Mullerian Ducts
Mixed Tumor, Mullerian
Anti-Mullerian Hormone
Adenosarcoma
Wolffian Ducts
Hormones
46, XX Disorders of Sex Development
Thyroid Hormones
Follicle Stimulating Hormone
Luteinizing Hormone
Receptors, Peptide
Parathyroid Hormone
Growth Inhibitors
Disorders of Sex Development
Gonadotropin-Releasing Hormone
Gonadal Steroid Hormones
Urogenital Abnormalities
Genitalia, Female
Sex Differentiation
Receptors, Thyroid Hormone
Human Growth Hormone
Adrenocorticotropic Hormone
Uterus
Receptors, Transforming Growth Factor beta
Testis
Pituitary Hormones
Glycoproteins
Subrenal Capsule Assay
Mixed Tumor, Malignant
Estradiol
Ovary
Urogenital System
Testosterone
Diethylstilbestrol
Triiodothyronine
Carcinosarcoma
Cystadenocarcinoma, Papillary
Juvenile Hormones
Butterflies
Hormone Replacement Therapy
Cryptorchidism
Fushi Tarazu Transcription Factors
Steroidogenic Factor 1
Freemartinism
Wnt4 Protein
Growth Hormone-Releasing Hormone
Virilism
Corticotropin-Releasing Hormone
Ovarian Neoplasms
Hysterosalpingography
Gonadal Dysgenesis
Hypothalamic Hormones
Peptide Hormones
Pituitary Gland
Thyroxine
Mesonephros
Predatory Behavior
Pregnancy
Gonadal Hormones
Molecular Sequence Data
Thyroid Hormone Receptors beta
Prolactin
Sertoli Cells
46, XY Disorders of Sex Development
Pituitary Hormones, Anterior
Base Sequence
RNA, Messenger
Thyrotropin
Cystadenocarcinoma, Serous
Immunohistochemistry
Progesterone
Gastrointestinal Hormones
Integumentary System Physiological Phenomena
Bone Morphogenetic Protein Receptors, Type I
Fallopian Tubes
Thyroid Hormone Receptors alpha
Glycoprotein Hormones, alpha Subunit
Insect Hormones
Hormone Antagonists
Embryonic Structures
Pituitary Hormone-Releasing Hormones
Invertebrate Hormones
Pituitary Hormones, Posterior
Sarcoma, Endometrial Stromal
Color
Gonadal Dysgenesis, 46,XY
Stereoisomerism
Endometrial Neoplasms
Receptors, Somatotropin
Estrogens
Radioimmunoassay
Amino Acid Sequence
Melanocyte-Stimulating Hormones
DNA
Broad Ligament
Follicle Stimulating Hormone, beta Subunit
Pituitary Gland, Anterior
Hydrocortisone
Smad8 Protein
Paracrine-mediated apoptosis in reproductive tract development. (1/492)
In mammalian development, the signaling pathways that couple extracellular death signals with the apoptotic machinery are still poorly understood. We chose to examine Mullerian duct regression in the developing reproductive tract as a possible model of apoptosis during morphogenesis. The TGFbeta-like hormone, Mullerian inhibiting substance (MIS), initiates regression of the Mullerian duct or female reproductive tract anlagen; this event is essential for proper male sexual differentiation and occurs between embryonic days (E) 14 and 17 in the rat. Here, we show that apoptosis occurs during Mullerian duct regression in male embryos beginning at E15. Female Mullerian ducts exposed to MIS also exhibited prominent apoptosis within 13 h, which was blocked by a caspase inhibitor. In both males and females the MIS type-II receptor is expressed exclusively in the mesenchymal cell layer surrounding the duct, whereas apoptotic cells localize to the epithelium. In addition, tissue recombination experiments provide evidence that MIS does not act directly on the epithelium to induce apoptosis. Based on these data, we suggest that MIS triggers cell death by altering mesenchymal-epithelial interactions. (+info)Ptx1 regulates SF-1 activity by an interaction that mimics the role of the ligand-binding domain. (2/492)
Ptx1 (Pitx1) is a bicoid-related homeobox transcription factor expressed from the onset of pituitary development. It was shown to cooperate with cell-restricted factors, such as Pit1, NeuroD1/PanI and steroidogenic factor 1 (SF-1), to establish a combinatorial code conferring lineage- and promoter-specific gene transcription in the pituitary. Transcriptional synergism between Ptx1 and SF-1 on two SF-1 target genes, pituitary luteinizing hormone beta and Mullerian-inhibiting substance (MIS), requires SF-1 binding to DNA and appears to result from direct physical interaction between these two proteins. The interaction between the C-terminus of Ptx1 and the N-terminal half of SF-1 results in transcriptional enhancement that equals the activity of a constitutively active SF-1 mutant and that may mimic the effect of a still unidentified SF-1 ligand. Thus, the unmasking of SF-1 activity by Ptx1 may represent a developmental mechanism to alleviate the need for SF-1 ligand in transcription and, possibly, at critical times during organogenesis. (+info)Reversion of the differentiated phenotype and maturation block in Sertoli cells in pathological human testis. (3/492)
To study the relationship between abnormal Sertoli cell differentiation and spermatogenic impairment, we examined the expression of Sertoli cell markers normally lost at puberty, cytokeratin 18 (CK18), anti-Mullerian hormone (AMH) and M2A antigen, in three children (aged 1-2 years), 50 adults (aged 19-45 years) with obstructive or non-obstructive azoospermia or oligozoospermia, and six patients (aged 1-18 years) with 5 alpha-reductase deficiency. There was CK18 and/or AMH expression, but never M2A antigen expression, associated with spermatogonial arrest or Sertoli cell-only (SCO) syndrome in infertile men. Loss of M2A antigen suggests the transition of Sertoli cells to an adult phenotype, while CK18 and/or AMH expression may be a manifestation of de-differentiation of Sertoli cells. In 5 alpha-reductase deficiency, there was a sequential loss of CK18, M2A antigen and AMH around puberty, associated with partial spermatogenesis. The persistence of immature Sertoli cells expressing M2A antigen was associated with prepubertal seminiferous cords and SCO syndrome. Therefore, 5 alpha-reductase deficiency may prevent the maturation of Sertoli cells, resulting in impairment of spermatogenesis, and loss of M2A antigen expression coincides with a critical step in the Sertoli cell maturation. High follicle stimulating hormone concentrations due to failure of normal Sertoli cell differentiation indicate a normal development pattern of the hypothalamic-pituitary-gonadal axis. (+info)Anti-Mullerian hormone as a seminal marker for spermatogenesis in non-obstructive azoospermia. (4/492)
Anti-Mullerian hormone (AMH) also known as Mullerian inhibiting substance or factor, is a Sertoli cell-secreted glycoprotein responsible in male embryos for Mullerian duct regression. However, its role in adults remains unknown. AMH seminal concentrations have been evaluated using an enzyme-linked immunoassay in three groups of young men: group 1, fertile donors (n = 18); group 2, obstructive azoospermia (n = 9) after vasectomy or associated with deferent duct agenesia; and group 3, non-obstructive azoospermia with spermatogenesis deficiency and normal karyotype (n = 23). AMH was present in seminal plasma of most fertile donors at concentrations ranging from undetectable (<3.5 pmol/l) up to 543 pmol/l (geometric mean: 153 pmol/l), higher than the serum level (range <3.5 up to 67 pmol/l, geometric mean: 10.7 pmol/l, n = 13). Seminal AMH concentrations were undetectable in all obstructive azoospermic patients, confirming its testicular origin. In non-obstructive azoospermia (group 3), seminal AMH concentration was lower (range <3. 5-68.5 pmol/l, geometric mean: 17 pmol/l) than in fertile donors (P < 0.003) without correlation with plasma follicle stimulating hormone values. In group 3, comparison of seminal AMH concentration and the results of histological analysis of testicular biopsies revealed that undetectable AMH found in 14 cases was associated in 11 of them with lack of spermatozoa, while detectable concentrations of AMH (10-68.5 pmol/l) found in nine cases were associated in seven of them with persistent spermatogenesis. In the adult, AMH is secreted preferentially towards the seminiferous lumen. Although its relationship with spermatogenesis requires further investigation, our results suggest that seminal AMH may represent a non-invasive marker of persistent hypospermatogenesis in cases of non-obstructive azoospermia which may indicate the likely success of testicular spermatozoa recovery before intracytoplasmic sperm injection. (+info)Reverse transcription-polymerase chain reaction analysis of genes involved in gonadal differentiation in pigs. (5/492)
In mammals, testis development is initiated in the embryo as a response to the expression of the sex-determining gene, SRY. The time course of SRY expression during gonadal differentiation in the male has been described in detail only in mice and sheep. In this study, we used reverse transcription-polymerase chain reaction analysis to define the SRY transcription profile in pig genital ridges. SRY transcripts were first detectable from 23 days postcoitum (dpc), then declined sharply after 35 dpc. None were detected at 60 dpc. In addition, we analyzed temporal expression of other genes known to be involved in mammalian sex determination: WT-1, SF-1, SOX9, and AMH. A key stage seems to be 28 dpc, in which SOX9 expression switches between the male and female, and AMH expression begins to attest to Sertoli cell differentiation and to correspond to seminiferous cord formation in the male. Expression of gonadotropin receptors and aromatase was also investigated in porcine gonads, and we showed that their transcripts were detected very early on, especially in the male: 25 dpc for the LH receptor (rLH) and aromatase, and 28 dpc for the FSH receptor (rFSH). In the female, aromatase transcripts were not detected until 70 dpc, and rFSH expression occurred later: at 45 dpc at the onset of meiosis. Moreover, no difference was observed between the sexes for the onset of rLH transcription at 25 dpc. Such a thorough study has never been performed on pigs; developmental analysis will be useful for investigating sex-reversed gonads and determining ontogeny in intersexuality, a common pathology in pigs. (+info)Targeted mutagenesis of the endogenous mouse Mis gene promoter: in vivo definition of genetic pathways of vertebrate sexual development. (6/492)
Mutations were introduced into conserved steroidogenic factor 1 (SF1)- and SOX9-binding sites within the endogenous mouse Mullerian inhibiting substance (Mis) promoter. Male mice homozygous for the mutant SF1-binding site correctly initiated Mis transcription in fetal testes, although at significantly reduced levels. Surprisingly, sufficient MIS was produced to eliminate the MUllerian ducts. In contrast, males homozygous for the mutant SOX9-binding site did not initiate Mis transcription, resulting in pseudohermaphrodites. These studies suggest an essential role for SOX9 in the initiation of Mis transcription, whereas SF1 appears to act as a quantitative regulator of Mis transcript levels, perhaps for influencing non-Mullerian duct tissues. Comparative studies of Mis expression in vertebrates indicate that the Mis promoter receives transcriptional inputs that vary between species but result in the same functional readout. (+info)Human ovarian cancer, cell lines, and primary ascites cells express the human Mullerian inhibiting substance (MIS) type II receptor, bind, and are responsive to MIS. (7/492)
Six human ovarian cancer cell lines and samples of ascites cells isolated from 27 patients with stage III or IV ovarian papillary serous cystadenocarcinoma were studied individually to test whether recombinant human Mullerian inhibiting substance (rhMIS) acts via its receptor. To do these experiments, we scaled up production of rhMIS and labeled it successfully with biotin for binding studies, cloned the human MIS type II receptor for mRNA detection, and raised antibodies to an extracellular domain peptide for protein detection. These probes were first tested on the human ovarian cancer cell lines and then applied to primary ovarian ascites cells. rhMIS inhibited colony growth of five of six cell lines that expressed the human MIS type II receptor mRNA by Northern analysis while not inhibiting receptor-negative COS cells. Flow cytometry performed on MIS-sensitive ovarian cancer cell lines demonstrated specific and saturable binding of rhMIS (Kd = 10.2 nM). Ascites cells from 15 of 27 or 56% of patients tested bound biotinylated MIS (MIS-biotin) and, of the 11 that grew in soft agarose, 9 of 11 or 82% showed statistically significant inhibition of colony formation. Of the 15 patients who bound biotinylated MIS, mRNA was available for analysis from 9, and 8 of 9 expressed MIS type II receptor mRNA by reverse transcription-PCR, showing a statistically significant correlation, compared with binding, by chi2 analysis (P = 0.025). Solid ovarian cancers were positive for the MIS type II receptor protein by immunohistochemical staining, which colocalized with staining for antibody to CA-125 (OC-125). Thus, the detection of the MIS type I receptor by flow cytometry may be a useful predictor of therapeutic response to MIS and may be a modality to rapidly choose patients with late-stage ovarian cancer for treatment with MIS. (+info)Postnatal sex reversal of the ovaries in mice lacking estrogen receptors alpha and beta. (8/492)
Mice lacking estrogen receptors alpha and beta were generated to clarify the roles of each receptor in the physiology of estrogen target tissues. Both sexes of alphabeta estrogen receptor knockout (alphabetaERKO) mutants exhibit normal reproductive tract development but are infertile. Ovaries of adult alphabetaERKO females exhibit follicle transdifferentiation to structures resembling seminiferous tubules of the testis, including Sertoli-like cells and expression of Mullerian inhibiting substance, sulfated glycoprotein-2, and Sox9. Therefore, loss of both receptors leads to an ovarian phenotype that is distinct from that of the individual ERKO mutants, which indicates that both receptors are required for the maintenance of germ and somatic cells in the postnatal ovary. (+info)The term "mixed tumor" refers to a tumor that contains multiple types of cells or tissue, in this case, both epithelial and stromal components. "Müllerian" refers to the embryonic origins of the tumor, which are derived from the müllerian ducts, which eventually develop into the uterus, cervix, and fallopian tubes.
Endometrial stromal sarcoma is the most common type of mixed tumor, müllerian. It is a rare and aggressive cancer that arises in the uterus, typically in the endometrium (the lining of the uterus). It can be difficult to diagnose and treat, and may require surgery, radiation therapy, and/or chemotherapy.
Other types of mixed tumors, müllerian include:
* Endometrial carcinoma with stromal overgrowth
* Uterine papillary serous carcinoma with stromal components
* Mucinous adenocarcinoma with stromal components
It is important to note that while these tumors are considered "mixed", they are still classified based on the predominant cell type present. For example, a tumor that contains both epithelial and stromal components would be classified as an endometrial stromal sarcoma, rather than an endometrial adenocarcinoma with stromal overgrowth.
The exact cause of adenosarcoma is not known, but it is believed to be linked to genetic mutations that occur during the development of soft tissue cells. The risk of developing adenosarcoma increases with age, and it is more common in men than women.
Symptoms of adenosarcoma may include:
* Painless lumps or swelling in the affected area
* Pain or discomfort in the affected area
* Limited range of motion in the affected limb
* Night sweats
* Fever
If adenosarcoma is suspected, a doctor may perform a series of tests to confirm the diagnosis, including:
* Imaging tests, such as X-rays, CT scans, or MRI scans, to visualize the tumor and determine its size and location.
* Biopsy, where a sample of tissue is taken from the affected area and examined under a microscope for cancer cells.
* Blood tests to check for certain substances in the blood that are associated with adenosarcoma.
Treatment options for adenosarcoma may include:
* Surgery to remove the tumor and surrounding tissue.
* Radiation therapy to kill cancer cells using high-energy rays.
* Chemotherapy to kill cancer cells using drugs.
* Targeted therapy, which uses drugs or other substances to target specific molecules that are involved in the growth and spread of cancer cells.
The prognosis for adenosarcoma is generally good if the tumor is small and has not spread to other parts of the body. However, the cancer can be challenging to treat if it has spread to surrounding tissues or organs. The 5-year survival rate for adenosarcoma is approximately 70%.
The term DSD is used to describe a range of conditions that were previously referred to as intersex conditions or hermaphroditism. The use of the term DSD is intended to be more neutral and less stigmatizing than previous terms, as it emphasizes the variability and complexity of these conditions rather than their perceived abnormality.
The most common 46,XX DSDs include:
1. Androgen insensitivity syndrome (AIS): A condition in which individuals with male genitalia are born without the ability to respond to androgens (male hormones), resulting in a female physical appearance.
2. Congenital adrenal hyperplasia (CAH): A condition caused by a deficiency of an enzyme necessary for the production of cortisol and aldosterone, leading to the overproduction of androgens.
3. Turner syndrome: A condition in which individuals are born with only one X chromosome, resulting in short stature, infertility, and other physical and developmental abnormalities.
4. Triple X syndrome: A condition in which individuals are born with three X chromosomes, leading to a range of physical and developmental abnormalities.
5. XX males: A condition in which individuals with female chromosomes (46,XX) are born with male genitalia.
The diagnosis and management of 46,XX DSDs can be complex and require a multidisciplinary approach involving endocrinologists, geneticists, pediatricians, and psychosocial experts. Treatment options may include hormone therapy, surgery, and gender confirmation surgeries.
It is important to note that the term DSD is not without controversy, as some advocates argue that it pathologizes and stigmatizes individuals with intersex traits rather than recognizing their diversity and human rights. The use of the term DSD should be carefully considered in clinical practice and education, and language that is respectful and inclusive of all individuals should be used to describe those with intersex traits.
In conclusion, 46,XX DSDs are a group of rare genetic disorders that can result in a range of physical and developmental abnormalities. The diagnosis and management of these disorders require a multidisciplinary approach and sensitivity to the needs and preferences of individuals with intersex traits.
The term "Disorders of Sex Development" was introduced in the early 2000s as a more inclusive and neutral way to describe these conditions, replacing outdated and stigmatizing terms such as "intersex." DSD includes a wide range of conditions, some of which may be genetic in origin, while others may result from hormonal or environmental factors.
The diagnosis and management of DSD can be complex and require a multidisciplinary team of healthcare providers, including endocrinologists, geneticists, urologists, and psychologists. Treatment options may include hormone therapy, surgery, and counseling, and the goals of treatment are to alleviate symptoms, improve quality of life, and support the individual's self-identification and gender expression.
It is important to note that DSD is a medical term and does not have any implications for an individual's gender identity or expression. All individuals with DSD have the right to live as their authentic selves, regardless of their gender identity or expression.
Examples of Urogenital Abnormalities:
1. Congenital Anomalies: Conditions that are present at birth and affect the urinary tract or genitalia, such as hypospadias (a condition where the urethra opens on the underside of the penis instead of the tip), undescended testes (testes that fail to descend into the scrotum), or interrupted or absent vas deferens (tubes that carry sperm from the epididymis to the penis).
2. Infections: Bacterial or viral infections that can cause urogenital abnormalities, such as pyelonephritis (a kidney infection) or prostatitis (an inflammation of the prostate gland).
3. Trauma: Injuries to the urinary tract or genitalia, such as those caused by sexual assault or accidents, can lead to urogenital abnormalities.
4. Neurological Conditions: Certain neurological conditions, such as spina bifida (a birth defect that affects the spine and spinal cord), can cause urogenital abnormalities.
5. Cancer: Cancer of the urinary tract or genitalia, such as bladder cancer or prostate cancer, can cause urogenital abnormalities.
Symptoms of Urogenital Abnormalities:
Depending on the specific condition, symptoms of urogenital abnormalities may include:
1. Difficulty urinating or painful urination
2. Blood in the urine or semen
3. Frequent urination or incontinence
4. Pain during sexual activity
5. Abnormalities in the shape or size of the genitalia
6. Testicular atrophy or swelling
7. Discharge from the vagina or penis
8. Foul-smelling urine
Diagnosis and Treatment of Urogenital Abnormalities:
Diagnosis of urogenital abnormalities typically involves a combination of physical examination, medical history, and diagnostic tests such as urinalysis, blood tests, and imaging studies (such as X-rays or ultrasound). Treatment depends on the specific condition causing the abnormality. Some common treatments include:
1. Medications to treat infections or inflammation
2. Surgery to repair or remove damaged tissue
3. Lifestyle changes, such as diet and exercise modifications
4. Pelvic floor exercises to strengthen the muscles that control urination and bowel movements
5. Assistive devices, such as catheters or prosthetic limbs
6. Hormone therapy to treat hormonal imbalances or gender identity issues.
Examples of mixed tumors, malignant include:
1. Melanoma-squamous cell carcinoma: This type of skin cancer is a mix of melanocytes (the cells that produce pigment) and squamous cells (thin, flat cells that make up the outer layer of skin).
2. Adenoid cystic carcinoma with squamous differentiation: This type of head and neck cancer has features of both adenoid cystic carcinoma (a type of salivary gland cancer) and squamous cell carcinoma.
3. Uterine leiomyosarcoma with endometrial adenocarcinoma: This type of uterine cancer is a mix of leiomyosarcoma (a type of smooth muscle cancer) and endometrial adenocarcinoma (a type of glandular cancer).
4. Metanephric stromal tumor with oncocytic changes: This type of kidney cancer is a mix of metanephric stromal tumor (a type of connective tissue cancer) and oncocytic changes (abnormal cells that resemble normal cells but have lost their ability to regulate growth).
5. Synovial sarcoma with osteoclast-like giant cells: This type of soft tissue cancer is a mix of synovial sarcoma (a type of connective tissue cancer) and osteoclast-like giant cells (large cells that resemble bone-forming cells).
Treatment for mixed tumors, malignant can vary depending on the specific types of cancer present and the extent of the disease. Surgery, radiation therapy, and chemotherapy may be used alone or in combination to treat the tumor. In some cases, a clinical trial may be an option.
Mixed tumors, malignant are often more aggressive and difficult to treat than single-type tumors because they contain multiple types of cancer cells that can grow and spread differently. However, advances in cancer diagnosis and treatment have improved the outlook for some patients with mixed tumors. The prognosis and treatment options for mixed tumors depend on the specific types of cancer present, the stage of the disease, and other individual factors.
A patient's age, overall health, and the presence of any other medical conditions can also affect their prognosis and treatment options. If you or a loved one has been diagnosed with a mixed tumor, it is essential to discuss your treatment options with a qualified healthcare professional who specializes in cancer care. They can help you understand the specific types of cancer present, the stage of the disease, and the most appropriate treatment plan for your individual situation.
In some cases, a clinical trial may be an option. Clinical trials are research studies that evaluate new treatments or combinations of treatments to see if they are safe and effective. Participating in a clinical trial may give you access to innovative therapies that are not yet widely available. However, it is essential to discuss the potential risks and benefits of clinical trials with your healthcare professional before making a decision.
In summary, mixed tumors are complex cancer diagnoses that can be challenging to treat. However, advances in cancer diagnosis and treatment have improved the outlook for some patients. If you or a loved one has been diagnosed with a mixed tumor, it is essential to discuss your treatment options with a qualified healthcare professional who specializes in cancer care. They can help you understand the specific types of cancer present, the stage of the disease, and the most appropriate treatment plan for your individual situation.
In some cases, a clinical trial may be an option. Clinical trials are research studies that evaluate new treatments or combinations of treatments to see if they are safe and effective. Participating in a clinical trial may give you access to innovative therapies that are not yet widely available. However, it is essential to discuss the potential risks and benefits of clinical trials with your healthcare professional before making a decision.
1. Endometrial carcinoma (cancer that starts in the lining of the uterus)
2. Uterine papillary serous carcinoma (cancer that starts in the muscle layer of the uterus)
3. Leiomyosarcoma (cancer that starts in the smooth muscle of the uterus)
4. Adenocarcinoma (cancer that starts in the glands of the endometrium)
5. Clear cell carcinoma (cancer that starts in the cells that resemble the lining of the uterus)
6. Sarcoma (cancer that starts in the connective tissue of the uterus)
7. Mixed tumors (cancers that have features of more than one type of uterine cancer)
These types of cancers can affect women of all ages and are more common in postmenopausal women. Risk factors for developing uterine neoplasms include obesity, tamoxifen use, and a history of endometrial hyperplasia (thickening of the lining of the uterus).
Symptoms of uterine neoplasms can include:
1. Abnormal vaginal bleeding (heavy or prolonged menstrual bleeding, spotting, or postmenopausal bleeding)
2. Postmenopausal bleeding
3. Pelvic pain or discomfort
4. Vaginal discharge
5. Weakness and fatigue
6. Weight loss
7. Pain during sex
8. Increased urination or frequency of urination
9. Abnormal Pap test results (abnormal cells found on the cervix)
If you have any of these symptoms, it is essential to consult your healthcare provider for proper evaluation and treatment. A diagnosis of uterine neoplasms can be made through several methods, including:
1. Endometrial biopsy (a small sample of tissue is removed from the lining of the uterus)
2. Dilation and curettage (D&C; a surgical procedure to remove tissue from the inside of the uterus)
3. Hysteroscopy (a thin, lighted tube with a camera is inserted through the cervix to view the inside of the uterus)
4. Imaging tests (such as ultrasound or MRI)
Treatment for uterine neoplasms depends on the type and stage of cancer. Common treatments include:
1. Hysterectomy (removal of the uterus)
2. Radiation therapy (uses high-energy rays to kill cancer cells)
3. Chemotherapy (uses drugs to kill cancer cells)
4. Targeted therapy (uses drugs to target specific cancer cells)
5. Clinical trials (research studies to test new treatments)
It is essential for women to be aware of their bodies and any changes that occur, particularly after menopause. Regular pelvic exams and screenings can help detect uterine neoplasms at an early stage, when they are more treatable. If you experience any symptoms or have concerns about your health, talk to your healthcare provider. They can help determine the cause of your symptoms and recommend appropriate treatment.
Carcinosarcomas are typically slow-growing and can occur in various parts of the body, including the abdomen, pelvis, and extremities. They can be difficult to diagnose because they often have a mix of cancerous and noncancerous cells, making it challenging to determine the exact type of tumor.
The treatment of carcinosarcoma depends on the location, size, and stage of the tumor, as well as the patient's overall health. Surgery is often the first line of treatment, followed by radiation therapy and/or chemotherapy. In some cases, a combination of all three may be necessary.
Overall, carcinosarcoma is a rare and aggressive form of cancer that requires careful management and coordinated care from a multidisciplinary team of healthcare professionals. With proper treatment, many patients with carcinosarcoma can achieve long-term survival and a good quality of life.
Example sentences:
1. The patient was diagnosed with a rare form of cancer called carcinosarcoma, which is a combination of both carcinoma and sarcoma.
2. The carcinosarcoma had spread to the patient's lymph nodes and required aggressive treatment, including surgery, radiation therapy, and chemotherapy.
3. Due to the rarity of carcinosarcoma, the oncologist consulted with a team of specialists to develop a personalized treatment plan for the patient.
Also known as:
* Cystadenocarcinoma, papilliferum
* Papillary adenocarcinoma
* Glandular neoplasm, papillary
Synonyms:
* Adenocarcinoma, papillary
* Carcinoma, papillary
* Mucinous cystadenocarcinoma
* Cystic papillary carcinoma
Epithelial tumors of the breast with a glandular or mixed (glandular and ductal) pattern account for approximately 15% of all breast cancers. The most common histologic type is papillary adenocarcinoma, which accounts for about 70% of all glandular tumors.
Papillary carcinoma (PC) was first described by Miles in 1932 as a distinct clinical and pathological entity. It typically affects women between the ages of 40 to 60 years, with rare cases occurring in men. The incidence is 1/1,800,000 for invasive PC and 1/3,500,000 for DCIS.
The majority of papillary carcinomas are confined to the breast and regional lymph nodes; however, there have been case reports of distant metastases.
PC is a slow-growing tumor with an average diameter of 15-20 mm, and most patients present with a palpable mass or nipple discharge. The microscopic features include a glandular or acinar pattern, with papillary structures lined by bland-appearing cells.
The malignant potential of PC is less than that of ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC). The 5-year survival rate for PC is approximately 90%, and the risk of recurrence is low.
Treatment options include surgery, radiation therapy, and hormone therapy. Surgical excision is the primary treatment, with a wide local excision being preferred over lumpectomy or simple mastectomy. Radiation therapy may be recommended for patients with positive axillary nodes or large tumors. Hormone therapy may be considered for postmenopausal women with ER-positive tumors.
Despite its relatively low malignant potential, PC should be treated aggressively to prevent local recurrence and possible distant metastases. The prognosis is generally excellent, but long-term follow-up is essential to monitor for any signs of recurrence or new primary cancers.
Cryptorchidism can be classified into two types:
1. Abdomenal cryptorchidism: In this type, the testis is located in the abdominal cavity above the inguinal ring and is not covered by any skin or membrane.
2. Inguinoscrotal cryptorchidism: In this type, the testis is located in the inguinal canal and may be covered by a thin layer of skin or membrane.
Cryptorchidism is usually diagnosed at birth or during childhood, and it can occur as an isolated condition or as part of other congenital anomalies. Treatment options for cryptorchidism include:
1. Watchful waiting: In mild cases, doctors may choose to monitor the child's development and delay any treatment until they are older.
2. Surgical repair: In more severe cases or those that cause discomfort or other complications, surgery may be recommended to move the testes into the scrotum.
3. Hormone therapy: In some cases, hormone therapy may be used to stimulate the descent of the testes.
4. Assisted reproductive technology (ART): In cases where fertility is a concern, ART such as in vitro fertilization (IVF) may be recommended.
It's important to note that cryptorchidism can increase the risk of complications such as testicular cancer, infertility, and twisting or inflammation of the testes (torsion). Regular check-ups with a healthcare provider are essential for monitoring and managing this condition.
Freemartinism is caused by the abnormal development of the reproductive system of the calves. During fetal development, the two female calves may fail to fully separate from each other, leading to a shared uterus and vagina. This can result in a range of physical and reproductive abnormalities, including:
* Unusual genitalia: The shared uterus and vagina can cause the genitalia to appear abnormal or incomplete.
* Reproductive difficulties: Freemartinism can make it difficult or impossible for the calves to breed or conceive.
* Health problems: Freemartinism can increase the risk of health problems, such as urinary tract infections and reproductive tract infections.
Freemartinism is typically diagnosed through ultrasound examination during pregnancy or after birth. Treatment options for freemartinism are limited, and may include surgery to correct physical abnormalities and hormone therapy to stimulate reproductive function. In some cases, euthanasia may be necessary due to the severity of the condition.
Prevention of freemartinism is not possible, as it is a congenital condition that occurs during fetal development. However, careful breeding practices and proper veterinary care can help reduce the risk of complications associated with this condition.
Hematometra can be caused by several factors, including:
1. Uterine fibroids: These are non-cancerous growths in the uterus that can cause bleeding and accumulation of blood.
2. Endometrial polyps: These are growths in the lining of the uterus that can cause bleeding and hematometra.
3. Adenomyosis: This is a condition where tissue similar to the lining of the uterus grows into the muscle wall of the uterus, leading to bleeding and hematometra.
4. Cervical polyps: These are growths on the cervix that can cause bleeding and hematometra.
5. Cervical cancer: This is a rare but serious condition that can cause bleeding and hematometra.
6. Injury or trauma to the uterus: This can cause bleeding and hematometra.
7. Surgical complications: Hematometra can occur as a complication of surgery, such as a hysterectomy or endometrial ablation.
Symptoms of hematometra may include:
1. Severe pain in the abdomen, pelvis, or lower back
2. Heavy bleeding that lasts for more than 7 days
3. Fever and chills
4. Anemia and fatigue
5. Difficulty urinating or constipation
Diagnosis of hematometra is typically made through a combination of physical examination, medical history, and imaging tests such as ultrasound or MRI. Treatment depends on the underlying cause of hematometra and may include medications to control bleeding, surgery to remove blood clots or fibroids, or other interventions to address underlying conditions.
In conclusion, hematometra is a rare but potentially serious condition that can cause severe pain, anemia, and other complications. It is important to be aware of the risk factors and symptoms of hematometra and seek medical attention promptly if they occur. With proper diagnosis and treatment, most cases of hematometra can be effectively managed and resolved.
The causes of virilism can be due to various factors including:
1. Congenital adrenal hyperplasia (CAH): A genetic disorder that affects the production of hormones by the adrenal glands, leading to excessive levels of androgens such as testosterone.
2. Androgen insensitivity syndrome (AIS): A condition where the body is unable to respond to androgens, leading to virilization.
3. 5-alpha-reductase deficiency: A rare genetic disorder that affects the production of the enzyme 5-alpha-reductase, which is important for the development of male characteristics.
4. Genetic mutations: Some individuals may have genetic mutations that lead to the overproduction of androgens or the underproduction of anti-androgens.
5. Hormonal imbalances: Imbalances in hormone levels, such as high testosterone and low estrogen, can also cause virilism.
Virilism can be diagnosed through a combination of physical examination, medical history, and laboratory tests such as hormone level measurements. Treatment options for virilism depend on the underlying cause and may include hormone replacement therapy, surgery, or psychological counseling.
In summary, virilism is a condition characterized by the excessive development of male characteristics in individuals who are not biologically male, and it can be caused by various genetic or hormonal factors. It is important to seek medical attention if symptoms persist or worsen over time, as early diagnosis and treatment can improve outcomes.
Benign ovarian neoplasms include:
1. Serous cystadenoma: A fluid-filled sac that develops on the surface of the ovary.
2. Mucinous cystadenoma: A tumor that is filled with mucin, a type of protein.
3. Endometrioid tumors: Tumors that are similar to endometrial tissue (the lining of the uterus).
4. Theca cell tumors: Tumors that develop in the supportive tissue of the ovary called theca cells.
Malignant ovarian neoplasms include:
1. Epithelial ovarian cancer (EOC): The most common type of ovarian cancer, which arises from the surface epithelium of the ovary.
2. Germ cell tumors: Tumors that develop from germ cells, which are the cells that give rise to eggs.
3. Stromal sarcomas: Tumors that develop in the supportive tissue of the ovary.
Ovarian neoplasms can cause symptoms such as pelvic pain, abnormal bleeding, and abdominal swelling. They can also be detected through pelvic examination, imaging tests such as ultrasound and CT scan, and biopsy. Treatment options for ovarian neoplasms depend on the type, stage, and location of the tumor, and may include surgery, chemotherapy, and radiation therapy.
The term "gonadal dysgenesis" is used to describe a wide spectrum of abnormalities that affect the development of the gonads, including:
1. Turner Syndrome: A rare genetic disorder caused by a missing or partially deleted X chromosome, which can result in short stature, infertility, and characteristic physical features such as a small head, ears, and hands.
2. Klinefelter Syndrome: A condition in which an individual has an extra X chromosome, leading to infertility, hypogonadism, and a range of physical characteristics such as breast enlargement and small testes.
3. Androgen Insensitivity Syndrome (AIS): A condition in which the body is unable to respond to androgens (male hormones), resulting in female physical characteristics despite the presence of XY chromosomes.
4. Persistent Mullerian Duct Syndrome (PMDS): A rare condition in which the müllerian ducts (the precursors of the uterus and fallopian tubes) do not properly develop, leading to a range of physical and reproductive abnormalities.
5. Congenital Adrenal Hyperplasia (CAH): An inherited disorder that affects the production of hormones by the adrenal glands, which can lead to ambiguous genitalia and other physical symptoms.
The exact cause of gonadal dysgenesis is not always known, but it can be due to genetic mutations, chromosomal abnormalities, or environmental factors. Diagnosis is typically made based on a combination of clinical features, hormone levels, and genetic testing. Treatment options vary depending on the specific condition and may include hormone therapy, surgery, and/or psychological support.
The term 'disorders of sex development' (DSD) is used to encompass a wide range of conditions that affect the development of the reproductive and sexual systems in individuals with chromosomes XY. The term 'intersex' is sometimes used interchangeably with DSD, but some intersex advocates argue that this term can be problematic, as it has been historically used to pathologize and stigmatize individuals with these conditions.
The 46, XY disorders of sex development can be broadly classified into two categories: (1) genetic and hormonal, and (2) anatomical. Examples of genetic and hormonal DSDs include Klinefelter syndrome (47, XXY), Turner syndrome (45, X), and androgen insensitivity syndrome (AIS). Anatomical DSDs can include a range of physical characteristics, such as ambiguous genitalia, hypospadias, or undescended testes.
The management of 46, XY disorders of sex development is often complex and multidisciplinary, involving specialists from fields such as endocrinology, urology, gynecology, psychology, and social work. Treatment may include hormone therapy, surgery, or other interventions to support the individual's physical and emotional well-being, as well as their gender identity and expression.
It is important to note that the term 'disorder' in '46, XY disorders of sex development' can be problematic, as it can imply that there is something inherently wrong or abnormal about these conditions. Some advocates argue that a more neutral term, such as ' variations of sex development,' would be more appropriate and respectful of individuals with these conditions.
Congenital Abnormalities are relatively common, and they affect approximately 1 in every 30 children born worldwide. Some of the most common types of Congenital Abnormalities include:
Heart Defects: These are abnormalities that affect the structure or function of the heart. They can range from mild to severe and can be caused by genetics, viral infections, or other factors. Examples include holes in the heart, narrowed valves, and enlarged heart chambers.
Neural Tube Defects: These are abnormalities that affect the brain and spine. They occur when the neural tube, which forms the brain and spine, does not close properly during fetal development. Examples include anencephaly (absence of a major portion of the brain), spina bifida (incomplete closure of the spine), and encephalocele (protrusion of the brain or meninges through a skull defect).
Chromosomal Abnormalities: These are changes in the number or structure of chromosomes that can affect physical and mental development. Examples include Down syndrome (an extra copy of chromosome 21), Turner syndrome (a missing or partially deleted X chromosome), and Klinefelter syndrome (an extra X chromosome).
Other types of Congenital Abnormalities include cleft lip and palate, clubfoot, and polydactyly (extra fingers or toes).
Congenital Abnormalities can be diagnosed before birth through prenatal testing such as ultrasound, blood tests, and amniocentesis. After birth, they can be diagnosed through physical examination, imaging studies, and genetic testing. Treatment for Congenital Abnormalities varies depending on the type and severity of the condition, and may include surgery, medication, and other forms of therapy. In some cases, the abnormality may be minor and may not require any treatment, while in other cases, it may be more severe and may require ongoing medical care throughout the person's life.
Examples of syndromes include:
1. Down syndrome: A genetic disorder caused by an extra copy of chromosome 21 that affects intellectual and physical development.
2. Turner syndrome: A genetic disorder caused by a missing or partially deleted X chromosome that affects physical growth and development in females.
3. Marfan syndrome: A genetic disorder affecting the body's connective tissue, causing tall stature, long limbs, and cardiovascular problems.
4. Alzheimer's disease: A neurodegenerative disorder characterized by memory loss, confusion, and changes in personality and behavior.
5. Parkinson's disease: A neurological disorder characterized by tremors, rigidity, and difficulty with movement.
6. Klinefelter syndrome: A genetic disorder caused by an extra X chromosome in males, leading to infertility and other physical characteristics.
7. Williams syndrome: A rare genetic disorder caused by a deletion of genetic material on chromosome 7, characterized by cardiovascular problems, developmental delays, and a distinctive facial appearance.
8. Fragile X syndrome: The most common form of inherited intellectual disability, caused by an expansion of a specific gene on the X chromosome.
9. Prader-Willi syndrome: A genetic disorder caused by a defect in the hypothalamus, leading to problems with appetite regulation and obesity.
10. Sjogren's syndrome: An autoimmune disorder that affects the glands that produce tears and saliva, causing dry eyes and mouth.
Syndromes can be diagnosed through a combination of physical examination, medical history, laboratory tests, and imaging studies. Treatment for a syndrome depends on the underlying cause and the specific symptoms and signs presented by the patient.
The term "serous" refers to the fact that the tumor produces a fluid-filled cyst, which typically contains a clear, serous (watery) liquid. The cancer cells are typically found in the outer layer of the ovary, near the surface of the organ.
Cystadenocarcinoma, serous is the most common type of ovarian cancer, accounting for about 50-60% of all cases. It is often diagnosed at an advanced stage, as it can be difficult to detect in its early stages. Symptoms may include abdominal pain, bloating, and changes in bowel or bladder habits.
Treatment for cystadenocarcinoma, serous usually involves a combination of surgery and chemotherapy. Surgery may involve removing the uterus, ovaries, and other affected tissues, followed by chemotherapy to kill any remaining cancer cells. In some cases, radiation therapy may also be used.
Prognosis for cystadenocarcinoma, serous varies depending on the stage of the cancer at diagnosis. Women with early-stage disease have a good prognosis, while those with advanced-stage disease have a poorer outlook. However, overall survival rates have improved in recent years due to advances in treatment and screening.
In summary, cystadenocarcinoma, serous is a type of ovarian cancer that originates in the lining of the ovary and grows slowly over time. It can be difficult to detect in its early stages, but treatment typically involves surgery and chemotherapy. Prognosis varies depending on the stage of the cancer at diagnosis.
Peritoneal neoplasms are relatively rare, but they can be aggressive and difficult to treat. The most common types of peritoneal neoplasms include:
1. Peritoneal mesothelioma: This is the most common type of peritoneal neoplasm and arises from the mesothelial cells that line the abdominal cavity. It is often associated with asbestos exposure.
2. Ovarian cancer: This type of cancer originates in the ovaries and can spread to the peritoneum.
3. Appendiceal cancer: This type of cancer arises in the appendix and can spread to the peritoneum.
4. Pseudomyxoma peritonei: This is a rare type of cancer that originates in the abdominal cavity and resembles a mucin-secreting tumor.
5. Primary peritoneal cancer: This type of cancer originates in the peritoneum itself and can be of various types, including adenocarcinoma, squamous cell carcinoma, and sarcoma.
The symptoms of peritoneal neoplasms vary depending on the location and size of the tumor, but may include abdominal pain, distension, and difficulty eating or passing stool. Treatment options for peritoneal neoplasms depend on the type and stage of the cancer, but may include surgery, chemotherapy, and radiation therapy. Prognosis for peritoneal neoplasms is generally poor, with a five-year survival rate of around 20-30%.
Some examples of multiple abnormalities include:
1. Multiple chronic conditions: An individual may have multiple chronic conditions such as diabetes, hypertension, arthritis, and heart disease, which can affect their quality of life and increase their risk of complications.
2. Congenital anomalies: Some individuals may be born with multiple physical abnormalities or birth defects, such as heart defects, limb abnormalities, or facial deformities.
3. Mental health disorders: Individuals may experience multiple mental health disorders, such as depression, anxiety, and bipolar disorder, which can impact their cognitive functioning and daily life.
4. Neurological conditions: Some individuals may have multiple neurological conditions, such as epilepsy, Parkinson's disease, and stroke, which can affect their cognitive and physical functioning.
5. Genetic disorders: Individuals with genetic disorders, such as Down syndrome or Turner syndrome, may experience a range of physical and developmental abnormalities.
The term "multiple abnormalities" is often used in medical research and clinical practice to describe individuals who have complex health needs and require comprehensive care. It is important for healthcare providers to recognize and address the multiple needs of these individuals to improve their overall health outcomes.
Benign vaginal neoplasms include:
1. Vaginal papilloma: A small, finger-like growth on the wall of the vagina.
2. Vaginal polyps: Growths that protrude from the wall of the vagina.
3. Vaginal cysts: Fluid-filled sacs that can develop in the vaginal wall.
Malignant vaginal neoplasms include:
1. Vaginal squamous cell carcinoma: Cancer that develops in the thin, flat cells that line the vagina.
2. Adenocarcinoma of the vagina: Cancer that develops in the glandular cells that line the vagina.
3. Melanoma of the vagina: Rare cancer that develops in the pigment-producing cells of the vagina.
4. Sarcoma of the vagina: Cancer that develops in the connective tissue of the vagina.
Causes and risk factors:
The exact cause of vaginal neoplasms is not known, but certain factors can increase the risk of developing them, such as:
1. HPV (human papillomavirus) infection: A common sexually transmitted virus that can lead to cancer.
2. Smoking: Can increase the risk of developing cancer.
3. Weakened immune system: Can increase the risk of developing cancer.
4. Family history of cancer: Can increase the risk of developing cancer.
Symptoms:
The symptoms of vaginal neoplasms can vary depending on the type and location of the tumor, but may include:
1. Abnormal bleeding or discharge
2. Pain during sex
3. Itching or burning sensation in the vagina
4. A lump or mass in the vagina
5. Difficulty urinating
6. Painful urination
7. Vaginal wall thickening
Diagnosis:
A diagnosis of vaginal neoplasm is typically made through a combination of physical examination, imaging tests such as ultrasound or MRI, and a biopsy to confirm the presence of cancer cells.
Treatment:
The treatment of vaginal neoplasms depends on the type and stage of the cancer, but may include:
1. Surgery: Removal of the tumor and surrounding tissue.
2. Radiation therapy: Use of high-energy rays to kill cancer cells.
3. Chemotherapy: Use of drugs to kill cancer cells.
4. Hysterectomy: Removal of the uterus and/or vagina.
5. Pelvic exenteration: Removal of the pelvic organs, including the bladder, rectum, and reproductive organs.
Prognosis:
The prognosis for vaginal neoplasms depends on the type and stage of the cancer at the time of diagnosis. In general, the earlier the cancer is detected and treated, the better the prognosis.
Complications:
Some possible complications of vaginal neoplasms include:
1. Recurrence of the cancer
2. Infection
3. Incontinence or other urinary problems
4. Sexual dysfunction
5. Emotional distress
Prevention:
There is no sure way to prevent vaginal neoplasms, but some risk factors can be reduced by:
1. Practicing safe sex to reduce the risk of HPV infection
2. Getting regular Pap smears to detect and treat precancerous changes early
3. Avoiding tobacco and limiting alcohol consumption
4. Maintaining a healthy diet and exercising regularly
5. Getting vaccinated against HPV if you are under 26 years old
Note: This information is intended for educational purposes only and should not be considered medical advice. If you have any concerns or questions about vaginal neoplasms, you should consult a healthcare professional for personalized advice and treatment.
The symptoms of sarcoma, endometrial stromal can include abnormal vaginal bleeding, pelvic pain, and a mass in the pelvis. The tumor can be small or large, and it may or may not have spread to other parts of the body (metastasized) at the time of diagnosis.
The exact cause of sarcoma, endometrial stromal is not known, but there are several risk factors that have been associated with an increased risk of developing this type of cancer. These include:
* Previous radiation therapy to the pelvis
* Family history of uterine cancer
* Early onset of menstruation (before age 12) or late menopause (after age 55)
* Never being pregnant or having few or no full-term pregnancies
* Obesity
* Use of tamoxifen, a medication used to treat certain types of breast cancer
To diagnose sarcoma, endometrial stromal, a doctor may perform a physical exam, take a medical history, and use one or more of the following tests:
* Pelvic exam: The doctor will insert a speculum into the vagina to examine the cervix and uterus for any abnormalities.
* Imaging tests: Such as ultrasound, CT scan, or MRI to look for any tumors in the pelvis.
* Biopsy: A sample of tissue is taken from the suspected tumor and examined under a microscope for cancer cells.
* Endometrial biopsy: A sample of tissue is taken from the lining of the uterus to check for any abnormalities.
Treatment for sarcoma, endometrial stromal usually involves a combination of surgery and hormone therapy. The specific treatment plan will depend on the stage and location of the cancer, as well as the patient's overall health. Some common treatments include:
* Surgery: To remove the tumor and any affected tissues.
* Hysterectomy: Removal of the uterus is often necessary to treat sarcoma, endometrial stromal.
* Radiation therapy: Use of high-energy beams to kill cancer cells.
* Chemotherapy: Use of drugs to kill cancer cells.
It's important for women to talk to their doctor about their risk factors and any symptoms they may be experiencing, so that they can be monitored closely and receive appropriate treatment if necessary.
Individuals with this condition may have a range of symptoms, including:
* Undescended testes (cryptorchidism) or absent testes
* Infertility or lack of secondary sexual characteristics (such as beard growth or deepened voice)
* Variations in the shape and structure of the testes
* Chromosomal abnormalities, such as an extra X or Y chromosome
The cause of gonadal dysgenesis, 46,XY is not fully understood, but it is thought to be related to genetic mutations that affect the development of the testes during fetal development. Treatment options for this condition may include hormone replacement therapy, surgery to correct undescended testes, and assisted reproductive technology (such as in vitro fertilization) to achieve pregnancy.
It is important to note that gonadal dysgenesis, 46,XY is a rare condition and may not be the sole cause of infertility or other reproductive issues. A thorough medical evaluation and genetic testing may be necessary to determine the underlying cause of these issues.
Endometrial neoplasms are abnormal growths or tumors that develop in the lining of the uterus, known as the endometrium. These growths can be benign (non-cancerous) or malignant (cancerous). The most common type of endometrial neoplasm is endometrial hyperplasia, which is a condition where the endometrium grows too thick and can become cancerous if left untreated. Other types of endometrial neoplasms include endometrial adenocarcinoma, which is the most common type of uterine cancer, and endometrial sarcoma, which is a rare type of uterine cancer that develops in the muscle or connective tissue of the uterus.
Endometrial neoplasms can be caused by a variety of factors, including hormonal imbalances, genetic mutations, and exposure to certain chemicals or radiation. Risk factors for developing endometrial neoplasms include obesity, early onset of menstruation, late onset of menopause, never being pregnant or having few or no full-term pregnancies, and taking hormone replacement therapy or other medications that can increase estrogen levels.
Symptoms of endometrial neoplasms can include abnormal vaginal bleeding, painful urination, and pelvic pain or discomfort. Treatment for endometrial neoplasms depends on the type and stage of the condition, and may involve surgery, radiation therapy, chemotherapy, or hormone therapy. In some cases, a hysterectomy (removal of the uterus) may be necessary.
In summary, endometrial neoplasms are abnormal growths that can develop in the lining of the uterus and can be either benign or malignant. They can be caused by a variety of factors and can cause symptoms such as abnormal bleeding and pelvic pain. Treatment depends on the type and stage of the condition, and may involve surgery, radiation therapy, chemotherapy, or hormone therapy.
Some common types of uterine diseases include:
1. Endometriosis: A condition in which tissue similar to the lining of the uterus grows outside the uterus, causing pain, inflammation, and infertility.
2. Fibroids: Noncancerous growths that develop in the uterus, often causing heavy menstrual bleeding, pelvic pain, and infertility.
3. Adenomyosis: A condition where tissue similar to the lining of the uterus grows into the muscle wall of the uterus, leading to heavy menstrual bleeding, pain, and infertility.
4. Uterine polyps: Growths that develop on the inner lining of the uterus, often causing abnormal bleeding or spots on the uterine lining.
5. Uterine cancer: Cancer that develops in the cells of the uterus, often caused by factors such as obesity, hormonal imbalances, or family history of cancer.
6. Endometrial hyperplasia: A condition where the lining of the uterus becomes thicker than normal, often due to hormonal imbalances or excessive estrogen exposure.
7. Asherman's syndrome: Scar tissue that develops inside the uterus, often after a D&C procedure, leading to infertility and irregular menstrual bleeding.
8. Uterine septum: A congenital condition where a wall of tissue divides the uterus into two compartments, often causing irregular menstrual bleeding and fertility problems.
9. Endometrial cysts: Fluid-filled sacs that develop on the inner lining of the uterus, often causing abnormal bleeding or pelvic pain.
10. Uterine tuberculosis: A rare condition where the uterus becomes infected with tuberculosis bacteria, often caused by poor sanitation and hygiene.
These are just a few of the many conditions that can affect the uterus and cause abnormal bleeding. It's important to consult with a healthcare provider if you experience any unusual or persistent vaginal bleeding to determine the underlying cause and receive proper treatment.
There are two main types of dysmenorrhea: primary and secondary. Primary dysmenorrhea is caused by uterine muscle contractions that occur during menstruation, while secondary dysmenorrhea is caused by an underlying medical condition such as endometriosis, fibroids, or pelvic inflammatory disease.
Symptoms of dysmenorrhea may include:
* Cramping pain in the lower abdomen, usually beginning before or at the onset of menstruation and lasting for 1-3 days
* Pain that can be sharp, dull, or throbbing
* Pelvic discomfort or heaviness
* Nausea and vomiting
* Diarrhea or constipation
* Headache
* Fatigue
* Mild fever
While dysmenorrhea is not a life-threatening condition, it can significantly impact a woman's quality of life, particularly during her reproductive years. The exact cause of primary dysmenorrhea is not fully understood, but it is believed to be related to the production of prostaglandins, hormone-like substances that cause uterine muscle contractions and increased blood flow to the pelvis.
Treatment for dysmenorrhea may include over-the-counter pain relievers such as ibuprofen or naproxen, as well as home remedies such as heat application, exercise, and relaxation techniques. In some cases, prescription medications or surgery may be necessary to address underlying conditions that are contributing to the dysmenorrhea.
It's important for women who experience severe or persistent dysmenorrhea to seek medical attention to rule out any underlying conditions that may need treatment. With proper diagnosis and management, most women with dysmenorrhea can find relief from their symptoms and lead normal, active lives.
Anti-Müllerian hormone receptor
Paramesonephric duct
Age and female fertility
Anti-Müllerian hormone
BRCA mutation
Female infertility
Polycystic ovary syndrome
Mullerian anomalies
Seminal vesicles
Human reproductive ecology
Ovary
Ovarian drilling
Follicular atresia
Intermediate mesoderm
Activin and inhibin
Azoospermia
Ovarian follicle activation
Ovarian reserve
Congenital adrenal hyperplasia due to 21-hydroxylase deficiency
Persistent Müllerian duct syndrome
WNT4 deficiency
List of diseases (H)
Partial androgen insensitivity syndrome
Mimicry
Complete androgen insensitivity syndrome
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SSAMH B
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Inhibin4
- Within the 2001-2002 National Health and Nutrition Examination Survey (NHANES) Serum Anti-Müllerian Hormone (AMH) and inhibin B concentrations among men were measured to evaluate variation by age and race/ethnicity. (cdc.gov)
- As levels of progesterone, estradiol, and inhibin decline 2-3 days before menses, the pituitary begins to release higher levels of follicle-stimulating hormone (FSH), which recruits oocytes for the next menstrual cycle. (medscape.com)
- 18. Comparison of anti-Müllerian hormone and inhibin immunolabeling in canine and equine granulosa cell tumors. (nih.gov)
- Detection of anti-mullerian hormone, inhibin, and testosterone. (tamu.edu)
Follicle-stimula1
- 1 , 2 , 3 , 4 This test measures the amount of follicle-stimulating hormone (FSH) or luteinizing hormone (LH)-hormones made by the pituitary gland-in your blood to determine if your ovaries are working properly. (nih.gov)
Serum8
- Description: A competitive inhibition quantitative ELISA assay kit for detection of Human Anti-Mullerian Hormone (AMH) in samples from serum, plasma, tissue homogenates, cell lysates, cell culture supernates or other biological fluids. (unicoupi.com)
- Description: This is Competitive Enzyme-linked immunosorbent assay for detection of Rat Anti-Mullerian Hormone (AMH) in serum, plasma, tissue homogenates, cell lysates, cell culture supernates and other biological fluids. (unicoupi.com)
- One-year impact of bariatric surgery on serum anti-Mullerian-hormone levels in severely obese women. (bvsalud.org)
- To evaluate changes in serum anti-Mullerian hormone (AMH) levels in reproductive-age severely obese women after bariatric surgery (BS). (bvsalud.org)
- 2. Biological and clinical significance of anti-Müllerian hormone determination in blood serum of the mare. (nih.gov)
- This study was conducted to determine serum anti-Müllerian hormone (AMH) concentration influence on pregnancy outcome. (nel.edu)
- Moreover, it cannot be excluded that presence of anti-thyroid antibodies and increased insulin serum concentration may be connected to diminished ovarian reserve measured by AMH concentration. (nel.edu)
- 6. Anti-Mullerian hormone is a sensitive serum marker for gonadal function in women treated for Hodgkin's lymphoma during childhood. (nih.gov)
Sertoli2
Granulosa cells3
- Immediately prior to ovulation, the combination of E 2 and FSH leads to the production of luteinizing-hormone (LH) receptors on the granulosa cells surrounding the lead follicle. (medscape.com)
- 15. Vitamin D regulates anti-Mullerian hormone expression in granulosa cells of the hen. (nih.gov)
- 16. Concentrations of anti-Müllerian hormone in fluid from small human antral follicles show a negative correlation with CYP19 mRNA expression in the corresponding granulosa cells. (nih.gov)
Gonadotropin-releasi2
- Gonadotropin therapy or the use of pulsatile gonadotropin-releasing hormone (GnRH) therapy may be required to induce ovulation in patients with infertility whose underlying pathology cannot be reversed. (medscape.com)
- The hypothalamus is the initiator of the follicular phase via gonadotropin-releasing hormone (GnRH). (medscape.com)
Receptor2
- 7. Anti-müllerian hormone and anti-müllerian hormone type II receptor messenger ribonucleic acid expression in rat ovaries during postnatal development, the estrous cycle, and gonadotropin-induced follicle growth. (nih.gov)
- Aecently, amh and its type II receptor, amhrII have been cloned from teleosts, which do not contain the tissue of Mullerian duct. (ncl.edu.tw)
Pituitary1
- Consideration of the target organs of these reproductive hormones (hypothalamus, pituitary, ovary, uterus) is helpful for identifying the disease process responsible for a patient's amenorrhea. (medscape.com)
Concentrations4
- Urinary phthalate metabolite concentrations are negatively associated with follicular fluid anti-müllerian hormone concentrations in women undergoing fertility treatment. (nih.gov)
- Our objective was to investigate whether urinary phthalate metabolite concentrations were associated with pre-ovulatory follicular fluid (FF) anti-müllerian hormone (AMH) concentrations in women undergoing fertility treatment. (nih.gov)
- 13. Molecular changes in the equine follicle in relation to variations in antral follicle count and anti-Müllerian hormone concentrations. (nih.gov)
- Sex hormone concentrations differ, on average, in different individuals. (freethoughtblogs.com)
Thyroid-stimula1
- 1 , 2 , 3 This test measures the amount of thyroid-stimulating hormone (TSH) in your blood, which can help determine if your thyroid is working properly. (nih.gov)
Ovarian follicles2
- Your health care provider may also evaluate the level of anti-Mullerian hormone (AMH), which is produced by the ovarian follicles. (nih.gov)
- The assessment involves checking various hormones involved in the ovulation process, including your AMH, aka anti-mullerian hormone , which is produced by your ovarian follicles that release eggs, and can therefore give your doctors a sense of your ovarian reserve, or full bank of eggs. (instyle.com)
Follicular2
Duct2
- Anti-Mullerian hormone (AMH) plays an important role in the process of mammalian male development, which major function is inhibition of Mullerian duct activity of female reproduction tissue. (ncl.edu.tw)
- In males, defects of this hormone result in persistent Mullerian duct, a form of MALE PSEUDOHERMAPHRODITISM . (nih.gov)
Progesterone2
- EMPROGEST EV 200MG TABLET contains Progesterone which belongs to the group of medicines called Steroid hormones. (netmeds.com)
- EMPROGEST EV 200MG TABLET is a steroid hormone used to treat progesterone deficiency in the body. (netmeds.com)
Ovary3
- 4. Early postnatal methoxychlor exposure inhibits folliculogenesis and stimulates anti-Mullerian hormone production in the rat ovary. (nih.gov)
- 8. [Study on the anti-müllerian hormone served as a marker for granulosa cell tumor of ovary]. (nih.gov)
- High levels of anti-Mullerian hormone (AMH) have traditionally been thought of as merely a passive byproduct of polycystic ovary syndrome (PCOS), but a new preclinical study by Weill Cornell Medicine researchers suggests that the hormone plays an active role in the disorder and may contribute to problems with ovulation and fertility. (news-medical.net)
Reproductive2
Hormonal1
- When she remarked that males and females have hormonal differences, her colleagues told her that hormones are not real, they were only made up by a conspiracy of male scientists. (freethoughtblogs.com)
Fertility10
- Daoud A, Bataineh H, Otoom S, Abdul-Zahra E. The effect of Vigabatrin, Lamotrigine and Gabapentin on the fertility, weights, sex hormones and biochemical profiles of male rats. (nel.edu)
- An easy and affordable fertility hormone test you can use to be proactive about your fertility. (ro.co)
- I've been using Modern Fertility's Hormone Test since 2020 to help me better understand my body and where I'm at fertility-wise based upon my age and lifestyle. (ro.co)
- Modern Fertility gives you insight into your ovarian reserve, thyroid health, and other hormone factors. (ro.co)
- We'll test between two and seven hormones based on your birth control method, and deliver custom reports to help you learn about your fertility. (ro.co)
- The same fertility hormone test typically offered in clinics. (ro.co)
- Information garnered from a fertility hormone panel can help people understand how their fertility changes over time so that they can take action and be proactive about their fertility planning. (ro.co)
- Low levels of Anti-Mullerian Hormone can cause reduced fertility and difficulty conceiving, typically caused by age, genetics, illness or cancer treatment. (goodbodyclinic.com)
- Check your levels of common female hormones which can impact your mood, fertility, energy levels, weight, skin and hair condition, sex drive and fitness levels. (goodbodyclinic.com)
- Check your levels of common male hormones which can impact your mood, energy levels, libido and erectile function, fertility, weight, fitness and sports performance. (goodbodyclinic.com)
Evaluate1
- We also evaluate correlations with previously measured sex-steroid hormone measurements. (cdc.gov)
Ovaries3
- 1. Expression of anti-Müllerian hormone (AMH) in equine granulosa-cell tumors and in normal equine ovaries. (nih.gov)
- All women have a different level of AMH (anti-mullerian hormone) which is a hormone found in the blood which is released by the eggs being developed in the ovaries. (gemivf.com)
- A sex hormone produced by the ovaries. (ro.co)
Steroid1
- Vitamin D is a steroid hormone well known for its role in calcium homeostasis and bone mineralization. (vitamindwiki.com)
Levels4
- AMH levels were measured retrospectively in 39 women (mean age 34.6 ± 1.1 years, range 18-45) that underwent a sleeve gastrectomy or Roux-en-Y gastric bypass (RYGB) at baseline, and 6 and 12 months after BS. (bvsalud.org)
- 1 , 2 , 3 Androgens are sometimes called "male hormones" because men need higher levels of these hormones than woman do for overall health. (nih.gov)
- MF gave me a ground to stand on when I had to stand up to doctors who said I was too young to have hormone levels that low. (ro.co)
- Check your levels of the HCG hormone to identify pregnancy from 10 days after a missed period. (goodbodyclinic.com)
Deficiency1
- In conditions leading to estrogen deficiency, hormone replacement therapy is required to maintain bone density, and it may have other possible health benefits in patients whose underlying pathology cannot be reversed to restore normal endocrine function. (medscape.com)
Clinical1
- The use of stimulation (gonadotropins) and targeted pre- and posttreatment hormone monitoring during this clinical trial aims to characterize more fully the transition from PRP dosing, embryogenesis, IVF and conception. (clinicaltrials.gov)
Regulation2
Type1
- A newly discovered hormone named fabkin helps regulate metabolism and may play an important role in the development of both type 1 and type 2 diabetes, according to research led by the Sabri Ülker Center for Metabolic Research at Harvard T.H. Chan School of Public Health. (news-medical.net)
Exposure1
- Vitamin D is a secosteroid hormone mainly produced in the skin after sunlight exposure and is primarily known for its role in bone health and mineralization.1 In the last few years, the extraskeletal actions of vitamin D have emerged as a significant area of intensive scientific interest. (vitamindwiki.com)
Pregnancy2
Normal1
- Hormone replacement therapy is required to achieve peak bone density in patients whose underlying pathology cannot be reversed to restore normal endocrine function. (medscape.com)
Test2
Women3
- This research extends earlier work conducted by Inovium associates in Athens, Greece who demonstrated efficacy of intraovarian injection of autologous PRP for resumption of menses, hormone stabilization, and conception after IVF in multiple women following PRP+natural cycle IVF (i.e., without gonadotropin stimulation). (clinicaltrials.gov)
- Increased androgen, anti-Müllerian hormone, and sporadic anovulation in healthy, eumenorrheic women: a mild PCOS-like phenotype? (nih.gov)
- 9. Anti-Müllerian hormone follow-up in young women treated by chemotherapy for lymphoma: preliminary results. (nih.gov)
Eggs1
- Turns out, when I came up with the idea of contending with my conundrum by undergoing egg freezing - an 11-ish day process in which you take hormone injections to spur the growth of, ideally, mature eggs that can be retrieved under anesthesia and then cryopreserved (aka frozen) with the hope that they could be fertilized down the road - I was also in good company. (instyle.com)
Study1
- The current study seeks to describe how PRP works to rejuvenate immune system and ovarian stem cells, restore menses, provide hormone stability, and generate successful IVF sequences and conceptions. (clinicaltrials.gov)