Remission of Angiographically Confirmed Minocycline-induced Renal Polyarteritis Nodosa: A Case Report and Literature Review.

A 23-year-old man presented with severe hypertension. Based on his history of minocycline treatment for over three years and clinical symptoms, such as myalgias and renovascular hypertension with multiple intrarenal aneurysms, he was diagnosed with minocycline-induced renal polyarteritis nodosa (PAN). After minocycline treatment cessation and management of the hypertension, his blood pressure, renin-aldosterone levels, and urinary protein levels gradually improved. Seven and a half years later, repeated angiography found that the aneurysms had resolved. This is the first report in English describing a case of minocycline-induced renal PAN that was reversed functionally and morphologically without steroids or immunosuppressive drugs.

Case Report of Empagliflozin-Induced Cutaneous Polyarteritis Nodosa.

Polyarteritis nodosa (PAN) is a rare vasculitis affecting medium-sized vessels. Cutaneous PAN is a clinical variant, and we report the first case of empagliflozin-induced cutaneous PAN in a 69-year-old man. After starting empagliflozin, the patient presented with tender subcutaneous nodules on his legs, which showed a medium-sized vessel vasculitis on histopathology. Upon cessation of this medication, he had full resolution of these nodules. This case illustrates that empagliflozin can induce cutaneous PAN, and further attention to this medication's association with cutaneous PAN is warranted.

Minocycline-induced polyarteritis nodosa-like vasculitis presenting as brainstem stroke.

Minocycline use has been associated with the development of autoimmune disorders, including drug-induced vasculitis. Previously published reports suggest that clinical manifestations are limited to cutaneous, constitutional, or musculoskeletal symptoms. To our knowledge there has been only one reported patient with ischemic stroke in the setting of minocycline-induced vasculitis. We describe a 26-year-old woman, with no vascular risk factors, who had an ischemic pontine stroke in the setting of biopsy-proven minocycline-induced polyarteritis nodosa-like vasculitis. Discontinuation of minocycline resulted in resolution of the vasculitis, and she has not had any recurrent ischemic events. This report shows that ischemic strokes may occur as a result of minocycline-induced vasculitis. While this is likely a rare association, recognition is important given the widespread use of minocycline and the potential for devastating consequences in a young population. Consequently, drug-induced vasculitis should be considered in patients with an ischemic stroke taking minocycline.

Minocycline-induced renal polyarteritis nodosa.

Minocycline is a bacteriostatic, long-acting, lipid-soluble tetracycline that is generally well tolerated, but has been associated with polyarteritis nodosa (PAN). This is a case report of a 21-year-old woman presented to her primary care physician with several months of fatigue, mylagias, weight loss and intermittent severe bi-temporal headaches without changes in vision. Her medications included an Ortho-Tri-Cyclen Lo and Minocycline, which she started 2 years prior for acne. On presentation, she was tachycardic and severely hypertensive. Initial laboratory evaluation showed hyponatraemia and hypokalaemia as well as elevation of inflammatory markers. Autoimmune work-up was positive for perinuclear antineutrophil cytoplasmic antibodies. Renal arteriogram was characteristic of PAN and along with her other symptoms, she fulfilled the necessary criteria of American College of Rheumatology for diagnosis of PAN. Minocycline as a possible causative agent was discontinued since it was reported to cause cutaneous PAN in the literature. Cyclophosphamide and prednisone were initiated for treatment of her vasulculitis. Her symptoms and hypertension improved over the next several months. This is the first report of the minocycline-induced renal PAN.

Polyarteritis nodosa-like vasculitis in association with minocycline use: a single-center case series.

OBJECTIVE: To describe the clinical features, treatment, and outcomes of polyarteritis nodosa (PAN)-like vasculitis in association with minocycline therapy. METHODS: We identified all subjects ≥18 years old with PAN-like vasculitis in the context of minocycline use seen at our institution between January 1995 and October 2010. Cases of hepatitis B-associated PAN were excluded. PAN was defined based on angiographic findings or tissue biopsy. Minocycline use was defined as medication use at the time of onset of first symptom. RESULTS: We identified 9 patients (5 females; 56%) with a median age of 30 (range 18 to 55) years. Four patients (44%) had isolated cutaneous disease, while 5 cases (56%) had systemic involvement including renal artery microaneurysms (2 patients), cholecystitis (1 patient), mononeuritis multiplex (2 patients), and mesenteric vasculitis (1 patient). Median duration of minocycline use was 2 (range 1 to 4) years. Three patients had a positive antinuclear antibody with negative extractable nuclear antigen antibodies. All patients had positive antineutrophil cytoplasmic antibody in a perinuclear pattern but specificity to myeloperoxidase was observed in 2 patients (22%). Diagnosis was confirmed by histopathology in 6 patients (67%) and angiography in 3 patients (33%). Minocycline was discontinued in all cases. Further immunosuppressive therapy was added in 6 cases (67%). CONCLUSIONS: Cutaneous, as well as systemic, PAN-like vasculitis may occur in association with minocycline use. Clinicians should consider the possibility of drug-induced vasculitis, especially in cases of medium-vessel vasculitis with atypical antineutrophil cytoplasmic antibody serologies or in patients with negative hepatitis B testing.

[Necrotic leg ulcers induced by vitamin K antagonists: five cases]. / Ulcères de jambe nécrotiques induits par les anti-vitamines K : à propos de cinq cas.

BACKGROUND: Vitamin K antagonists (VKAs) are widely used in thromboembolic diseases. We report five cases of necrotic leg ulcers having a particularly severe course and in which withdrawal of VKA treatment alone enabled healing. CASE REPORTS: Five patients presented with necrotic leg ulcers clinically evocative of necrotic angiodermatitis or vasculitis. Histological features were variable, including inconstantly inflammatory lesions (leukocytoclastic vasculitis) and microthrombosis. None of the patients had laboratory signs of autoimmune disease. Healing occurred in all patients only after withdrawal of VKA therapy (fluindione or acenocoumarol). Associated vascular diseases included superficial venous, distal arterial insufficiency and postphlebitic disease. In three cases, thrombotic factors were observed: hyperhomocysteinaemia or heterozygous Factor V Leiden mutation. DISCUSSION: Although the causative role of VKAs is based solely on chronological criteria, this potential side effect deserves publication because of its practical therapeutic consequences. The physiopathological mechanisms accounting for the role of VKAs, including immunoallergic phenomena and, above all, microcirculatory thrombotic processes, are hypothetical and not universally accepted.

Minocycline-induced cutaneous polyarteritis nodosa.

Minocycline is a tetracycline derivative with multiple clinical uses including the treatment of various infections, acne vulgaris, and rosacea. Numerous adverse events have been reported ranging from minor complaints such as nausea, to serious life-threatening toxicities such as acute renal failure, hepatotoxicity, and systemic lupus erythematosus. We report the case of an 18-year-old female patient who developed minocycline-induced cutaneous polyarteritis nodosa after taking minocycline for acne vulgaris. The vasculitis resolved after discontinuation of the minocycline without need for corticosteroids. This case is the eighth biopsy-confirmed case of minocycline-induced polyarteritis nodosa. Although minocycline is an effective medication with a wide variety of clinical uses, clinicians must be aware of its potential side effects including autoimmune-related disorders such as polyarteritis nodosa or systemic lupus erythematosus.

Minocycline-induced vasculitis fulfilling the criteria of polyarteritis nodosa.

A 47-year-old man who had been taking minocycline for palmoplantar pustulosis developed fever, myalgias, polyneuropathy, and testicular pain, with elevated C-reactive protein (CRP). Neither myeloperoxidase- nor proteinase-3-antineutrophil cytoplasmic antibody was positive. These manifestations met the American College of Rheumatology 1990 criteria for the classification of polyarteritis nodosa. Stopping minocycline led to amelioration of symptoms and normalization of CRP level. To our knowledge, this is the second case of minocycline-induced vasculitis satisfying the criteria. Differential diagnosis for drug-induced disease is invaluable even for patients with classical polyarteritis nodosa.

Antineutrophil cytoplasmic antibody (ANCA)-associated autoimmune diseases induced by antithyroid drugs: comparison with idiopathic ANCA vasculitides.

Clinical and serological profiles of idiopathic and drug-induced autoimmune diseases can be very similar. We compared data from idiopathic and antithyroid drug (ATD)-induced antineutrophil cytoplasmic antibody (ANCA)-positive patients. From 1993 to 2003, 2474 patients were tested for ANCA in the Laboratory for Allergy and Clinical Immunology in Belgrade. Out of 2474 patients, 72 (2.9%) were anti-proteinase 3 (PR3)- or anti-myeloperoxidase (MPO)-positive and their clinical and serological data were analyzed. The first group consisted of ANCA-associated idiopathic systemic vasculitis (ISV) diagnosed in 56/72 patients: 29 Wegener's granulomatosis (WG), 23 microscopic polyangiitis (MPA) and four Churg-Strauss syndrome. The second group consisted of 16/72 patients who became ANCA-positive during ATD therapy (12 receiving propylthiouracil and four receiving methimazole). We determined ANCA and antinuclear (ANA) antibodies by indirect immunofluorescence; PR3-ANCA, MPO-ANCA, anticardiolipin (aCL) and antihistone antibodies (AHA) by ELISA; and cryoglobulins by precipitation. Complement components C3 and C4, alpha-1 antitrypsin (alpha1 AT) and C reactive protein (CR-P) were measured by nephelometry. Renal lesions were present in 3/16 (18.8%) ATD-treated patients and in 42/56 (75%) ISV patients (p <0.001). Skin lesions occurred in 10/16 (62.5%) ATD-treated patients and 14/56 (25%) ISV patients (p <0.01). ATD-treated patients more frequently had MPO-ANCA, ANA, AHA, aCL, cryoglobulins and low C4 (p <0.01). ISV patients more frequently had low alpha1 AT (p = 0.059) and high CR-P (p <0.001). Of 16 ATD-treated patients, four had drug-induced ANCA vasculitis (three MPA and one WG), while 12 had lupus-like disease (LLD). Of 56 ISV patients, 13 died and eight developed terminal renal failure (TRF). There was no lethality in the ATD-treated group, but 1/16 with methimazole-induced MPA developed pulmonary-renal syndrome with progression to TRF. ANCA-positive ISV had a more severe course in comparison with ATD-induced ANCA-positive diseases. Clinically and serologically ANCA-positive ATD-treated patients can be divided into two groups: the first consisting of patients with drug-induced WG or MPA which resemble ISV and the second consisting of patients with LLD. Different serological profiles could help in the differential diagnosis and adequate therapeutic approach to ANCA-positive ATD-treated patients with symptoms of systemic disease.