Fabry disease, also known as Anderson–Fabry disease, is a rare genetic disease that can affect many parts of the body, including the kidneys, heart, and skin. Fabry disease is one of a group of conditions known as lysosomal storage diseases. The genetic mutation that causes Fabry disease interferes with the function of an enzyme that processes biomolecules known as sphingolipids, leading to these substances building up in the walls of blood vessels and other organs. It is  inherited in an X-linked manner. Fabry disease is sometimes diagnosed using a blood test that measures the activity of the affected enzyme called alpha-galactosidase, but genetic testing is also sometimes used, particularly in females. The treatment for Fabry disease varies depending on the organs affected by the condition, and the underlying cause can be addressed by replacing the enzyme that is lacking. The first descriptions of the condition were made simultaneously by  dermatologist Johannes Fabry and the surgeon William Anderson in 1898. Signs and symptoms
Symptoms are typically first experienced in early childhood and can be very difficult to diagnose; the rarity of Fabry disease to many clinicians sometimes leads to misdiagnoses. Manifestations of the disease usually increase in number and severity as an individual ages. Pain
Full-body or localized pain to the extremities (known as acroparesthesia) or gastrointestinal (GI) tract is common in patients with Fabry disease. This pain can increase over time. This acroparesthesia is believed to be related to the damage of peripheral nerve fibers that transmit pain.
Escherichia coli
Proteus mirabilis
Klebsiella pneumoniae
Enterobacter species
Coagulase-negative Staphylococcus species, including S. saprophyticus
Streptococcus pneumoniae
Haemophilus influenzae

Side effects
Common
Nauseas
Change in taste
Vomiting
Diarrhea
Rashes
Sun sensitivity
Itchiness

Rare
Can cause thrombocytopenia (low levels of platelets) by lowering folic acid levels; this may also cause megaloblastic anemia. Trimethoprim antagonizes the epithelial sodium channel  in the distal tubule, thus acting like amiloride. This can cause increased potassium levels in the body (hyperkalemia). Can compete with creatinine for secretion into the renal tubule. This can cause an artificial rise in the serum creatinine. Use in EHEC infections may lead to an increase in expression of Shiga toxin. Contraindications
Known hypersensitivity to trimethoprim
History of megaloblastic anemia due to folate deficiency

Pregnancy
Based on the studies that show that trimethoprim crosses the placenta and can affect folate metabolism, there has been growing evidence of the risk of structural birth defects associated with trimethoprim, especially during the first trimester of pregnancy. It may be involved in a reaction similar to disulfiram when alcohol is consumed after it is used, in particular when used in combination with sulfamethoxazole. The trophoblasts in the early fetus are sensitive to changes in the folate cycle. A recent study has found a doubling in the risk of miscarriage in women exposed to trimethoprim in the early pregnancy. Mechanism of action
Trimethoprim binds to dihydrofolate reductase and inhibits the reduction of dihydrofolic acid (DHF) to tetrahydrofolic acid (THF). THF is an essential precursor in the thymidine synthesis pathway and interference with this pathway inhibits bacterial DNA synthesis.