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Acute attacks could occur during the convalescent phase of COVID-19 illness, more commonly in patients with a history of frequent attacks. However it is unclear whether the acute attacks during the convalescent phase are specifically triggered by COVID-19 or not.
Acute attacks could occur during the convalescent phase of COVID-19 illness, more commonly in patients with a history of frequent attacks.
an uncontrolled 13-patient series cannot distinguish COVID-associated attacks from usual disease activity
in our cohort, only 31% of HAE patients developed attacks during SARS-CoV-2 infection.
the four-of-thirteen count is consistent, although the attack window is labelled inconsistently
it is unclear whether the acute attacks during the convalescent phase are specifically triggered by COVID-19 or not.
the observational design directly warrants uncertainty about COVID-19-specific triggering
it adds to the evidence that patients with a good HAE disease control are at low risk of developing angioedema attacks.
nine non-attacking patients without a matched baseline cannot establish a reliable low-risk estimate
Derived from the full evaluation — not a separate score.
Strengths
The four-centre registry addresses a concrete question for people with HAE and reports both the attack proportion and its association with baseline disease activity.
↳ Methods and Results, pp. 948–949; Table 2
Tables 1–2 provide HAE subtype, prophylaxis, COVID-19 testing, comorbidity, attack location, treatment, baseline frequency, and follow-up information suitable for interpreting this small series.
↳ Tables 1–2; Results, pp. 948–949
The Abstract and final summary distinguish observed convalescent attacks from proof that COVID-19 specifically triggered them.
↳ Abstract; final summary paragraph, p. 949
Limitations
The analysis does not compare convalescent attacks with an equivalent pre-COVID period within the same patients, leaving usual high-frequency HAE activity incompletely separated from infection-associated attacks.
↳ Table 2; Results and final summary paragraph, p. 949
Table 1 labels attacks as during COVID-19, Table 2 refers to status after disease while also using during-infection rows, and the narrative specifies convalescence. This limits temporal interpretation of the central observation.
↳ Tables 1–2; Abstract and Results, pp. 948–949
The conclusion that well-controlled patients are at low risk rests on nine patients without attacks and does not provide a validated risk estimate.
↳ Table 2; final summary paragraph, p. 949
The prospective registry and detailed tables support a descriptive finding that four of 13 patients experienced attacks and that these patients had higher baseline attack frequency. The main causal statement is appropriately restrained, but the absence of a matched pre-COVID period prevents separation of infection-associated attacks from usual disease activity. Aggregate follow-up is reported, yet inconsistent descriptions of attacks as during COVID-19, after disease, or during convalescence reduce temporal precision. Direct comparison with Grumach et al. supports an incremental contribution, while the small uncontrolled sample keeps translation and transferability limited.
Nabu’s assessment, alongside the field’s view.
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Sound3.2
Confidence mediumThe registry adds a second small cohort and identifies higher pre-existing attack frequency among patients reporting convalescent attacks. The contribution remains incremental because the design cannot determine whether COVID-19 caused those attacks.
“it is unclear whether the acute attacks during the convalescent phase are specifically triggered by COVID-19 or not”
Patient characteristics, treatments, attack locations, aggregate timing, and follow-up are reported in Tables 1–2 and the Results. The absence of a matched pre-COVID observation window leaves usual disease activity and other triggers incompletely separated from COVID-associated attacks.
“median time between first symptoms and the end of follow-up: 90 days”
The report follows a concise rationale-to-results-to-conclusion sequence and explicitly preserves uncertainty about causation. Reporting is reduced by inconsistent timing labels and by a low-risk inference that is stronger than the 13-patient dataset supports.
“Nonetheless, it adds to the evidence that patients with a good HAE disease control are at low risk”
The paper connects ACE2 and bradykinin biology to HAE and quantitatively compares its attack proportion with a directly relevant prior cohort. Limitations are acknowledged, but the consequences of lacking a matched baseline period are not fully traced through the risk interpretation.
“These results are in line with those of Grumach et al.”
Caveats4 of 4 checks
The reported count of four affected patients is consistent, but the temporal classification of their attacks varies across the title, tables, Abstract, and Results. This ambiguity affects whether the observations are described as occurring during infection, after disease, or specifically during convalescence.
Ethics approval and oral consent are declared, conflicts are disclosed as absent, and the restricted data-on-request statement is internally coherent. No text-grounded research-conduct concern was identified.
Flags: 3 declared / 5 total
10 of 10 checkable references verified
10 references in manuscript the reference list may be incompletely parsed; counts are indicative
No retraction notice found in Retraction Watch.
Sources: Retraction Watch ✓
Where this paper’s evidence sits on the path from initial observation to real-world use.
The result is a small observational association rather than a validated prognostic estimate or tested intervention. Substantial controlled and larger-scale work would be required before it could direct management.
“This current study has, however, several limitations among them, the small sample size.”
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