The adverse effects of anti-tumour necrosis factor alpha (TNFα) drugs include an increase in the risk of infections, congestive heart failure, lupus-like syndrome, and the onset or worsening of various demyelinating diseases such as, multiple sclerosis, optic neuritis, and Guillain-Barrè syndrome (GBS), among others. We describe the case of a patient who developed GBS while she was on treatment with adalimumab. A 50-year-old woman with rheumatoid arthritis (RA) was admitted to the hospital due to progressive severe bilateral symmetric weakness of the legs, which quickly extended to the upper limbs and to the respiratory muscles. Adalimumab was started 13 months before. GBS was diagnosed and the anti-TNFα therapy discontinued. The serological test for Campylobacter jejuni was positive. She required invasive mechanical ventilatory support for 9 months. Twelve months later, the patient was using a wheelchair following a rehabilitation programme, and at 24 months she was walking a few steps with assistive devices. The relevant literature on the relationship between GBS and anti-TNFα is reviewed. Twenty three cases of GBS occurring during anti-TNFα therapy have been reported so far in the literature. In several cases, there was no clear temporal association, more than half had a possible previous infection, and in two cases the drug was reintroduced without recurrence of GBS. Our case, which is best explained by C. jejuni infection, as well as some of the cases described are probably not a direct result of anti-TNFα treatment, but an accidental coincidence. We also discuss the potential therapeutic options after anti-TNFα discontinuation.

A case of carbamazepine-induced systemic lupus erythematosus (CBZ-DILE) is presented, along with a literature review, with the aim to define the clinical and serological characteristics of this group, and compare them with systemic lupus erythematosus (SLE) triggered by other drugs (DILE). A 31-year-old woman presented with a 6-month history of hand arthritis and nasal ulcers. She had been diagnosed with epilepsy at 12 years of age and had continued treatment with carbamazepine (CBZ) for the past 18 years with excellent clinical control. Laboratory data revealed antinuclear antibodies (ANA) positive to a titer of 1/1280, and positive anti-nucleosome antibodies. The patients’ clinical symptoms disappeared after the CBZ discontinuation and did not reappear during the 1-year follow-up period. A search was made in the PubMed/Medline database of the (CBZ-DILE) published cases. A total of 26 cases of CBZ-DILE were found in the search. CBZ-DILE cases are characterized by variable latency periods that often last for years and are not related to the dose of CBZ. Most frequent clinical findings of CBZ-DILE in patients are arthralgia/arthritis, mucocutaneous manifestations, constitutional symptoms, and pleuritis or pericarditis. The renal involvement has not been reported in CBZ-DILE. Antihistone antibodies were observed less frequently, and anti-dsDNA antibodies were observed more frequently than in the “classic” DILE. The ANA remained positive in over 60% of cases during the follow-up after withdrawal. The CBZ-DILE has significant clinical and laboratory manifestations that distinguish it from classic DILE or idiopathic SLE.

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The case is reported of a 75-year-old woman diagnosed with polymyalgia rheumatica (PMR), treated with low doses of prednisone, and with clinical and analytical remission. Two years later, she presented with a clinical picture of giant cell arteritis (GCA), including headache, diplopia, jaw pain, feeling of swelling in both temples, and elevation of acute phase reactants. Symptoms spontaneously subsided two weeks later, while analytical parameters improved without any treatment. A high-resolution color Doppler ultrasound showed thickening of the intima-media complex with “halo” sign in the right temporal artery. A biopsy of the right temporal artery was performed, although it was not successful, as no artery could be found, and the procedure became more complicated with an eyebrow ptosis due to a lesion of the frontal branch of the facial nerve. GCA diagnosis was based on the clinical, laboratory and ultrasound findings. The patient was treated with prednisone and methotrexate, without clinical or analytical relapse. Comments are presented on the described cases of GCA with spontaneous remission and the most appropriate treatment in these cases are discussed. Other peculiarities of the case are also mentioned, such as the progression to GCA more than two years after the onset of PMR, and the complications from the temporal artery biopsy.