Evidence map›Paper›PMID 31832276›Full record

ArticleAdvances in wound care2019

Lymphovenous Anastomosis Aids Wound Healing in Lymphedema: Relationship Between Lymphedema and Delayed Wound Healing from a View of Immune Mechanisms.

Shuhei Yoshida, Isao Koshima, Yuichi Hamada, Ayano Sasaki, Yumio Fujioka, Shogo Nagamatsu, Kazunori Yokota, Mitsunobu Harima, Shuji Yamashita

Open access · greenAbstract readNews
In one paragraph

Article in Advances in wound care, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Shuhei YoshidaThe International Center for Lymphedema, Hiroshima University Hospital, Hiroshima, Japan.
Isao KoshimaThe International Center for Lymphedema, Hiroshima University Hospital, Hiroshima, Japan.
Yuichi HamadaPlastic and Reconstructive Surgery, Japanese Red Cross Fukuoka Hospital, Fukuoka, Japan.
Ayano SasakiPlastic and Reconstructive Surgery, Hiroshima University, Hiroshima, Japan.
Yumio FujiokaPlastic and Reconstructive Surgery, Hiroshima University, Hiroshima, Japan.
Shogo NagamatsuPlastic and Reconstructive Surgery, Hiroshima University, Hiroshima, Japan.
Kazunori YokotaPlastic and Reconstructive Surgery, Hiroshima University, Hiroshima, Japan.
Mitsunobu HarimaPlastic and Reconstructive Surgery, Tokyo University, Tokyo, Japan.
Shuji YamashitaPlastic and Reconstructive Surgery, Tokyo University, Tokyo, Japan.
Hiroshima University · JPHiroshima University Hospital · JPTokyo Medical University · JPJapanese Red Cross Fukuoka Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Delayed wound healing in lymphedema is assumed to be caused by two reasons, pathophysiological and immunological effects of lymphedema. The aim of this review is to establish how impaired lymphatics alter wound healing pathophysiologically and immunologically, and to propose treatment modalities that can promote wound healing in lymphedema. Lymphaticovenular anastomoses (lymphovenous anastomoses [LVAs]) were performed on patients who had recurrent cellulitis several times with lymphorrhea and developed severe ulcers that were refractory to skin grafts, flaps, and conservative therapy. The lymphorrhea and the ulcer had healed by 4 weeks. Moreover, the lymphedema improved without compression therapy. Lymphedema is characterized pathophysiologically by localized peripheral edema that compresses the microvasculature and lymphatic vasculature and impairs tissue remodeling. Another suspected mechanism is an imbalance in the differentiation of participating immune cells. Profound suppression of T helper (Th)1 cells is likely to increase the risk of infection, and excessive differentiation of Th2 cells, including M2 macrophage polarization, may promote fibrosis, which disrupts the carefully orchestrated wound healing process. Although negative-pressure wound therapy is useful for the treatment of delayed wound healing in lymphedema, LVAs may be necessary to treat the fundamental problem of lymphedema. LVAs are considered to create a bypass to the lymph nodes through which dendritic cells (DCs) can transmit antigen information to T cells. LVAs are considered to neutralize chronic inflammation by allowing more DCs to return into the circulation, thereby improving wound healing.

Indexed as

chronic inflammationimmunodeficiencyimmunologylymphedemalymphovenous anastomosiswound healing

Identifiers

PMID31832276
PMCPMC6906758
OpenAlexW2910633885

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.