Metabolic defects of fatty acid oxidation
More than 20 human genetic defects in fatty acid transport or oxidation have been identified. In case of fatty acid oxidation defects, acyl-carnitines accumulate in mitochondria and are transferred into the cytosol, and then into the blood. Plasma levels of acylcarnitine in newborn infants can be detected in a small blood sample by tandem mass spectrometry.When β oxidation is defective because of either mutation or deficiency in carnitine, the ω (omega) oxidation of fatty acids becomes more important in mammals. Actually, the ω Oxidation of Fatty Acids is another pathway for F-A degradation in some species of vertebrates and mammals that occurs in the endoplasmic reticulum of the liver and kidney, it is the oxidation of the ω carbon—the carbon most far from the carboxyl group (in contrast to 
  
    
      
        β
      
    
    {\displaystyle \beta }
   oxidation which occurs at the carboxyl end of fatty acid, in the mitochondria). Physiological effects
As an example of normal synthesis, a 70 kilograms (150 lb) person would produce 11–34 mg of carnitine per day. Adults eating mixed diets of red meat and other animal products ingest some 60–180 mg of carnitine per day, while vegans consume about 10–12 mg per day. Most (54–86%) carnitine obtained from the diet is absorbed in the small intestine before entering the blood.
Anagen effluvium is the pathologic loss of anagen or growth-phase hairs. Classically, it is caused by radiation therapy to the head and systemic chemotherapy, especially with alkylating agents. : 753–4 Anagen effluvium is due to an acute injury to the hair follicles by an endogenous or exogenous cause, resulting in sudden diffuse shedding of structurally damaged hairs. Diffuse alopecia (hair loss) may occur over a period of days. The alopecia is non-scarring. Pathophysiology
Any insult that impairs mitosis of hair follicle keratinocytes can cause anagen effluvium. Disruption to cell division in the hair matrix makes the hair narrowed at its base and susceptible to breakage just above the zone of keratinisation. The necrotic matrix forms plugs consisting of melanin, keratin and inner root sheath which are extruded through the follicular opening. This process is known as trichomalacia. The main causes of anagen effluvium are an infection, a drug, a toxin, radiation or an autoimmune disease.Toxins that can interrupt hair growth include:

Chemotherapy agents, usually prescribed to treat cancer, especially when multiple drugs are used or they are in high dose. Severe hair loss is reported from doxorubicin, the nitrosoureas, and cyclophosphamide. Other causes are bleomycin, dactinomycin, daunorubicin, systemic fluorouracil, and high-dose methotrexate. Other medicines such as colchicine and ciclosporin (ciclosporin more often causes increased hair growth)
Poisons such as thallium, arsenic, gold and bismuth. Evaluation
A biopsy is rarely necessary, as a diagnosis can usually be made on history and physical exam findings alone. If a biopsy is requested or necessary for diagnosis, it can help exclude telogen effluvium.