Hepatotoxicity Minocycline therapy is associated with two forms of clinically apparent liver injury, an acute hepatitis-like syndrome that arises within 1 to 3 months of starting therapy and a chronic hepatitis-like syndrome typically with autoimmune features that occurs with long term therapy, sometimes after several years of use. There is some overlap between these two presentations of minocycline hepatotoxicity, both are associated with a hepatocellular pattern of serum enzyme elevations and both can be associated with autoantibodies and immunological features.
Minocycline has been linked to cases of an acute hepatitis with jaundice that typically arises within a few weeks or months of starting therapy. The enzyme elevations are typically hepatocellular and resemble acute viral hepatitis. Immunoallergic features are common and may be prominent with fever, rash and eosinophilia and some cases with facial edema, lymphoadenopathy and lymphocytosis that may resemble acute mononucleosis.
The liver injury is usually self limited with complete resolution within 1 to 2 months of stopping. Some patients have autoimmune markers and these also improve upon stopping minocycline. Some of the observed adverse events are not entirely surprising. Minocycline is a small kDa , highly lipophilic molecule capable of crossing the blood—brain barrier BBB.
Because of the large volume of distribution of minocycline, the drug accumulates in tissues other than the CNS, including the eye and prostate, and it is detectable in high concentration in tears, saliva and breast milk [20].
The pharmacological half-life of minocycline is approximately 18 hours. Thus, high and frequent dosing is required. Preliminary data on the efficacy of minocycline in patients with MS are promising. In an ongoing clinical trial of minocycline in a relatively small number of patients with relapsing-remitting MS, study participants received oral minocycline mg twice daily for 6 months after a 3-month run-in period [21].
A month treatment extension is ongoing. The preliminary results of this trial demonstrated that minocycline therapy reduces gadolinium-enhancing lesions on magnetic resonance imaging MRI [21]. Fortunately, no serious adverse effects of minocycline in MS have been reported thus far. Since then, it has been shown that this disease can be paraneoplastic and nonparaneoplastic, and occur in both genders and at any age Irani et al. In this disorder, many patients present with marked behavioral and cognitive abnormalities and a small proportion were reported to have isolated psychiatric features at presentation or during relapse 0.
Among those with isolated psychiatric episodes, psychotic symptoms, including delusional thinking, auditory or visual hallucinations, and aggressiveness, were the most common. Taking this into account, and considering the frequent normality of the paraclinical investigations, these patients present a diagnostic challenge.
Indeed, in these conditions there may be minor serum aminotransferase elevations indicative of a mild component of hepatic injury. The important differential diagnosis for drug induced autoimmune hepatitis is, of course, spontaneous or idiopathic autoimmune hepatitis, a disease that can have spontaneous remissions and relapses, but that is typically severe and progressive without adequate immunosuppressive therapy.
Some cases of drug induced autoimmune hepatitis do not resolve completely upon withdrawal of the medication, and some require long term immunosuppressive therapy and have had relapses some severe when corticosteroids were stopped. In these instances, it is not clear whether the autoimmune hepatitis-like syndrome was actually caused by the medication or was a co-incidence, arising spontaneously in a patient being treated long term with a common medication.
An intermediate hypothesis is also possible, that the medication triggered the onset of autoimmune hepatitis in a susceptible patient that may have ultimately developed the disease, even without the medication. Often, this last possibility cannot be excluded. Spontaneous, idiopathic autoimmune hepatitis obviously has triggering factors for its onset and a medication or liver injury may be such a trigger.
These issues call for careful clinical investigation of cases of autoimmune hepatitis associated with medications for genetic and environmental factors that might reveal the cause of this important syndrome. The pathogenesis of autoimmune hepatitis due to medications is not clear. However, it is likely that hepatocytes, owing to their ability to metabolize drugs, can form drug-protein adducts which may be immunogenic. The current medication options will be reviewed below.
Corticosteroids such as prednisone, prednisolone, or budesonide are usually used to help suppress the immune system so the liver is not attacked and calm down the inflammation in the liver. Prednisone is a common first treatment. It has been used for many years and tends to work for many.
Unfortunately, there are several side effects of these medications including bone loss osteoporosis , high blood sugar, increased appetite, insomnia, mood changes, muscle pain, depression, and anxiety. Budesonide tends to have fewer of the side effects, but has been less studied. Azathioprine Imuran is commonly started during the tapering of prednisone. This medication tends to have less severe side effects compared to the prednisone so it is usually the drug of choice for long-term use.
There is an increased risk of lymphoma with this medication. Some people are unable to metabolize this medication which can be determined with some additional blood tests. While on this medication, white blood cell counts need to be monitored. Mycophenolate mofetil Cellcept is another option if one cannot tolerate azathioprine.
It can also cause a significant amount of GI symptoms including abdominal pain, nausea, vomiting, diarrhea, constipation, and anorexia. Some may also have their kidney function affected by this medication so that must be monitored by bloodwork. Females of childbearing age must take a pregnancy test prior to starting this medication and use two forms of birth control while on the medication because it is associated with birth defects.
Breastfeeding must be avoided until 6 months after this medication has been stopped because it is unknown if it is excreted in the breast milk. The well-known but well-kept secret. Friedlander IR "Minocycline and ototoxicity. Mensing H, Kowalzick L "Acute febrile neutrophilic dermatosis Sweet's syndrome caused by minocycline. Yamamoto T, Minatohara K "Minocycline-induced acute generalized exanthematous pustulosis in a patient with generalized pustular psoriasis showing elevated level of sELAM Wetter DA "Minocycline hyperpigmentation.
Caro I "Discoloration of the teeth related to minocycline therapy for acne. Boyle MP "Minocycline-induced pancreatitis in cystic fibrosis. Gorard DA "Late-onset drug fever associated with minocycline. Quilty B, Mchugh N "Lupus-like syndrome associated with the use of minocycline. Hess EV "Minocycline and autoimmunity. LePaw MI "Fixed drug eruption due to minocycline-report of one case. Case series and literature review. Kaufmann D, Pichler W, Beer JH "Severe episode of high fever with rash, lymphadenopathy, neutropenia, and eosinophilia after minocycline therapy for acne.
Ferner RE, Moss C "Minocycline for acne - first line antibacterial treatment of acne should be with tetracycline or oxytetracycline. Rosin MA "Viral-like syndrome associated with minocycline. Margolis DJ, Hoffstad O, Bilker W "Association or lack of association between tetracycline class antibiotics used for acne vulgaris and lupus erythematosus.
Case series in the West of Scotland.
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