Seventh-nerve Palsy and Hepatitis Associated with Nitrofurantoin

1986 ◽  
Vol 5 (6) ◽  
pp. 387-388 ◽  
Author(s):  
R.G. Thomson ◽  
O.F.W. James
Keyword(s):  
Side Effects ◽  
Chronic Active Hepatitis ◽  
Nerve Palsy ◽  
Repeated Treatment ◽  
First Case ◽  
Seventh Nerve ◽  
Hepatic Reaction

Adverse hepatic reactions to nitrofurantoin therapy are well reported and range from acute cholestatic or hepatitic injury to chronic active hepatitis [R. G. Penn & J. P. Griffin (1982) Br. Med. J., 284, 1440-1442]. Neurological side-effects, predominantly sensorimotor peripheral poly-neuropathy, have also been documented [R. G. Penn & J. P. Griffin (1982)]. We report the first case of combined neurological and hepatic reaction to nitrofurantoin; this occurred during repeated treatment with the drug.

scholarly journals Recent advances in understanding NRF2 as a druggable target: development of pro-electrophilic and non-covalent NRF2 activators to overcome systemic side effects of electrophilic drugs like dimethyl fumarate

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 2138 ◽  
Author(s):  
Takumi Satoh ◽  
Stuart Lipton
Keyword(s):  
Side Effects ◽  
Specific Interaction ◽  
Dimethyl Fumarate ◽  
Carnosic Acid ◽  
European Medicines Agency ◽  
Related Factor ◽  
Inflammatory Phase ◽  
First Case ◽  
Systemic Side Effects ◽  
Transcriptional Pathway

Dimethyl fumarate (DMF) is an electrophilic compound previously called BG-12 and marketed under the name Tecfidera®. It was approved in 2013 by the US Food and Drug Administration and the European Medicines Agency for the treatment of relapsing multiple sclerosis. One mechanism of action of DMF is stimulation of the nuclear factor erythroid 2-related factor 2 (NRF2) transcriptional pathway that induces anti-oxidant and anti-inflammatory phase II enzymes to prevent chronic neurodegeneration. However, electrophiles such as DMF also produce severe systemic side effects, in part due to non-specific S-alkylation of cysteine thiols and resulting depletion of glutathione. This mini-review presents the present status and future strategy for NRF2 activators designed to avoid these side effects. Two modes of chemical reaction leading to NRF2 activation are considered here. The first mode is S-alkylation (covalent reaction) of thiols in Kelch-like ECH-associated protein 1 (KEAP1), which interacts with NRF2. The second mechanism involves non-covalent pharmacological inhibition of protein-protein interactions, in particular domain-specific interaction between NRF2 and KEAP1 or other repressor proteins involved in this transcriptional pathway. There have been significant advances in drug development using both of these mechanisms that can potentially avoid the systemic side effects of electrophilic compounds. In the first case concerning covalent reaction with KEAP1, monomethyl fumarate and monoethyl fumarate appear to represent safer derivatives of DMF. In a second approach, pro-electrophilic drugs, such as carnosic acid from the herb Rosmarinus officinalis, can be used as a safe pro-drug of an electrophilic compound. Concerning non-covalent activation of NRF2, drugs are being developed that interfere with the direct interaction of KEAP1-NRF2 or inhibit BTB domain and CNC homolog 1 (BACH1), which is a transcriptional repressor of the promoter where NRF2 binds.

scholarly journals Drug-Induced Autoimmune Hepatitis following Treatment with Zoledronic Acid

2017 ◽  
Vol 11 (2) ◽  
pp. 440-445 ◽  
Author(s):  
Jenny Sarah Schneider ◽  
Matteo Montani ◽  
Felix Stickel
Keyword(s):  
Liver Disease ◽  
Zoledronic Acid ◽  
Side Effects ◽  
Liver Injury ◽  
Drug Reactions ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
First Case ◽  
Alternative Drugs

Adverse drug reactions are among the most frequent side effects of synthetic and complementary alternative drugs and represent the premier causes of license revocations and acute liver failure. Drug-induced liver injury can resemble literally any other genuine liver disease and usually responds well to drug dechallenge. However, in some cases autoimmune-like hepatitis can evolve, requiring short- and sometimes long-term immunosuppression. Here, we present the hitherto first case of autoimmune-like hepatitis following treatment with zoledronic acid.

Successful evacuation of a pontine hematoma secondary to rupture of a pathologically diagnosed “cryptic” vascular malformation

1973 ◽  
Vol 39 (1) ◽  
pp. 104-108 ◽  
Author(s):  
Ben B. Scott ◽  
Joachim F. Seeger ◽  
Richard C. Schneider
Keyword(s):  
Arteriovenous Malformation ◽  
Brain Stem ◽  
Posterior Fossa ◽  
Vascular Malformation ◽  
Nerve Palsy ◽  
Neurological Deficits ◽  
Content Type ◽  
Brain Stem Lesion ◽  
Seventh Nerve ◽  
Fine Print

✓ A posterior fossa exploration was performed on a child thought initially to have an inoperable brain stem lesion. A pontine hematoma was discovered and evacuated. The pathological specimen was designated as a “cryptic” arteriovenous malformation. All preoperative neurological deficits disappeared except for a minimal left seventh nerve palsy.

Tinnitus related to eyelid blinking

1992 ◽  
Vol 106 (1) ◽  
pp. 44-45 ◽  
Author(s):  
V. Rajah
Keyword(s):  
Nerve Palsy ◽  
Palatal Myoclonus ◽  
First Case

AbstractTinnitus due to muscular causes is rare. The commonest pathological muscular cause of tinnitus is palatal myoclonus.A case of bilateral tinnitus, related to eyelid blinking, is presented. This is the first case reported in the literature. Previous reported cases of tinnitus related to eyelid blinking have all been unilateral and associated with recovery from a VII nerve palsy. The treatment of the condition is discussed.

Temporalis transfer for lagophthalmos due to seventh nerve palsy

1966 ◽  
Vol 37 (6) ◽  
pp. 578
Author(s):  
F. W. Masters ◽  
D. W. Robinson ◽  
J. N. Simons
Keyword(s):  
Nerve Palsy ◽  
Seventh Nerve

scholarly journals Isolated Hypoglossal Nerve Palsy Due to Endovascular Treatment of a Dural Arteriovenous Fistula with Onyx-18

2010 ◽  
Vol 16 (3) ◽  
pp. 286-289 ◽  
Author(s):  
W. Pei ◽  
S. Huai-Zhang ◽  
X. Shan-Cai ◽  
G. Cheng ◽  
Z. Di
Keyword(s):  
Endovascular Treatment ◽  
Arteriovenous Fistula ◽  
Nerve Palsy ◽  
Dural Arteriovenous Fistula ◽  
Hypoglossal Nerve ◽  
Transvenous Embolization ◽  
Prednisolone Therapy ◽  
Hypoglossal Nerve Palsy ◽  
Hypoglossal Canal ◽  
First Case

We describe a patient with dural arteriovenous fistula (DAVF) treated with Onyx-18 who developed isolated hypoglossal nerve palsy. This is the first case of isolated hypoglossal nerve palsy caused by Onyx-18 embolization. This complication suggests that over embolization with Onyx-18 in the treatment of hypoglossal canal DAVFs should be avoided, and transvenous embolization may be safer. Furthermore, prednisolone therapy should be carried out in the prophase of nerve palsy.

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