Connective Tissue Diseases
Molecular Sequence Data
Amino Acid Sequence
Sugar Alcohol Dehydrogenases
3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)
Endothelial Growth Factors
Fetal Membranes, Premature Rupture
Pyruvate Dehydrogenase (Lipoamide)
3-Hydroxyacyl CoA Dehydrogenases
Glucosephosphate Dehydrogenase Deficiency
3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)
Dihydrouracil Dehydrogenase (NADP)
Uridine Diphosphate Glucose Dehydrogenase
11-beta-Hydroxysteroid Dehydrogenase Type 1
Some common types of connective tissue diseases include:
1. Rheumatoid arthritis (RA): A chronic autoimmune disorder that causes inflammation and joint damage.
2. Systemic lupus erythematosus (SLE): An autoimmune disorder that can affect multiple systems in the body, including the skin, joints, and kidneys.
3. Sjogren's syndrome: An autoimmune disorder that causes dry eyes and mouth, as well as joint pain and swelling.
4. Fibromyalgia: A chronic condition characterized by widespread muscle pain and fatigue.
5. Myositis: Inflammatory diseases that affect the muscles, such as dermatomyositis and polymyositis.
6. Giant cell arteritis: A condition that causes inflammation of the blood vessels, particularly in the head and neck.
7. Takayasu arteritis: A condition that causes inflammation of the blood vessels in the aorta and its branches.
8. Polyarteritis nodosa: A condition that causes inflammation of the blood vessels, particularly in the hands and feet.
9. IgG4-related disease: A condition characterized by inflammation and damage to various organs, including the pancreas, salivary glands, and liver.
Connective tissue diseases can cause a wide range of symptoms, including joint pain and stiffness, fatigue, skin rashes, fever, and weight loss. Treatment options vary depending on the specific disease and its severity, but may include medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs). In some cases, surgery or physical therapy may also be necessary.
Premature rupture of fetal membranes is diagnosed through a combination of physical examination, ultrasound, and laboratory tests. Treatment options for PROM include:
1. Expectant management: In this approach, the woman is monitored closely without immediately inducing labor. This option is usually chosen if the baby is not yet ready to be born and the mother has no signs of infection or preterm labor.
2. Induction of labor: If the baby is mature enough to be born, labor may be induced to avoid the risks associated with preterm birth.
3. Cesarean delivery: In some cases, a cesarean section may be performed if the woman has signs of infection or if the baby is in distress.
4. Antibiotics: If the PROM is caused by an infection, antibiotics may be given to treat the infection and prevent complications.
5. Steroids: If the baby is less than 24 hours old, steroids may be given to help mature the lungs and reduce the risk of respiratory distress syndrome.
Prevention of premature rupture of fetal membranes includes good prenatal care, avoiding activities that can cause trauma to the abdomen, and avoiding infections such as group B strep. Early detection and management of PROM are crucial to prevent complications for the baby.
The condition is inherited in an X-linked recessive pattern, meaning that the gene for G6PD deficiency is located on the X chromosome and affects males more frequently than females. Females may also be affected but typically have milder symptoms or may be carriers of the condition without experiencing any symptoms themselves.
G6PD deficiency can be caused by mutations in the G6PD gene, which can lead to a reduction in the amount of functional enzyme produced. The severity of the condition depends on the specific nature of the mutation and the degree to which it reduces the activity of the enzyme.
Symptoms of G6PD deficiency may include jaundice (yellowing of the skin and eyes), fatigue, weakness, and shortness of breath. In severe cases, the condition can lead to hemolytic anemia, which is characterized by the premature destruction of red blood cells. This can be triggered by certain drugs, infections, or foods that contain high levels of oxalic acid or other oxidizing agents.
Diagnosis of G6PD deficiency typically involves a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment is focused on managing symptoms and preventing complications through dietary modifications, medications, and avoidance of triggers such as certain drugs or infections.
Overall, G6PD deficiency is a relatively common genetic disorder that can have significant health implications if left untreated. Understanding the causes, symptoms, and treatment options for this condition is important for ensuring appropriate care and management for individuals affected by it.
Aryl-alcohol dehydrogenase (NADP+)
List of MeSH codes (D08)
List of EC numbers (EC 1)
NDF-RT Code NDF-RT Name
YRC Public Data Repository - Protein Overview - dhs-16 / CE08067
Aldehydes. Medical search
DeCS 2016 - June 12, 2016 version
Pesquisa | Portal Regional da BVS
Thick Acsending Limb Transcriptomic Database
NEW (2006) MESH HEADINGS WITH SCOPE NOTES (UNIT RECORD FORMAT; 9/3/2005
Code System Concept
DeCS 2017 - December 21, 2017 version
Pesquisa | Prevenção e Controle de Câncer
- It acts by inhibiting aldehyde dehydrogenase. (lookformedical.com)
- It is caused by mutation of gene encoding microsomal fatty ALDEHYDE DEHYDROGENASE leading to defect in fatty alcohol metabolism. (lookformedical.com)
- We demonstrated that two e-liquids and three aldehyde flavoring agents (cinnamaldehyde, benzaldehyde, and ethyl vanillin) exhibited dose-dependent inhibition of cellular CYP2A6. (bvsalud.org)
- A subclass of enzymes which includes all dehydrogenases acting on primary and secondary alcohols as well as hemiacetals. (lookformedical.com)