Nitrofurantoin and Minocycline–Associated Vasculitic Neuropathy: Case Reports and Literature Review : Journal of Clinical Neuromuscular Disease

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Nitrofurantoin and Minocycline–Associated Vasculitic Neuropathy: Case Reports and Literature Review

Aladawi, Mohammad MD*; Shelly, Shahar MD; Dyck, P. James B. MD; Koster, Matthew MD; Engelstad, JaNean§; Piccione, Ezequiel A. MD*; Naddaf, Elie MD

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Journal of Clinical Neuromuscular Disease 24(2):p 85-94, December 2022. | DOI: 10.1097/CND.0000000000000404
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Vasculitic neuropathies are a group of inflammatory neuropathies, characterized by inflammation of the vasa nervorum. They are classified as systemic versus nonsystemic vasculitis, the latter when they exclusively affect the nerve.1

Vasculitic neuropathy is routinely considered in the differential diagnosis of acute to subacute painful sensorimotor peripheral neuropathy. It typically presents with overlapping involvement of multiple individual nerves, with distal nerves preferentially involved compared with proximal ones.2 Most common patterns of involvement include a mononeuropathy, multiple mononeuropathies, or asymmetric polyradiculoneuropathy.3 However, vasculitic neuropathy may present as a symmetric length-dependent peripheral neuropathy or polyradiculoneuropathy and may also be painless.4

Drug-induced vasculitic neuropathy is considered a secondary cause of vasculitis. Beside antibiotics, there have been various classes of medications reported in association with vasculitis. Nevertheless, association does not necessarily indicate causation.

Among drug-associated vasculitic neuropathy, minocycline has been the most frequently reported offending drug. In this article, we report a novel case of nitrofurantoin-associated and an illustrative case of minocycline-associated vasculitic neuropathy with a literature review detailing the pathological and laboratory findings.


We present 2 cases of drug-associated vasculitic neuropathy. Case 1 was seen at the Mayo Clinic, and case 2 was seen at the University of Nebraska Medical Center. The nerve biopsies of both were processed at the Mayo Clinic peripheral nerve laboratory using routine laboratory histological techniques.5 We searched PubMed, Google Scholar, and EMBACE to identify all cases of vasculitic neuropathy associated with nitrofurantoin and minocycline use. We summarize all identified cases in a table comparing the patient's demographics, the indication of antibiotics uses duration of antibiotics treatment, clinical presentation, treatment, and neuropathy outcome.


Case 1

A 60-year-old woman was referred for painful progressive asymmetric muscle weakness. Two months before presentation, she received nitrofurantoin 100 mg BID for a urinary tract infection (UTI). Three days after initiation, she presented to a local emergency department for severe myalgias and arthralgias and was found to have elevated liver enzymes: alkaline phosphatase 353 U/L (normal 35–104), ALT 174 U/L (normal range 7–45), AST 71 U/L (normal range 8–43), normal bilirubin, and CRP 7.3 mg/dL (normal ≤0.5). Nitrofurantoin was discontinued. However, myalgia and arthralgia persisted, and 2 weeks later, bilateral hand weakness, numbness, tingling, and upper extremity lancinating shooting pain developed. Shortly after, bilateral lower limb weakness with shooting pain, tingling, and numbness from the knees down were noted. Review of systems was remarkable for dysphagia, orthopnea, and 11-pound weight loss; however, the patient denied any skin rash, hemoptysis, or hematuria.

Prednisone 60 mg/day was started resulting in reduction of myalgias, lancinating pain, and dysphagia, but no improvement in limb weakness. Tapering of prednisone to 30 mg resulted in return of severe neuropathic pain and dysphagia, prompting referral to our institution 2 months after the symptom onset.

At presentation to our institution, neurological examination was remarkable for complete paralysis of the left first and second digit flexion and right second finger flexion, 0/5 on the Medical Research Council (MRC) scale; moderate weakness (MRC 4-/5) in left wrist and fingers extension, bilateral fingers flexion (right first and third–fourth and left third–fourth), and bilateral thumb and fifth digit abduction with sparing of the first dorsal interossei; and mild weakness of left elbow flexion and extension. In the lower limbs, weakness was confined to the knee extension bilaterally (MRC 4-/5). Reflexes were absent at the knees and preserved elsewhere. Sensory examination showed absent pinprick sensation in the dorsum of the left hand (radial nerve distribution) and diminished pinprick sensation in the left more than right femoral nerve distribution and left more than right palmar aspect of hands and fingers. Vibration and joint position sensation were normal in fingers and toes. Gait was mildly wide based and cautious.

Nerve conduction studies (NCSs) were remarkable for absent left radial sensory nerve action potential while preserved on the right side. Needle electromyography showed dense fibrillation potentials and mildly long duration high amplitude, complex motor unit potentials in a patchy pattern involving bilateral femoral, median, ulnar and radial-innervated muscles—findings indicative of a subacute, sensory and motor, axonal, multifocal neuropathic process. Repeat liver enzymes and CRP had normalized. Additional evaluations included normal electrolytes, complete blood count, erythrocyte sedimentation rate, C-reactive protein (CRP), angiotensin-converting enzyme, serum monoclonal protein screen, fasting glucose, and hemoglobin A1c. Antinuclear antibodies (ANA), extractable nuclear antigens, rheumatoid factor, cryoglobulins, and antineutrophil cytoplasmic antibodies (ANCAs) were normal. A superficial radial nerve biopsy showed large epineural inflammatory cell collections surrounding and invading epineural microvessel walls, suggestive of microvasculitis (Fig. 1). Overnight oximetry was in keeping with neuromuscular respiratory insufficiency.

Left superficial radial nerve biopsy from a patient with nitrofurantoin-associated vasculitic neuropathy: (A) Teased nerve fibers all in the early stages of axonal degeneration suggesting a severe insult occurring at one time point; (B) longitudinal paraffin section stained with LFB/PAS showing degenerating nerve fiber profiles at a similar stage to what is seen in the teased nerve fibers; (C) longitudinal paraffin section reacted to CD20 (B-cell marker) showing an epineural perivascular inflammatory collection surrounding and involving the wall of a microvessel; and (D) serial longitudinal paraffin sections stained with H&E (E) and reacted to CD45 (F) and CD68 (macrophage marker) showing a large collection of perivascular epineural inflammatory cells surrounding and involving a microvessel. There is no clear evidence of vessel wall destruction or necrosis. These findings are suggestive of fulminant axonal injury due to microvasculitis of nerve.

Taken altogether, the symptoms, clinical findings, and nerve biopsy results are mostly in keeping with a nonsystemic vasculitic neuropathy. The timing of abrupt and progressive development after exposure without identified systemic etiology resulted in the diagnosis of nitrofurantoin-induced nonsystemic vasculitic neuropathy. Owing to ongoing symptoms despite high-dose oral glucocorticoids, oral cyclophosphamide (target 2 mg/kg/day) was added. On follow-up, 3 months later, her myalgias and arthralgias have resolved and the progression of her neuropathic symptoms was halted. On examination, there was improvement in her lower limb strength, with otherwise stable examination findings. She was switched to azathioprine (target dose of 100 mg daily) while continuing to taper down prednisone.

Case 2

A 23-year-old woman was referred for subacute right foot drop of 2-week duration. Symptoms started suddenly with inability to dorsiflex the right foot and numbness and prickling paresthesia in the right foot and leg. She had a history of seronegative inflammatory arthritis diagnosed 8 months before and acne vulgaris that had been treated with oral minocycline 50 mg twice daily for 1 year. Review of symptoms was otherwise unremarkable with no history of asthma, nasal polyposis, skin rash, hemoptysis, or hematuria. Neurologic examination demonstrated severe weakness in right ankle dorsiflexion, foot eversion, and toe extension (MRC 0/5) and mild weakness (4/5) in right ankle plantar flexion, foot inversion, and toe flexion. There was reduced pinprick and light touch sensation in the right common peroneal nerve distribution. Increased joint stiffness and swelling in the distal interphalangeal joints bilaterally was noted.

On NCS/EMG, right peroneal compound muscle action potential was absent, recording from extensor digitorum brevis (EDB), and had a low-amplitude recording from tibialis anterior (TA), without focal slowing or conduction block, and the right superficial peroneal sensory nerve action potential was absent. Needle examination showed fibrillation potentials and no activated motor unit potentials in right peroneal-innervated muscles. These findings indicate as a right subacute poorly localizable common peroneal mononeuropathy.

Three weeks later, the patient woke up with new left ankle dorsiflexion weakness and left foot numbness and paresthesia. In addition to the examination findings from the previous assessment, neurologic examination showed mild weakness (4/5) in left ankle dorsiflexion, foot eversion, and toe extension. There was reduced pinprick and light touch sensation in the left superficial peroneal and left median sensory distribution. Repeat NCS/EMG showed low amplitude in left peroneal compound muscle action potential recording from EDB and TA. Needle examination revealed fibrillation potentials in left extensor hallucis longus and EDB. In addition, there was reduced recruitment of normal motor unit potentials in peroneal-innervated muscles.

Laboratory studies were remarkable for positive ANA (1:1280, normal < 1:160), with elevated chromatin autoantibodies (8.0 IA, normal < 1.0 AI) but normal double-stranded DNA autoantibodies (dsDNA), and elevated perinuclear ANCA (1:10240, normal <1:20) and myeloperoxidase (MPO) (54 AU/mL, normal < 19) antibody titers, but normal serine protease 3 (PR3) titer. Furthermore, antihistone antibodies were elevated (7.8 U, normal < 0.9). Laboratory workup was otherwise unremarkable including complete blood count, erythrocyte sedimentation rate, CRP, complete metabolic panel, hemoglobin A1c, serum monoclonal protein screen, rheumatoid factor, citrullinated protein antibody, and complement 3 and 4.

Based on the patient's history of minocycline use before the development of her rheumatologic and neurologic symptoms, she was suspected of having minocycline-induced inflammatory arthritis and vasculitic neuropathy. A sural nerve biopsy was obtained and showed large perivascular inflammatory collections invading the wall of a large epineural large arteriole with occluded lumen, diagnostic of vasculitis (Fig. 2). The patient was hence diagnosed with ANCA-associated vasculitis.6,7 Minocycline was discontinued, and the patient was started on intravenous high-dose methylprednisolone for 5 days followed by weekly infusions for 3 months. Three months later, left foot drop resolved with partial recovery of the right foot weakness.

Right sural nerve biopsy from a patient with minocycline-associated vasculitic neuropathy showing diagnostic features of nerve large arteriole vasculitis. A, Paraffin transverse section stained with H&E shows large arteriole vasculitis with perivascular and vessel wall inflammation and total luminal occlusion (star); serial transverse paraffin sections of the occluded epineural arteriole immunoreacted to CD45 (B), smooth muscle actin (SMACTIN) (C), CD3 (T cells) (D), and CD20 (B cells) (E). These images show the inflammatory process consist of a mixture of B and T cells with vessel wall disruption and fragmentation and luminal occlusion; these findings are diagnostic of vasculitis.


We present 2 cases of drug-associated vasculitic neuropathy, one with nitrofurantoin, an entity not previously described, and another with minocycline. Both cases presented with subacute multiple mononeuropathies in a stepwise progression. A drug-induced process was suspected given the temporal correlation with antibiotic initiation and lack of an alternative etiology for a vasculitic neuropathy.

The peripheral neuropathy associated with exposure to nitrofurantoin is typically length-dependent sensory predominant and occurs in approximately 0.0007% of users.8 Distal motor involvement has been reported in severe cases.9 It is reported more in females than males, especially the elderly, likely because the drug is most often used to treat UTI which are more common in females. It is believed to be independent of dose and treatment duration, and impaired renal function is considered a risk factor.10 Nitrofurantoin-associated neurotoxicity is believed to be due to the drug limiting the synthesis of citrate and coenzyme A by interfering with pyruvate oxidation.11 Most of the reported cases were in patients who had medical conditions associated with peripheral neuropathy (renal failure, diabetes melilites, and anemia) and whose neuropathy was probably unmasked by nitrofurantoin.12,13 Our patient had multiple mononeuropathies (also known as mononeuritis multiplex), rather than a length-dependent neuropathy, which raised suspicion for an inflammatory or vasculitic process, not previously reported with nitrofurantoin. There is only a case series of 2 patients who presented with non–length-dependent neuropathic pain after therapy with nitrofurantoin and demonstrated substantial morphologic changes of aggregated swellings of terminal nerve fibers in their skin biopsy.14 However, nitrofurantoin-associated vasculitis, not involving nerves, has been rarely reported. These reports consisted mostly of a pulmonary reaction with occasional vasculitic changes on biopsy.15–17 In addition, there have been 2 reported cases of systemic vasculitis with skin and renal involvement and no peripheral nerve involvement, associated with positive p-ANCA and MPO antibodies.18,19 Both patients (a 67-year-old female and a 45-year-old male) were treated for a UTI and developed symptoms 3–4 days later, with resolution of the symptoms after treatment with oral prednisone and stopping nitrofurantoin. No biopsy was performed in the second case. Finally, nitrofurantoin has also been related to autoimmune hepatitis.20 It remains unclear what predisposed our patient to develop such a rare, not previously reported, complication.

Regarding minocycline-associated vasculitic neuropathy, there have been 11 reported cases, summarized in Table 1. In addition, there are 2 case reports of CNS vasculitis, one of which involved the spinal cord.21,22 Minocycline-associated vasculitic neuropathy has been more commonly reported in females between the second and fifth decade, likely reflecting the population that is prescribed this drug.23 The duration of minocycline use ranged from 2 weeks to 36 months.24–26 Positive ANA was seen in the most of the cases, and positive p-ANCA were seen in 3 of 9 cases tested.23 Nine patients were treated with corticosteroids alone or in combination with other agents. Limited description of outcomes is provided with only 3 patients with sufficient follow-up, all with recovery, but the remaining 8 cases had no outcome data available. Similar to our case, the typical neurologic presentation of these cases is subacute neuropathic pain, paresthesia, and weakness that involved one extremity, followed by the involvement of other extremities in a stepwise fashion.27,28 Remission of symptoms was typically achieved in 3–6 months after the initiation of immunomodulatory treatment. Rash, fever, myalgia, and arthralgia have been reported in minocycline-associated vasculitic neuropathy.29 Our patient had inflammatory arthritis, possibly indicative of a systemic process.

TABLE 1. - Literature Review of Minocycline-Associated Vasculitic Neuropathy
Author Age/Sex Minocycline Indication Treatment Duration Neurologic Symptoms Systemic Symptoms ANA p-ANCA Treatment Recovery
Baratta 24 17 F Acne 36 Months Left forearm pain, numbness, and weakness
Left leg weakness
None + Methylprednisolone NA
Baratta 24 33 M Acne 24 Months Left foot pain and weakness Fever
Testicular pain
+ Oral prednisone
3 Months
McMillan 41 ,* 17 M Acne 6 Months Bilateral foot dysesthesias Arthralgia + NA Methylprednisolone NA
Thaisetthawatkul 25 28 F Acne 2 weeks Left foot pain, numbness, and weakness None +(SSA) Methylprednisolone 3 Months
Kang 27 47 F Acne 3 Months Left arm and wrist pain
Right foot numbness
Left foot pain
Night sweats
Joint swelling
Oral prednisone NA
Kang 27 37 M Acne Several years Left forearm weakness and paresthesia
Right leg pain and foot drop
Hyperpigmentation of the feet
+(DS-DNA) Oral prednisone
Conlee 28 17 F Acne NA Left forearm pain, numbness, and weakness
Left leg numbness
None NA NA Rituximab NA
Kermani 23 18 F Acne 24 months Left hand numbness Fever
+(MPO) Oral prednisone
Kermani 23 40 F Acne NA Limb paresthesia
Foot drop
Vision loss
Fatigue arthralgias
+(ENA) +(MPO) Prednisone
Kermani 23 36 F Acne 18 months Limb paresthesia Arthralgia
Abdominal pain
NA + None NA
Ogawa 26 70F Prosthetic joint infection 6 months Limb paresthesia
Foot drop
Weight loss
+ Methylprednisolone 3 months
*Minocycline was held initially after the presence of arthralgia; 1 month later, neurologic symptoms started 1 month after minocycline was resumed by the patient due to severe acne.
+, positive; −, negative; DS-DNA, double-stranded DNA antibody; ENA, extractable nuclear antigen antibody; SSA, Sjogren syndrome autoantibodies.

Minocycline-induced autoimmune syndromes have been linked with ANA and p-ANCA.30 Most of the reported cases of minocycline-induced vasculitic neuropathy showed ANA and p-ANCA positivity. However, positive ANA is a nonspecific finding and does not necessarily indicate an underlying autoimmunity as shown in a study comparing patients with acne with and without exposure to minocycline.31 The development of a p-ANCA immunofluorescence pattern in patients exposed to minocycline has been associated with antibody development against minor antigens, such as elastase, cathepsin G, or bactericidal/permeability-increasing proteins, and rarely myeloperoxidase (MPO).21,23,32 Usually, immune stimulus from drug exposure results in positive p-ANCA with negative MPO; however, in minocycline, patients may have positive MPO without necessarily having systemic ANCA vasculitis. The exact mechanism by which minocycline exposure can induce autoimmunity is still unclear. However, there have been few theories purposed. Processing of minocycline by neutrophils or hepatocytes can result in reactive metabolites: minocycline degradation products bind degrading enzymes such as MPO forming haptens, which stimulates p-ANCA formation.33 Another suggested mechanism is that these reactive metabolites can induce autoimmune reaction directed against class II MHC antigens, as similarly reported in hydralazine-associated lupus, where HLA-DR4 carriers are susceptible to drug-induced lupus.34 Interestingly, there is a report of 2 patients with positive HLA-DRB1 * 09:01 allele, who presented with minocycline-induced p-ANCA vasculitis after treatment for palmoplantar pustulosis, which might emphasize the role of HLA allele in the predisposition to this condition.35

In patients with generalized symptoms, drug-induced vasculitis can be reversible after discontinuation of the36 offending agent. In addition to discontinuing the offending medication, immunomodulatory treatment is usually considered. Our patient with nitrofurantoin neuropathy required treatment similar to systemic vasculitis to stop progression, given the inability to taper down oral prednisone to less than 35 mg per day, whereas the second patient was successfully treated with corticosteroids monotherapy, emphasizing the need to tailor treatment on a case-by-case basis. Induction therapy consists of glucocorticoids.37 In glucocorticoid-refractory cases, adjuvant therapy may be required based on the severity of the symptoms present, for example, mild-to-moderate symptoms may require glucocorticoids only or in combination with additional disease-modifying agents (azathioprine, mycophenolate, and methotrexate), whereas severe cases may necessitate the use of cyclophosphamide or rituximab. No clinical trials, however, have formally addressed the use of immunosuppression in induction to remission for drug-induced vasculitis. Consequently, guidance on treatment is often generally extrapolated from the management of other small-vessel vasculitides, particularly ANCA-associated vasculitis (AAV). In severe AAV, rituximab is considered safer and more effective compared with cyclophosphamide.38 Although cyclophosphamide is typically reserved for severe cases with cardiac and central nervous system involvement39 in patients with AAV, discrete guidance on which agent should be used in drug-induced vasculitis is lacking and should be determined based on the severity of disease and the patient's comorbidities. Management with these cytotoxic therapies should be undertaken by providers with familiarity and experience. Once remission is achieved with induction therapy, maintenance therapy should be continued with oral azathioprine, methotrexate, mycophenolate mofetil, or a maintenance regimen of rituximab.40

Finally, a causative effect of the mentioned drugs may not be established based on case reports because it would require epidemiologic studies. This is particularly relevant in the nitrofurantoin case given its rarity. Our patient may have had unique risk factors that predisposed her to develop such complication. Nevertheless, raising awareness of such potential complication would help ensure accurate diagnosis, timely treatment, and stopping of the offending agent.


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vasculitic neuropathy; peripheral neuropathy; minocycline; nitrofurantoin; drug-induced vasculitis

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