Central Nervous System: Seizures, tremors, muscular twitching, confusion, agitation, ataxia, and hallucinations. Skin reactions
Hepatotoxicity
Infertility
Hair Loss

Pharmacology
Mechanism of action
Chlorambucil produces its anti-cancer effects by interfering with DNA replication and damaging the DNA in a cell. The DNA damage induces cell cycle arrest and cellular apoptosis via the accumulation of cytosolic p53 and subsequent activation of Bcl-2-associated X protein, an apoptosis promoter.Chlorambucil alkylates and cross-links DNA during all phases of the cell cycle, inducing DNA damage via three different methods of covalent adduct generation with double-helical DNA:
Attachment of alkyl groups to DNA bases, resulting in the DNA being fragmented by repair enzymes in their attempts to replace the alkylated bases, preventing DNA synthesis and RNA transcription from the affected DNA. DNA damage via the formation of cross-links which prevents DNA from being separated for synthesis or transcription. Induction of mispairing of the nucleotides leading to mutations.The precise mechanisms by which chlorambucil acts to kill tumor cells are not yet completely understood. Limitations to bioavailability
A recent study has shown Chlorambucil to be detoxified by human glutathione transferase Pi (GST P1-1), an enzyme that is often found over-expressed in cancer tissues.This is important since chlorambucil, as an electrophile, is made less reactive by conjugation with glutathione, thereby making the drug less toxic to the cell. Shown above, chlorambucil reacts with glutathione as catalyzed by hGSTA 1-1 leading to the formation of the monoglutathionyl derivative of chlorambucil. Chemistry
Chlorambucil is a white to pale beige crystalline or granular powder with a slight odor.
From the gallbladder, bile enters the intestine in individual portions. In the absence of a gallbladder, bile enters the intestine constantly, but in small quantities. Thus, it may be insufficient for the digestion of fatty foods. Postcholecystectomy syndrome treatment depends on the identified violations that led to it. Typically, the patient is recommended a dietary restriction table with fatty foods, enzyme preparations, antispasmodics, and sometimes cholagogue.If the pain is caused by biliary microlithiasis, oral ursodeoxycholic acid can alleviate the condition.A trial of bile acid sequestrant therapy is recommended for bile acid diarrhea.Functional dyspepsia is subdivided into Epigastric Distress Syndrome (EPS) and Post-Prandial Distress Syndrome (PDS). Treatment for EPS and PDS can both include proton pump inhibitors and dopamine antagonists. Tricyclic antidepressants have also been proven effective for nausea, vomiting, early satiety, impaired motility and other related symptoms.When investigation reveals no abnormalities within the abdominal cavity, the attending physician may consider Anterior cutaneous nerve entrapment syndrome (ACNES) as a possible cause. ACNES may present with pseudovisceral symptoms, including nausea, bloating, diarrhea and early satiety. References


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