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Serum Prolactin Levels (serum + prolactin_level)

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Medical Sciences	100%

Selected Abstracts

Prolactin Levels in Sudden Unexpected Death in Epilepsy

EPILEPSIA, Issue 1 2000
K. Opeskin
Summary: Purpose: To assess serum prolactin levels in sudden unexpected death in epilepsy (SUDEP) and control groups to test the hypothesis that if seizures occur routinely as a terminal event in SUDEP, then raised prolactin levels may be an indicator of terminal seizure. Methods: Blood was taken for measurement of prolactin levels from subjects with SUDEP and three control groups. The control groups were those with epilepsy dying from causes other than epilepsy (e.g., ischemic heart disease or injuries), physiologically stressed individuals without epilepsy (they were admitted to the hospital after an acute illness and died after several hours to 3 days), and nonepileptic rapid deaths (these people collapsed suddenly and died at the scene). In the SUDEP group, evidence for terminal seizure was considered to be at least one of the following: body found half on, half off the bed, or urinary incontinence at the scene, or bitten lips or tongue at autopsy. Results: There was evidence for terminal seizure at the scene or at autopsy in four of the 10 SUDEP cases. Serum prolactin levels were not significantly increased in the SUDEP group compared with the controls. None of the SUDEP subjects, including those with clinical evidence of a terminal seizure, had high prolactin levels characteristic of those observed after seizures in living subjects. Conclusions: Prolactin levels are not raised in SUDEP, even if there is evidence of terminal seizure. As prolactin takes 15,20 min to peak after a seizure in life, there may be insufficient time for a prolactin increase to occur in SUDEP. Thus prolactin levels cannot be used to determine if a deceased individual with epilepsy had a seizure or to answer the broad question whether SUDEP is always associated with a terminal seizure. [source]

An unusual association of pemphigus vulgaris with hyperprolactinemia

INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 10 2002
MNAMS, Sujay Khandpur MD
A 21-year-old unmarried woman presented with oral ulcerations and generalized, itchy, fluid-filled, skin lesions of 10 days' duration. The lesions ruptured spontaneously, resulting in extensive denuded areas covered by crusts. One month prior to this, she experienced pain and enlargement of both breasts with galactorrhea. Her menstrual cycles were normal initially, but later she developed menstrual irregularities. No past history suggestive of any other systemic or skin disease, including atopy or drug allergies, could be obtained. Her family history was not contributory. Dermatologic examination revealed multiple, flaccid bullae and extensive denuded areas of skin covered with crusts over the scalp, face, trunk, and upper and lower limbs (Fig. 1). Bulla spread sign and Nikolsky's sign were positive. The oral mucosa, including the lips, buccal surface, tongue, and palate, showed multiple erosions covered with necrotic slough. The rest of the mucocutaneous and systemic examination was within normal limits. Figure 1. Extensive erosions and flaccid bullae over the trunk with breast enlargement The patient's diagnostic work-up revealed: hemoglobin, 11.2 g%; total leukocyte count, 7400/mm3; differential leukocyte count, P62L34E2M2; erythrocyte sedimentation rate, 34 mm/h. A peripheral blood smear examination, urinalysis, blood sugar, and renal and liver function tests were normal. Venereal Disease Research Laboratory (VDRL) test and enzyme-linked immunoabsorbent assay (ELISA) for human immunodeficiency virus (HIV) were nonreactive. Antinuclear antibody, lupus erythematosus (LE) cell, rheumatoid factor, and anti-dsDNA levels were normal. Serum protein electrophoresis demonstrated increased levels of immunoglobulin G (IgG) antibody. The serum prolactin level was significantly raised to 139.49 ng/mL (normal, 3.6,18.9 ng/mL). The sex hormone levels, however, including follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol, and progesterone, were within normal limits. The thyroid hormone profile was also unaltered. Chest X-ray was normal. Ultrasound of the abdomen and pelvis revealed no visceral abnormality and computerized tomography (CT) scan of the pituitary sella showed no adenoma. Mammography was negative for breast malignancy. A Tzanck smear prepared from the base of the erosion showed multiple acantholytic cells and lymphocytes. Histologic examination from an intact vesicle was suggestive of pemphigus vulgaris (PV), showing a suprabasal cleft with acantholytic cells and the basal layer demonstrating a "row of tombstones" appearance (Fig. 2). Direct immunofluorescence (DIF) revealed the intercellular deposition of IgG and C3 throughout the epidermis in a "fishnet pattern." Indirect immunofluorescence (IIF) test performed on rat esophagus for circulating IgG antibody was positive in a titer of 1 : 120. Figure 2. Photomicrograph showing suprabasal cleft with "row of tombstones" appearance, suggestive of pemphigus vulgaris (hematoxylin and eosin, × 40) Based on the clinical and immunohistological features, a diagnosis of PV with idiopathic hyperprolactinemia was made. The patient was treated with bromocriptine mesylate (Tablet Proctinal, Glaxo Wellcome Ltd, India) at a dose of 2.5 mg twice a day. After 2 months of therapy, significant improvement in the skin lesions was observed. The existing lesions re-epithelialized with a drastic reduction in the number and distribution of new vesicles. However, no change in the mucosal erosions was noticed. IIF test demonstrated a lower antibody titer (1 : 40). The breast complaints also improved with a reduction in serum prolactin level to 6.5 ng/mL. The patient refused further treatment as she experienced nausea and dizziness with bromocriptine. After 2 weeks, the disease relapsed with the appearance of new vesicles over the forearms, abdomen, back, and thighs. She again complained of breast tenderness and galactorrhea, and the serum prolactin level was 95 ng/mL. The IgG titer increased to 1 : 120. Hence, treatment with oral prednisolone (2 mg/kg/day) and bromocriptine (2.5 mg twice a day) with an antiemetic was initiated. After 6 weeks, the skin lesions had cleared completely, the breast symptoms had improved, menses had become regular, and the prolactin level had decreased to 4 ng/mL. IIF test was negative for circulating antibody. Steroids were tapered off and maintenance therapy with bromocriptine at a dose of 2.5 mg/day was continued. [source]

Prolactin Levels in Sudden Unexpected Death in Epilepsy

Prolactin alters the mechanisms of B cell tolerance induction

ARTHRITIS & RHEUMATISM, Issue 6 2009
Subhrajit Saha
Objective Autoimmune diseases predominantly affect women, suggesting that female sex hormones may play a role in the pathogenesis of such diseases. We have previously shown that persistent mild-to-moderate elevations in serum prolactin levels induce a break in self tolerance in mice with a BALB/c genetic background. The aim of this study was to evaluate the effects of hyperprolactinemia on the mechanisms of B cell tolerance induction. Methods Effects of prolactin on splenic B cell subsets were studied in female BALB/c mice. B cell receptor (BCR),mediated apoptosis and proliferation of transitional B cells were analyzed by flow cytometry. Expression of apoptotic genes was examined by microarrays and real-time polymerase chain reaction analysis. B cells coexpressing ,/, light chains were assessed by flow cytometry and immunohistochemistry. Activation status of transitional type 3 (T3) B cells was evaluated by BCR-induced calcium influx studies. Results BCR-mediated apoptosis of the T1 B cell subset, a major checkpoint for negative selection of autoreactive specificities, was decreased in prolactin-treated mice. Microarray studies indicated that this event may be mediated by the prolactin-induced up-regulation of the antiapoptotic gene interferon-, receptor type II and down-regulation of the proapoptotic gene Trp63. Prolactin treatment also altered the amount of receptor editing, as indicated by the increased number of transitional B cells coexpressing ,/, light chains. Additionally, hyperprolactinemia modified the level of B cell anergy by increasing the degree of BCR-induced calcium influx in the T3 B cells. Conclusion Persistently elevated serum prolactin levels interfere with B cell tolerance induction by impairing BCR-mediated clonal deletion, deregulating receptor editing, and decreasing the threshold for activation of anergic B cells, thereby promoting autoreactivity. [source]

Single- and multiple-dose pharmacokinetics of ziprasidone under non-fasting conditions in healthy male volunteers

BRITISH JOURNAL OF CLINICAL PHARMACOLOGY, Issue S1 2000
J. J. Miceli
Aims, To evaluate the pharmacokinetics and tolerability of single and multiple oral doses of ziprasidone in healthy male volunteers, and to determine the influence of ziprasidone on serum prolactin levels. Methods, Single and multiple doses of ziprasidone were given orally (as two divided daily doses), at fixed dosages of 10 and 40 mg day,,1, and using titrated regimens of 40,80 and 40,120 mg day,,1, for 14 days. All dosages were taken immediately after food. The study adopted a randomized, double-blind, placebo-controlled design. Prolactin response, sedative properties, tolerability, and extrapyramidal symptoms were also investigated. Results, Steady-state exposure to ziprasidone was attained after 1 day of dosing. Mean Cmax and AUC(0,12 h) increased with increasing dose, with apparent dose-proportionality between the 20 and 60 mg dose levels. Trough-to-peak ratios at steady state ranged from 2 to 5. Accumulation ratios for the fixed-dose regimens were 1.49 and 1.48 at the 5 and 20 mg dose levels, respectively. Ziprasidone was associated with transient prolactin elevation but levels of prolactin returned to baseline within the dosing interval at steady state. There was a marginal, transient increase in serum prolactin levels which was not dose-related at the 80 and 120 mg day,,1 doses, and which was noted to attenuate with chronic dosing. Ziprasidone was generally well tolerated. The most frequent side-effect was mild or moderate headache. A minority of patients suffered first-dose postural hypotension. Ziprasidone was also associated with a mild sedative effect that became less pronounced as treatment continued. There were no drug-related changes in electrocardiogram or clinical laboratory variables that were of clinical importance. Conclusions, Ziprasidone is characterized by a predictable pharmacokinetic profile resulting in symptoms that reflect its pharmacological action. [source]