n terms in existing medical vocabularies. RESULTS: Removing case particles and using a context window size of 1+1 was a successful strategy for Medical Finding and Pharmaceutical Drug, while retaining case particles and using a window size of 8+8 was better for Body Part. For a 10n long candidate list, the use of different cluster sizes affected the result for Pharmaceutical Drug, while the effect was only marginal for the other two categories. For a list of top n candidates for Body Part, however, clusters with a size of up to two terms were slightly more useful than larger clusters. For Pharmaceutical Drug, the best settings resulted in a recall of 25 % for a candidate list of top n terms and a recall of 68 % for top 10n. For a candidate list of top 10n candidates, the second best results were obtained for Medical Finding: a recall of 58 %, compared to 46 % for Body Part. Only taking the top n candidates into account, however, resulted in a recall of 23 % for Body Part, compared to 16 % for Medical Finding. CONCLUSIONS: Different settings for corpus pre-processing, window sizes and cluster sizes were suitable for different semantic categories and for different lengths of candidate lists, showing the need to adapt parameters, not only to the language and text genre used, but also to the semantic category for which the vocabulary is to be expanded. The results show, however, that the investigated choices for pre-processing and parameter settings were successful, and that a Japanese blog corpus, which in many ways differs from those used in previous studies, can be a useful resource for medical vocabulary expansion.

Diagnostic Potential of Evaluation of SDF-1α and sRAGE Levels in Threatened Premature Labor.

Preterm birth remains the most prevalent cause of neonatal morbidity. This study aimed to evaluate the diagnostic value of SDF-1α, resistin, secretory RAGE (sRAGE), and endogenous secretory RAGE (esRAGE) in preterm labor. A total of 211 pregnant women participated in the study. Group A contained 72 women between 22 and 36 weeks of gestation, with premature labor, who finally had preterm birth. Group B contained 66 women in labor between 37 and 41 weeks of gestation. Women in group A had lower SDF-1α and sRAGE levels than those in group B. Moreover, in group A, SDF-1α and sRAGE levels were correlated with the latency period from the occurrence of premature labor symptoms until delivery. Sensitivity and specificity of studied parameters for prediction of preterm birth were 95% and 40% for SDF-1α and 51.3% and 93.5% for sRAGE, respectively. The prognostic value of plasma SDF-1α and sRAGE levels was comparable with that of cervical length ultrasound measurement and serum C-reactive protein levels. We conclude that SDF-1α and sRAGE appear to play a major role in the diagnosis of preterm birth and its evaluation could be convenient and useful for predicting preterm birth.

Using Doppler ultrasound of the uterine and umbilical arteries and disordered angiogenesis markers (sFlt-1/PlGF) in unified monitoring of ischemic placental syndrome patients.

OBJECTIVE: The shared pathogenesis of placental ischemia entitles us to create a single treatment model. We attempted to develop a unified method for monitoring ischemic placental syndrome patients using Doppler ultrasound of the uterine and umbilical arteries and disordered angiogenesis markers sFlt-1 and PlGF. MATERIAL AND METHODS: 182 pregnant women suffering from the ischemic placental syndrome were divided into four groups depending on the severity of their lesions revealed in the Doppler ultrasound examination and weeks of pregnancy. We analyzed the behavior of clinical and biochemical parameters in these groups and the correlations between the ultrasound examination and the disordered angiogenesis markers. RESULTS: In the group of patients demonstrating more severe Doppler ultrasound lesions, the clinical and biochemical parameters were significantly more expressed, whereas unfavorable obstetric events occurred either earlier or more frequently. Lesions revealed in Doppler occur more commonly in groups before 34th week of pregnancy. Disordered angiogenesis markers are significantly correlated with ultrasound examination results. CONCLUSIONS: A unified method for monitoring the ischemic placental syndrome based on pathogenetic, biophysical (Doppler ultrasound), and biochemical (sFlt-1/PlGF) parameters is feasible and constitutes a valuable supplement to the existing standards, while the high correlations between Doppler ultrasound examinations and both sFlt-1 and PlGF point to a shared pathogenesis of the lesions. Intensity of Doppler changes is connected with time of testing and pregnancy duration.

Ischemic placental syndrome--prediction and new disease monitoring.

The last decade has seen an improved understanding of the cause of the development of pathologies such as gestational hypertension, preeclampsia, intrauterine growth restriction, intrauterine fetal death or placental abruption. Nowadays, we know that most conditions within this group share the same pathogenesis, the cause of which is placental ischemia. The following review is an attempt to propose a new method for prediction, diagnosis and--above all--appropriate monitoring of pregnant women and fetuses developing the ischemic placental syndrome with the use of tests that are new but yet widely available in clinical diagnosis. They are closely related to the condition's pathogenesis, therefore their elevated levels may predate clinical symptoms, and--most importantly--they correlate with syndrome aggravation and the occurrence of complications. Perhaps, the new look will allow us to improve perinatal results by reducing mortality and severe complications in pregnant women and fetal deaths resulting from sudden intrauterine fetal death or placental abruption.

Development of a focal segmental glomerulosclerosis after pregnancy complicated by preeclampsia: case report and review of literature.

The global incidence of preeclampsia has been estimated at 3-5% of all pregnancies. It is the main cause of morbidity and mortality among pregnant women and their fetuses worldwide. In preeclampsia, the incorporation of cytotrofoblast into the spiral arteries is incomplete. Changed placenta releases into the mother's circulation soluble VEGF receptor-1 (sFlt-1) which causes many disorders including kidney damage. VEGF is produced by glomerular podocytes and is necessary for their normal function. The damage of podocytes leads to a glomerulosclerosis development. The damage of the critical number of podocytes contributes to the development of focal segmental glomerulosclerosis - kind of glomerulonephritis. We present a case of woman who as a result of preeclampsia developed focal segmental glomerulosclerosis manifested as nephritic syndrome. We describe a mechanism for the development of such changes in glomeruli in the course of preeclampsia.

Soluble and Endogenous Secretory Receptors for Advanced Glycation End Products in Threatened Preterm Labor and Preterm Premature Rupture of Fetal Membranes.

The aim of the study was to compare sRAGE and esRAGE plasma levels in pregnant women with (A) threatened premature labor (n = 41), (B) preterm premature rupture of membranes (n = 49), and (C) preterm rupture of membranes at term (n = 48). The relationship between these and classic intrauterine infection markers and the latent time from symptoms up to delivery depending on RAGE's concentration were investigated. In groups A and B, a positive correlation was found between plasma sRAGE and latent time (r = 0,422; p = 0,001; r = 0,413, p = 0,004, resp.). High prognostic values were found in both groups for plasma sRAGE concentration and the latent time from symptoms up to delivery. Groups B and C presented higher levels of esRAGE than group A (526,315 ± 129,453 pg/mL and 576,212 ± 136,237 pg/mL versus 485,918 ± 133,127 pg/mL, p< 0,05). The conclusion is that sRAGE concentration can be a favorable prognostic factor in the presence of symptoms of threatened premature labor. Higher esRAGE plasma level in case of the rupture of membranes in mature and premature pregnancy suggests its participation in fetal membranes destruction.

Soluble receptors for advanced glycation end products and receptor activator of NF-κB ligand serum levels as markers of premature labor.

BACKGROUND: This study aimed to determine the relationships between secretory and endogenous secretory receptors for advanced glycation end products (sRAGE, esRAGE), sRANKL, osteoprotegerin and the interval from diagnosis of threatened premature labor or premature rupture of the fetal membranes to delivery, and to evaluate the prognostic values of the assessed parameters for preterm birth. METHODS: Ninety women between 22 and 36 weeks' gestation were included and divided into two groups: group A comprised 41 women at 22 to 36 weeks' gestation who were suffering from threatened premature labor; and group B comprised 49 women at 22 to 36 weeks' gestation with preterm premature rupture of the membranes. Levels of sRAGE, esRAGE, sRANKL, and osteoprotegerin were measured. The Mann-Whitney test was used to assess differences in parameters between the groups. For statistical analysis of relationships, correlation coefficients were estimated using Spearman's test. Receiver operating characteristics were used to determine the cut-off point and predictive values. RESULTS: In group A, sRAGE and sRANKL levels were correlated with the latent time from symptoms until delivery (r = 0.422; r = -0.341, respectively). The sensitivities of sRANKL and sRAGE levels for predicting preterm delivery were 0.895 and 0.929 with a negative predictive value (NPV) of 0.857 and 0.929, respectively. In group B, sRAGE and sRANKL levels were correlated with the latent time from pPROM until delivery (r = 0.381; r = -0.439). The sensitivity of sRANKL and sRAGE for predicting delivery within 24 h after pPROM was 0.682 and 0.318, with NPVs of 0.741 and 0.625, respectively. Levels of esRAGE and sRANKL were lower in group A than in group B (median = 490.2 vs 541.1 pg/mL; median = 6425.0 vs 11362.5 pg/mL, respectively). CONCLUSIONS: Correlations between sRAGE, sRANKL, and pregnancy duration after the onset of symptoms suggest their role in preterm delivery. The high prognostic values of these biomarkers indicate their usefulness in diagnosis of pregnancies with threatened premature labor.

On the significance of new biochemical markers for the diagnosis of premature labour.

Preterm labour is defined as a birth taking place between 22nd and 37th weeks of gestation. Despite numerous studies on the aetiology and pathogenesis of preterm labour, its very cause still remains unclear. The importance of the cytokines and acute inflammation in preterm labour aetiology is nowadays well-proven. However, chronic inflammation as an element of the pathogenesis of premature labour is still unclear. This paper presents a literature review on the damage-associated molecular patterns (DAMPs), receptors for advanced glycation end products (RAGE), negative soluble isoforms of RAGE, chemokine-stromal cell-derived factor-1 (SDF-1) and one of the adipokines, resistin, in the pathogenesis of preterm labour. We conclude that the chronic inflammatory response can play a much more important role in the pathogenesis of preterm delivery than the acute one.

Urinary lysosomal enzyme excretion in pregnant women with hypertensive disorders.

BACKGROUND: The authors assessed proximal renal tubular dysfunction and/or damage in pregnant women with various types of hypertension by measuring the three urinary lysosomal enzyme levels: N-acetyl-ß-d-glucosaminidase (NAG), arylsulfatase A and ß-glucuronidase. METHODS: The study consisted of 120 pregnant women divided into four groups: 41 women in 20th week of gestation or more, with pregnancy-induced hypertension (PIH group), 28 pregnant women after 20 weeks of pregnancy with pre-eclampsia (PE group), 21 pregnant women with chronic hypertension, identified before 20th week of pregnancy (CH group) and 30 healthy, pregnant women (healthy controls (HC) group). RESULTS: Statistical analysis showed significantly higher levels of all the three of lysosomal enzymes in the urine of patients with PE compared with the healthy pregnant women, pregnant women with PIH and the ones with chronic hypertension. Additionally, significantly higher values of NAG were found in the group of pregnant women with PIH compared with healthy pregnancies. No correlation was found between the concentration of enzymes in urine and values of blood pressure in any of the analyzed groups of pregnant women. CONCLUSIONS: The authors conclude that higher values of all the studied enzymes in PE group, in the comparison with the other groups, indicate proximal tubular damage at the cellular level. The lack of correlation between the concentration of lysosomal enzymes and blood pressure suggests that the damage to these parts of kidney is complex. In addition, mechanisms other than hypertension realizing intracellular enzymes may be involved in this process.

Pregnancy delivery and puerperium in a patient with lysinuric protein intolerance--a case report.

The paper presents the course of pregnancy delivery and early postpartum period in a 23-year-old woman with lysinuric protein intolerance (LPI). The pregnancy was uneventful and resulted in a caesarean birth to a healthy baby at 37 weeks gestation. Nevertheless, the course of pregnancy in women with LPI is associated with a significantly increased risk of serious complications, including acute hyperammonemia, preeclampsia and postpartum bleeding, as well as fetus intrauterine growth retardation. In many cases, intensive metabolic monitoring and a proper diet with protein limitation and appropriate amino acids supplementation may significantly reduce the risk for both the mother and the newborn.