Prevalence of Vitamin D Deficiency in Burka-clad Pregnant Women in a 450-Bedded Maternity Hospital of Delhi.

AIM: To assess the prevalence of vitamin D deficiency in burka-clad pregnant women and to study feto-maternal outcome in these women. METHODS: 200 pregnant burka-clad women of 18-40-year age group irrespective of the period of gestation were recruited from the ANC OPD/ward of Kasturba hospital, and their vitamin D levels were estimated. Patients were categorized into vitamin D deficient, vitamin D inadequate, and vitamin D adequate according to The Endocrine Society Guidelines. The association of vitamin D deficiency with dietary/environmental factors was taken note of. Associations with preeclampsia, gestational diabetes mellitus (GDM), low birth weight (LBW), prematurity, APGAR score, and NICU admission were also studied. RESULTS: 78 patients (39.0 %) were vitamin D inadequate; 75 patients (37.5 %) were vitamin D deficient; and 47(23.5 %) were vitamin D adequate. Mean value of vitamin D level was 23.25 ng/ml ± 18.49 (SD). Fifteen patients (7.5 %) developed preeclampsia, and all 15 were vitamin D deficient; 13 (6.5 %) developed GDM; and only 5 (2.5 %) of them were vitamin D deficient. 19 patients (9.5 %) delivered LBW babies; mothers of 15 (7.5 %) of them were vitamin D deficient. 12 patients (6.0 %) delivered premature babies, and mothers of 4 (2 %) were vitamin D deficient; 12 babies had APGAR score <7 at 5 min; mothers of 4 (2.0 %) were vitamin D deficient. Babies of 12 patients (6 %) were admitted in NICU, and of these 12 babies, mothers of 5 (2.5 %) were vitamin D deficient. CONCLUSION: The prevalence of vitamin D deficiency was high among burka-clad pregnant women, and it is associated with adverse maternal and fetal outcomes. Routine screening of vitamin D levels is recommended in burka-clad women to improve the feto-maternal outcome.

Role of Thyroid Dysfunction in Patients with Menstrual Disorders in Tertiary Care Center of Walled City of Delhi.

OBJECTIVE: To study the prevalence of thyroid disorders and its correlation with menstrual disorders. METHODS: 100 women aged between 15 and 45 years who attended gyne OPD in Kasturba Hospital, Delhi, were included for this cross-sectional study. The study group comprised 50 patients presented with menstrual complaints. The control group consisted of 50 women of same age group with complaints other than menstrual disorders. Thyroid function tests, anti-TPO antibody estimation, and endometrial sampling were done in all patients. RESULTS: In patients with menstrual disorders, 44 % had thyroid disorders in which subclinical hypothyroidism was prevalent in 20 %, overt hypothyroidism in 14 %, and overt hyperthyroidism in 8 % of the women. Autoimmune thyroid antibodies were present in 30 % patients of women with menstrual disorders. On endometrial sampling, hypothyroid patients mainly had proliferative endometrium (42.85 %) whereas hyperthyroid had atrophic endometrium (60 %). CONCLUSIONS: Thyroid dysfunction is an important causative etiology of menstrual abnormalities. Assessment of thyroid function should be done in all patients with menstrual disorders to avoid unnecessary interventions like curettage and hysterectomy.

A Study of salt and fat Consumption pattern in Regional Indian diet among hypertensive and dyslipidemic PaTients - SCRIPT study.

BACKGROUND: Cardiovascular diseases are leading cause of mortality and morbidity. There is an increasing prevalence of hypertension and dyslipidemia due to globalization and adoption of westernized dietary habits in India. These transitions are manifest in dietary patterns and health outcomes. OBJECTIVE: To study the dietary salt and fat intake among patients diagnosed with hypertension and dyslipidemia in India. METHODS: SCRIPT study was a pilot exploratory, cross-sectional, observational, descriptive, multi-center study. It was conducted across hospitals and clinics in five metro cities of India, represented into four regional zones. In each region (North, n = 113; East, n = 98; West, n = 83; South, n = 152), patients diagnosed with hypertension and dyslipidemia were enrolled in the study. Socio-demographic and treatment details were recorded. Participants were interviewed by a dietician and their dietary intake was assessed by a three-day recall of food item questionnaire/ food diary. RESULTS: Overall the mean total daily salt consumption was 10.9 grams. Region-wise, the mean daily salt consumption in North, East, West and South were 14.13, 9.81, 10.12 and 9.38 grams respectively. The daily salt consumption in the North was significantly higher than other regions (P=0.012). The daily consumption of saturated fats (total saturated fat, ghee and butter) in the North was higher and statistically significantly in comparison to West, South and East (P <0.05). Overall, fats contributed to 24.1%, proteins contributed to 12.7% and carbohydrate contributed to 63.2% of total energy per day. The percentage of fat and protein contributing to total energy per day was within the acceptable range. CONCLUSIONS: Our study documented higher dietary salt intake than that recommended in India. There is an urgent need to address the issue of high salt and saturated fat consumption. Nutritional strategies for reducing salt intake, saturated fat and balancing energy nutrients should be urgently applied in Indian hypertensive and dyslipidemia patients.

Autoantibodies to ribosomal P antigens with immune complex glomerulonephritis in SJL mice treated with pristane.

BALB/c ByJ mice develop a lupus-like syndrome characterized by anti-nRNP/Sm and Su autoantibodies and immune complex glomerulonephritis after a single i.p. pristane injection. In contrast, mercuric chloride induces anti-fibrillarin Abs only in SJL and other H-2s mice, and not in BALB/c (H-2d) mice. In the present study, the specificities of autoantibodies induced by pristane and HgCl2 were compared in SJL and BALB/c mice to examine whether these strains are "programmed" to make different sets of autoantibodies in response to nonspecific immune stimulation. Unexpectedly, the predominant autoantibodies induced by pristane in SJL mice were neither those characteristic of HgCl2-treated SJL mice nor those associated with pristane-induced disease in BALB/c mice but, rather, anti-ribosomal P, another lupus-related specificity. The autoantibodies were strongly reactive with the C-terminal 22 amino acids of the ribosomal P2 protein, indicating that they exhibited similar fine specificities to anti-P Abs in human SLE and MRL/Ipr mice. Like BALB/c mice, pristane-treated SJL mice developed severe glomerulonephritis characterized by proteinuria, mesangial proliferation, and glomerular immune complex deposits. This is the first evidence that the induction of a lupus-like syndrome by pristane is not restricted to BALB/c mice. The predominance of anti-P Abs in SJL mice contrasts sharply with the predominance of anti-nRNP/Sm and Su, in pristane-treated BALB/c mice, even though the renal lesions were similar in both strains. The data suggest that H-2s does not program mice to produce anti-fibrillarin Abs in response to nonspecific immune stimulation, arguing that autoantibody induction by pristane involves Ag-specific mechanisms.

Autoantibodies that stabilize the molecular interaction of Ku antigen with DNA-dependent protein kinase catalytic subunit.

DNA-dependent protein kinase (DNA-PK) consists of a DNA binding subunit (Ku autoantigen), and a catalytic subunit (DNA-PKcs). In the present study, human autoantibodies that recognize novel antigenic determinants of DNA-PK were identified. One type of autoantibody stabilized the interaction of DNA-PKcs with Ku and recognized the DNA-PKcs -Ku complex, but not bio-chemically purified DNA-PKcs. Another type recognized purified DNA-PKcs. Autoantibodies to Ku (p70/p80 heterodimer), 'stabilizing' antibodies, and antibodies to DNA-PKcs comprise a linked autoantibody set, since antibodies recognizing purified DNA-PKcs were strongly associated with stabilizing antibodies, whereas stabilizing antibodies were strongly associated with anti-Ku. This hierarchical pattern of autoantibodies specific for components of DNA-PK (anti-Ku > stabilizing antibodies > anti-DNA-PKcs) may have implications for the pathogenesis of autoimmunity to DNA-PK and other chromatin particles. The data raise the possibility that altered antigen processing and/or stabilization of the DNA-PKcs-Ku complex due to autoantibody binding could play a role in spreading autoimmunity from Ku to the weakly associated antigen DNA-PKcs.

Changing autoantibody profiles with variable clinical manifestations in a patient with relapsing systemic lupus erythematosus and polymyositis.

The production of autoantibodies characteristic of different autoimmune disease subsets is thought to be controlled primarily by genetic factors, whereas non-genetic factors are generally believed to be of secondary importance. A patient with systemic lupus erythematosus (SLE) and polymyositis (PM) who experienced frequent relapses associated with changing clinical manifestations and autoantibody specificities is reported. Her initial presentation as SLE with anti-Sm antibodies shifted to the onset of PM with temporal production of a different set of autoantibodies. The latter antibodies disappeared when myositis resolved, followed by the reappearance of autoantibodies and clinical manifestations characteristic of SLE. The shifts of autoantibody profiles in association with variable clinical manifestations in this patient argue that environmental factors may play a more important role in autoimmunity than previously supposed, and that interplay between environmental triggers and genetic predisposing factors may lead to the constellation of autoimmune disease manifestations exhibited at a particular time.

Absence of autoantigen Ku in mature human neutrophils and human promyelocytic leukemia line (HL-60) cells and lymphocytes undergoing apoptosis.

The Ku autoantigen is a heterodimer of 70- and 80-kD proteins recognized by autoantibodies from patients with systemic lupus erythematosus and related diseases that is the DNA-binding component of a DNA-dependent protein kinase. The catalytic activity of DNA-dependent protein kinase is carried by a 350-kD subunit (p350). In light of the recently described role of Ku in repairing double-strand DNA breaks, we investigated the regulation of Ku and p350 levels in neutrophils, a terminally differentiated cell type destined to undergo apoptosis. Since the appearance of double-strand DNA breaks is characteristic of apoptosis, we were interested in the possibility that Ku might oppose programmed cell death. Analysis of peripheral blood cells by flow cytometry using anti-Ku and anti-p350 monoclonal antibodies revealed that neutrophils were unstained, whereas resting (G0) lymphocytes were positive. The absence of Ku in mature neutrophils was confirmed by Western blotting and enzyme-linked immunosorbent assay for Ku antigen. In contrast, the human promyelocytic leukemia line, HL-60, which undergoes differentiation toward neutrophils after dimethylsulfoxide treatment, was positive for Ku and p350. In view of the short lifespan of neutrophils and the prolonged half-life of Ku and p350 (> 5 d), these data suggested that Ku was actively degraded during myeloid differentiation. Analysis of HL-60 cells by flow cytometry revealed that Ku staining was bimodal. Cells in G1/G0, S, or G2/M were all stained positively, whereas cells with a subdiploid DNA content characteristic of apoptosis were Ku negative. Similar results were obtained with phytohemagglutin-stimulated human lymphocytes. These data suggest that the Ku antigen is actively degraded in both myeloid cells destined to undergo apoptosis and apoptotic lymphocytes, raising the possibility that degradation of Ku may help to prevent the inappropriate repair of fragmented nuclear DNA during apoptosis.

Association of autoantibodies to topoisomerase I and the phosphorylated (IIO) form of RNA polymerase II in Japanese scleroderma patients.

Autoantibodies to RNA polymerases (RNAP) I and III are highly specific for scleroderma (SSc), whereas autoantibodies to RNAP II are associated with systemic lupus erythematosus (SLE) and overlap syndromes, as well as SSc. The specificities of autoantibodies to RNAP I, II, and III in 129 SSc sera were investigated in the present study. Immunoprecipitation and pulse-chase analysis demonstrated several patterns of autoantibody recognition of RNAPs. Some sera immunoprecipitated RNAP II only after its largest subunit was phosphorylated, suggesting that they contained autoantibodies that recognized an epitope carrying a phosphoamino acid. Autoantibody recognition of all three classes of RNAPs was influenced strongly by race. Although in SLE, autoantibodies to the phosphorylated form of RNAP II (RNAP IIO) were identified in all races, in SSc, these autoantibodies were seen in 21% of Japanese and 5% of Black patients, but never in Caucasians. A striking association of anti-RNAP IIO with anti-topoisomerase I (topo I) autoantibodies was found in Japanese and Black SSc, but not SLE, patients. However, anti-topo I Abs were not associated with anti-RNAP IIO in Caucasians. Japanese SSc patients who were positive for both anti-RNAP IIO and anti-topo I Abs had a significantly higher frequency of diffuse disease, pigmentation changes, flexion contractures, and acro-osteolysis than patients having autoantibodies to topo I alone, and were diagnosed at a younger age (p < 0.05). These data suggest that genetic factors (possibly HLA-linked) influence autoantibody specificity, and that different autoantibody fine specificities may either cause, or be predictive of, different clinical outcomes.

Autoantibodies to RNA polymerase II are common in systemic lupus erythematosus and overlap syndrome. Specific recognition of the phosphorylated (IIO) form by a subset of human sera.

Autoantibodies to RNA polymerases (RNAP) I, II, and III are reported to be highly specific for the diagnosis of scleroderma (systemic sclerosis, SSc). In the present study, the specificity of autoantibodies to RNAP I and III for SSc was confirmed by immunoprecipitation of 35S-labeled proteins. However, we report here the previously unrecognized production of anti-RNAP II autoantibodies by 9-14% of patients with SLE and mixed connective tissue disease/overlap syndrome. 12 out of 32 anti-RNAP II positive sera (group 1) immunoprecipitated a diffuse 220-240-kD band identified as the largest subunit of RNAP II whereas the remaining 20 (group 2) immunoprecipitated preferentially the 240-kD phosphorylated (IIo) form of the large subunit. After pulse labeling, group 1 sera immunoprecipitated only the 220-kD (IIa) RNAP II subunit, whereas the diffuse IIa/IIo band plus the 145-kD second largest RNAP II subunit (IIc) were immunoprecipitated after several hours of cold chase, suggesting that these sera recognized primarily the largest subunit of RNAP II. Group 2 sera recognized the IIc subunit after pulse labeling, and immunoprecipitated the IIc and IIo, but not the IIa, subunits after cold chase. Although it has been suggested that autoantibodies to RNAP II are usually accompanied by anti-RNAP I/III in SSc, all but one of the anti-RNAP II positive sera from SLE or mixed connective tissue disease/overlap syndrome patients, as well as most of the SSc sera, were negative for anti-RNAP I/III. Moreover, in contrast to previous reports suggesting that anti-RNAP antibodies rarely coexist with other SSc subset marker antibodies, anti-RNAP II antibodies were often accompanied by anti-Ku, anti-nRNP, or anti-topoisomerase I autoantibodies in the present study. We conclude that autoantibodies to RNAP II are not a specific marker for SSc, whereas autoantibodies to RNAP I/III are associated primarily with SSc. In addition, we have identified two distinctive patterns of RNAP II antigen recognition by autoantibodies, one of them characterized by specific recognition of the transcriptionally active (phosphorylated) form of RNAP II. The clinical significance of these different patterns remains to be determined.

Onset of polymyositis with autoantibodies to threonyl-tRNA synthetase during pregnancy.

A 24-year-old black woman developed polymyositis with autoantibodies to threonyl-tRNA synthetase in the 2nd trimester of her 3rd pregnancy. This was complicated by fetal loss and the development of severe relapsing myositis resistant to corticosteroid and azathioprine therapy. These features were also common in other cases in the literature. Antisynthetase antibodies had not been reported in myositis occurring during pregnancy and may be of interest regarding the pathogenesis of inflammatory myopathy complicating pregnancy.

Recurrent annular erythema with anti-SSA/Ro and anti-SSB/La antibodies localized on palms and fingers in an elderly man.

A 69-year-old Japanese man with recurrent annular erythema localized on palms and flexor surface of fingers with anti-SSA/Ro and anti-SSB/La antibodies, is reported. The present case indicates that even in an elderly man with atypical localization, annular erythema with autoimmunity may be considered and serological analysis should be performed. Systematic studies will be required to understand the relationship between 'recurrent annular erythema associated with anti-SSB/La antibodies' in Japanese, subacute cutaneous lupus erythematosus (SCLE) and 'annular erythema associated with Sjogren's syndrome'.

Systemic lupus erythematosus. Antibodies to DNA, DNA-binding proteins, and histones.

Pathogenic autoantibodies to DNA are frequently associated with autoantibodies to chromatin-associated proteins such as histones or the Ku (p70/p80) antigens. In view of the increasing evidence that autoantibody production is antigen-driven, and because DNA is packaged with proteins in the cell, we suggest that anti-DNA antibodies may arise in response to DNA-protein complexes rather than naked DNA. Recent studies of the specificities of autoantibodies directed against the components of nucleosomes and transcriptional complexes are consistent with this hypothesis. The possible clinical significance of immune recognition of various types of chromatin complexes in autoimmune disease is discussed.

Intracranial arteriovenous malformation: contralateral steal phenomena.

Sixty-two patients with radiographically proven intracranial arteriovenous malformations underwent preoperative regional cerebral blood flow measurement with 133Xe single-photon emission computed tomography. Contralateral regions of hypoperfusion were detected in all cases. Steal severity was assessed according to the contralateral steal index [ISteal(c)]. ISteal(c) was greater than 0.7 (severe) in 22 (35%), 0.7-0.8 (intermediate) in 18 (29%), and greater than 0.8 (mild) in 22 (35%). ISteal(c) was more frequently severe or mild in females and more often intermediate in males (p less than 0.05). Hyperemic complications were encountered more frequently in patients with intermediate ISteal(c) (p = 0.086). An unfavorable outcome was associated with less severe contralateral steal (p = 0.12). A detailed clinical, radiographic, and hemodynamic profile may help to preoperatively identify patients at high risk for a poor surgical outcome.

Intracranial arteriovenous malformation: relationships between clinical and radiographic factors and cerebral blood flow.

Arteriovenous malformations (AVMs) dramatically alter normal cerebral circulatory dynamics. Clinical and radiographic data from 62 patients were analyzed to determine their impact on total brain blood flow (TBF) measured by single-photon emission computed tomography. 48% of patients presented with hemorrhage and 34% with progressive deficits. 37% had angiographic steal and 21% developed postoperative hyperemic complications. 40% were under 30 years old, 45% were between 30 and 50 years of age, and 15% were over 50. TBF was less than 70 ml/100 gm/min in 32% of patients, between 70 and 84 ml/100 gm/min in 40%, and greater than 84 ml/100 gm/min in 27%. Female patients had higher TBF than males; 42% of females but only 17% of males had values greater than 84 ml/100 gm/min (p less than 0.05). A trend toward decreased TBF with advancing age was noted. Intracranial hemorrhage was associated with lower TBF; 47% of patients with hemorrhage and 19% of those without had TBF of less than 70 ml/100 gm/min (p less than 0.05). 89% of patients with AVMs less than 5 cm in diameter had TBF of less than or equal to 84 ml/100 gm/min, and 65% of those with larger AVMs had similarly low flows (p less than 0.05). A trend toward lower TBF was observed in patients with unfavorable outcomes.

The effect of acetazolamide on regional cerebral blood flow in patients with Alzheimer's disease or stroke as measured by single-photon emission computed tomography.

Regional cerebral blood flow (rCBF) was assessed in 35 patients with possible or probable Alzheimer's disease (AD) and in 16 patients known to have had at least one stroke. Patients were evaluated before and after the administration of 1 g acetazolamide (ACZ) by means of a rotating four-detector single-photon emission computed tomograph (SPECT) and inhaled Xe-133. RCBF values in mL/minute/100 g were derived from eight cortical regions of interest (ROI), and from the whole transverse section as a measure of whole brain flow (WBF). ROI/WBF ratios were calculated for each ROI in paired determinations done before and 15 minutes after the administration of ACZ. Results were compared with those previously obtained in a study of 15 normal, healthy volunteer subjects. ROI/WBF ratios greater than 2 standard deviations (SD) below the mean for a given ROI in the normal group were regarded as probably abnormal, whereas ratios greater than 4 SD below the mean were considered definitely abnormal. After ACZ administration, the number of ROI greater than 2 SD below the normal mean decreased significantly in the AD group and was unchanged in the stroke patients. However, the number of ROI/WBF ratios greater than 4 SD below the normal mean fell in the AD group and rose in the stroke group, with the difference in behavior highly statistically significant. Thus, the response of low-flow areas to ACZ differs in AD and in stroke, which could be of ultimate diagnostic significance.

Intracranial arteriovenous malformation: relationships between clinical and radiographic factors and ipsilateral steal severity.

Intracranial arteriovenous malformations (AVMs) are high flow shunts that may jeopardize the perfusion of adjacent tissue. Clinical and radiographic data from 62 patients were analyzed to determine their relationship to the severity of steal measured by single photon emission computed tomography (SPECT). The ipsilateral steal index [ISteal(i)] was determined by dividing regional cerebral blood flow (rCBF) values within hand-drawn regions of hypoperfusion in the ipsilateral hemisphere by total brain flow, which was calculated as the average rCBF of each hemisphere. Of the patients, 40% were less than 30 years of age, 45% were 30 to 50 years old, and 15% were over 50. Forty-eight per cent presented with hemorrhage and 34% presented with progressive deficits. There was angiographic steal in 37%, and postoperative hyperemic complications developed in 21%. All patients had ipsilateral regions of hypoperfusion. The ISteal(i) was less than 0.7 in 23 (37%), 0.7 to 0.8 in 20 (32%), and greater than 0.8 in 19 (31%). The ISteal(i) was significantly less severe in the patients over 50; 78% of these patients had an ISteal(i) of greater than 0.8 (P less than 0.01). A history of hemorrhage was associated with less severe steal than that in patients who had not bled (P = 0.088). Patients presenting with a history of progressive deficits had increased severity of steal compared with those without progressive deficits (P less than 0.05). A trend toward decreased severity of steal was noted in patients with unfavorable outcomes.(ABSTRACT TRUNCATED AT 250 WORDS)