{'fraction_non_alphanumeric': 0.028101164191087918, 'fraction_numerical': 0.0004014452027298274, 'mean_word_length': 5.523560209424084, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Chronic myeloid leukemia presenting as multiple cranial nerve palsy

to progress after more than a decade. Another unusual point is the late-onset presentation for the familial disease. Early-onset disease is a prominent feature of familial forms of both SLE and DLE, as expected. Late-onset familial cases are rarely reported. Even after genome-wide association studies, it is estimated that genetic variation identified so far explains just approximately 8% of genetic SLE risk. So the genetic behavior of SLE is largely unknown. Patients with suspected SLE are classified into SLE with the aid of Systemic Lupus International Collaborating Clinics criteria. Besides research-related concerns, the set of these classification criteria is, indeed, an important clinical tool, especially for the non-rheumatologist physician. However, controversies exist about the applicability of these criteria in older adults, as advanced age, itself, is an atypical condition with infrequent presenting clinical scenarios in this age group. Although non-specific symptoms, such as weight loss, arthralgias, myalgias, weakness, pyrexia, cognitive and affective dysfunction, presentation with interstitial lung disease, sicca and cytopenias, and neurocognitive impairment with peripheral neuropathy, are much more common than in early-/adult-onset disease, late-onset lupus patients have less frequent seizures, psychosis, renal impairment, cutaneous findings and arthritis. As classification criteria are based on more frequent and more specific clinical and laboratory findings for inclusion–exclusion purposes, they do not include more probable presenting signs of elderly-onset disease. Instead of a criteria-based approach, a combination of clinical findings, although atypical, plus some disease-specific clues from laboratory, imaging or biopsy with a holistic approach might direct to a diagnosis in older adults. However, it is important not to forget that the prevalences of idiopathic pulmonary fibrosis, sicca symptoms and non-specific ANA positivity increase by age. Probably because of immunosenescence, older adults are more prone to immunosuppresive sideeffects, such as infections and malignancies. This issue should be of major concern while treating older adults with autoimmune diseases. In conclusion, familial DLE or SLE might present in older adults. Cases with DLE can progress to SLE even after a decade. Presenting symptoms and signs might be atypical in elderly-onset SLE cases.