TB or TB plus vasculitis: Occam versus Hickam – reply

Abstract

Dear Editor, We reported an unusual case of Mycobacterium tuberculosis infection complicated initially by fever, palpable purpura and mononeuropathy multiplex (MNM), and later by chylothorax [1]. The relationship between the purpura-associated ischaemic neuropathy, i.e. vasculitis, and the pulmonary tuberculosis was identified by the disease course, exclusion of other aetiologies, and the response to antituberculosis drugs. In our patient, the palpable purpura developed on the lower extremities concurrently with foot drop, where an electromyographic study showed the ischaemic change with active axonopathy. This was the clinical findings of cutaneous small vessel vasculitis with peripheral nerve system involvement. Cutaneous vasculitis has many causes. It may be a manifestation of systemic vasculitis, rheumatic diseases, hypersensitivity reactions, or malignancy. In addition, numerous viral and bacterial infections have been associated with the cutaneous vasculitis, including tuberculosis [2]. We have searched for an underlying cause for the development of palpable purpura and MNM in the patient. Pulmonary tuberculosis was proven to be the cause of fever of unknown origin, and other infectious, malignant, or immunological aetiologies were excluded after extensive studies. There were no clinical or laboratory evidences of eyes, kidney, musculoskeletal system or gastrointestinal tract involvement, which were more or less observed in systemic vasculitis or rheumatic diseases. The low-dose prednisolone therapy was prescribed for MNM at nearly 1 month postadmission. It is of low possibility to miss major clinical manifestations of a systemic vasculitis or rheumatic disease. Although palpable purpura, peripheral neuropathy and pulmonary involvement were common features of certain forms of vasculitis, such as Wegener's granulomatosis, Churg-Strauss syndrome, microscopic polyangiitis, there was little evidence to support the diagnosis in our patient. There were also a few diagnostic clues from the disease course and history to suspect Behçet's disease or Henoch-Schönlein purpura in the reported case, although these vasculitis were occasionally reported to cause chylothorax. Moreover, the results of serological tests including antineutrophil cytoplasmic antibody (ANCA) were all normal, except a mild elevated level of rheumatoid factor. Furthermore, there were no further relapses of palpable purpura, peripheral neuropathy, chylothorax or other vasculitis features after the completeness of antituberculosis therapy, even when the usage of prednisolone was discontinued. Relapses of the disease course, which were commonly seen in most systemic vasculitis, did not occur in this patient. This as a result also implied that the underlying cause of the cutaneous vasculitis was the M. tuberculosis infection. In conclusion, concurrence of MNM and chylothorax as the manifestations of pulmonary tuberculosis is a rare condition. The relationship between vasculitis and tuberculosis was indirect; however, it was reasonable to make the illation. This illation requires a longer follow up of the patient and more reported cases to support. No conflict of interest was declared.