Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (679 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal mucosa; buccal mucosa; and conjunctival mucosa.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Where it fits in the MeSH classification
- Broader topics
- Tuberculosis, Cutaneous
Related concepts
- Nasal Mucosa
- Buccal Mucosa
Research landscape
PubMed indexes 1,721 records tagged with the MeSH heading “Lupus Vulgaris” (counts retrieved 2026-10-29). 39 of them (2.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,276 records.
Reviews account for 130 records (7.6%) and meta-analyses for 0. Randomized controlled trials number 1 (0.1%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,276 |
| 2000-2009 | 294 |
| 2010-2019 | 112 |
| 2020 onward | 39 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 130 | 7.6% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 1 | 0.1% |
Method: PubMed query "Lupus Vulgaris"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in infectious diseases
Infectious disease evidence combines microbiology, epidemiology and clinical trials. Laboratory studies identify pathogens and how they cause harm; surveillance and outbreak investigations describe who is affected and how infection spreads; trials establish whether treatments and vaccines work. Results depend on place and time, because pathogens evolve and resistance patterns and population immunity change. Check when and where the data were collected, how cases were defined and how up to date the evidence is.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Low-dose exposure to inorganic mercury accelerates disease and mortality in acquired murine lupus | 2003 | Research article Design not recorded in structured metadata | 54 | cc by PMID 12896845 · DOI · PMC1241605 |
| Abnormal costimulatory phenotype and function of dendritic cells before and after the onset of severe murine lupus | 2006 | Research article Design not recorded in structured metadata | 37 | cc by PMID 16507174 · DOI · PMC1526610 |
| Lupus vulgaris mimicking hemangioma diagnosed 42 years after onset: a case report | 2015 | Research article Design not recorded in structured metadata | 3 | cc by PMID 26376746 · DOI · PMC4573701 |
| Diagnostic challenges of longstanding nasal cutaneous tuberculosis in an endemic setting: a case report | 2025 | Research article Design not recorded in structured metadata | 0 | cc by PMID 41116832 · DOI · PMC12535603 |
Low-dose exposure to inorganic mercury accelerates disease and mortality in acquired murine lupus [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Inorganic mercury (iHg) is known to induce autoimmune disease in susceptible rodent strains.
- Closing excerpt
- These results are consistent with the hypothesis that low-level, nontoxic iHg preexposure may interact with other risk factors, genetic or acquired, to promote subsequent autoimmune disease development.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (199 words)
Inorganic mercury (iHg) is known to induce autoimmune disease in susceptible rodent strains. Additionally, in inbred strains of mice prone to autoimmune disease, iHg can accelerate and exacerbate disease manifestations. Despite these well-known links between iHg and autoimmunity in animal models, no association between iHg alone and autoimmune disease in humans has been documented. However, it is possible that low-level iHg exposure can interact with disease triggers to enhance disease expression or susceptibility. To address whether exposure to iHg can alter the course of subsequent acquired autoimmune disease, we used a murine model of acquired autoimmunity, lupus-like chronic graft-versus-host disease (GVHD), in which autoimmunity is induced using normal, nonautoimmune prone donor and F1 recipient mice resistant to Hg-induced autoimmunity. Our results indicate that a 2-week exposure to low-dose iHg (20 or 200 micro g/kg every other day) to donor and host mice ending 1 week before GVHD induction can significantly worsen parameters of disease severity, resulting in premature mortality. iHg pretreatment clearly worsened chronic lupus-like disease, rather than GVHD worsening iHg immunotoxicity. These results are consistent with the hypothesis that low-level, nontoxic iHg preexposure may interact with other risk factors, genetic or acquired, to promote subsequent autoimmune disease development.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 12896845 · DOI · PMC1241605
Abnormal costimulatory phenotype and function of dendritic cells before and after the onset of severe murine lupus [2]
Abstract reading summary — source excerpts
- Opening excerpt
- We analyzed the activation and function of dendritic cells (DCs) in the spleens of diseased, lupus-prone NZM2410 and NZB-W/F1 mice and age-matched BALB/c and C57BL/6 control mice.
- Closing excerpt
- The increase in CD40 may instead participate in disease pathogenesis, being present months before any sign of autoimmunity, and its downregulation should be explored as an alternative to treatment with anti-CD40 ligand in lupus.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (213 words)
We analyzed the activation and function of dendritic cells (DCs) in the spleens of diseased, lupus-prone NZM2410 and NZB-W/F1 mice and age-matched BALB/c and C57BL/6 control mice. Lupus DCs showed an altered ex vivo costimulatory profile, with a significant increase in the expression of CD40, decreased expression of CD80 and CD54, and normal expression of CD86. DCs from young lupus-prone NZM2410 mice, before the development of the disease, expressed normal levels of CD80 and CD86 but already overexpressed CD40. The increase in CD40-positive cells was specific for DCs and involved the subset of myeloid and CD8alpha+ DCs before disease onset, with a small involvement of plasmacytoid DCs in diseased mice. In vitro data from bone marrow-derived DCs and splenic myeloid DCs suggest that the overexpression of CD40 is not due to a primary alteration of CD40 regulation in DCs but rather to an extrinsic stimulus. Our analyses suggest that the defect of CD80 in NZM2410 and NZB-W/F1 mice, which closely resembles the costimulatory defect found in DCs from humans with systemic lupus erythematosus, is linked to the autoimmune disease. The increase in CD40 may instead participate in disease pathogenesis, being present months before any sign of autoimmunity, and its downregulation should be explored as an alternative to treatment with anti-CD40 ligand in lupus.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 16507174 · DOI · PMC1526610
Lupus vulgaris mimicking hemangioma diagnosed 42 years after onset: a case report [3]
Abstract reading summary — source excerpts
- Opening excerpt
- IntroductionLupus vulgaris is the most common form of cutaneous tuberculosis.
- Closing excerpt
- ConclusionsThe lesion improved after antituberculous therapy, confirming the diagnosis of lupus vulgaris.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (108 words)
IntroductionLupus vulgaris is the most common form of cutaneous tuberculosis. It may easily be overlooked if a proper differential diagnosis is omitted.Case presentationA 46-year-old Turkish woman presented with a 42-year history of erythamatous plaque on her left arm. Ziehl-Neelsen and periodic acid-Schiff stains did not show any acid-fast bacilli. Culture from a biopsy specimen was negative for Mycobacterium tuberculosis. The result of a polymerase chain reaction-based assay for Mycobacterium was negative. Histopathologic findings revealed a tuberculoid granuloma containing epithelioid cells, lymphocytes and Langerhans-type giant cells. A diagnosis of lupus vulgaris was made by clinical and histopathologic findings.ConclusionsThe lesion improved after antituberculous therapy, confirming the diagnosis of lupus vulgaris.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26376746 · DOI · PMC4573701
Diagnostic challenges of longstanding nasal cutaneous tuberculosis in an endemic setting: a case report [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Nasal cutaneous tuberculosis (TB) is a rare manifestation of extrapulmonary tuberculosis and presents a diagnostic challenge, particularly in its paucibacillary form.
- Closing excerpt
- We propose that, in diagnostically difficult cases, the investigating team consider extending the specimen culture time to the maximum before definitively excluding tuberculous disease.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (159 words)
Nasal cutaneous tuberculosis (TB) is a rare manifestation of extrapulmonary tuberculosis and presents a diagnostic challenge, particularly in its paucibacillary form. As demonstrated in this case, achieving laboratory-confirmed diagnosis in paucibacillary TB remains a significant challenge, often resulting in missed or delayed diagnoses and increased severity of disease on presentation. We report an atypical case involving a 19-year-old male with extensive nasal destruction progressing for fourteen years. In this case, lupus vulgaris was ultimately diagnosed after extending the tissue culture duration beyond 35 days, despite prior exclusion of TB as the cause. The patient completed antituberculosis therapy with resolution of the active disease, and he was referred for further management of his facial deformity. The delayed diagnosis led to significant tissue destruction, which could have been prevented with earlier confirmation and treatment of the infection. We propose that, in diagnostically difficult cases, the investigating team consider extending the specimen culture time to the maximum before definitively excluding tuberculous disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41116832 · DOI · PMC12535603
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article A pivotal role for the natural interferon alpha-producing cells (plasmacytoid dendritic cells) in the pathogenesis of lupus [5]
- Research article Idiosyncratic drug reactions: the reactive metabolite syndromes [6]
- Research article Heart involvement in systemic lupus erythematosus, anti-phospholipid syndrome and neonatal lupus [7]
- Research article The cellular and genetic basis of murine lupus [8]
- Research article Macromolecular substrates for the ICE-like proteases during apoptosis [9]
- Research article Drug-induced lupus [10]
References
- Via CS, Nguyen P, Niculescu F, Papadimitriou J, Hoover D, Silbergeld EK. Low-dose exposure to inorganic mercury accelerates disease and mortality in acquired murine lupus. . 2003. PMID 12896845 · DOI · PMC1241605
- Colonna L, Dinnall JA, Shivers DK, Frisoni L, Caricchio R, Gallucci S. Abnormal costimulatory phenotype and function of dendritic cells before and after the onset of severe murine lupus. . 2006. PMID 16507174 · DOI · PMC1526610
- Yaldız M, Erdem T, Dikicier BS, Dilek FH. Lupus vulgaris mimicking hemangioma diagnosed 42 years after onset: a case report. . 2015. PMID 26376746 · DOI · PMC4573701
- van der Linden A, Elliot E, Borstlap R. Diagnostic challenges of longstanding nasal cutaneous tuberculosis in an endemic setting: a case report. . 2025. PMID 41116832 · DOI · PMC12535603
- Rönnblom L, Alm GV. A pivotal role for the natural interferon alpha-producing cells (plasmacytoid dendritic cells) in the pathogenesis of lupus. J Exp Med. 2001. PMID 11748288 · DOI · PMC2193578
- Knowles SR, Uetrecht J, Shear NH. Idiosyncratic drug reactions: the reactive metabolite syndromes. Lancet. 2000. PMID 11075787 · DOI
- Tincani A, Rebaioli CB, Taglietti M, Shoenfeld Y. Heart involvement in systemic lupus erythematosus, anti-phospholipid syndrome and neonatal lupus. Rheumatology (Oxford). 2006. PMID 16980725 · DOI
- Steinberg AD, Huston DP, Taurog JD, Cowdery JS, Ravecheé ES. The cellular and genetic basis of murine lupus. Immunol Rev. 1981. PMID 7016728 · DOI
- Rosen A, Casciola-Rosen L. Macromolecular substrates for the ICE-like proteases during apoptosis. J Cell Biochem. 1997. PMID 9015754 · DOI
- Rubin RL. Drug-induced lupus. Toxicology. 2005. PMID 15767026 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.