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In this observational study performed during 45 months we evaluated patients with chronic and recalcitrant diabetic ulcers who were treated with homologous platelet gel. Methods platelet gels were obtained from homologous platelet concentrates that were aliquoted and freezed, being then activated with calcium gluconate and applied in the ulcer after cleaning and debridement. We evaluated patient's comorbidities, wound characteristics (size, tissue, inflammatory signs, pain), number and time of treatment as well as outcome (classified as complete epithelialization; partial improvement- 50% reduction in wound size or pain relief; no evolution). Results Fifty-two patients (42 males, 10 females), with a median age of 65 years (range 43–85) were proposed for platelet gel. The following associated comorbidities were observed: hypertension (n = 41), dyslipidemia (n = 29), polyneuropathy (n = 30), peripheral arteriopathy (n = 32), retinopathy (n = 21), nephropathy (n = 15), cardiac ischemic disease (n = 14), obesity (n = 9). Thirty-eight patients presented with 3 or more associated comorbidities. The more frequent ulcer locations were sole of the foot (n = 13) and heel (n = 10). The median number of applications was 16, during 8.5 weeks. Nineteen patients (44%) achieved complete healing, 3 patients (7%) had a partial response and 21 (49%) had no progression. We did not observe a statistically significant relationship between patient age and response nor between number of comorbidities and response. We observed a more favorable evolution in patients with good compliance and good glycemic control. Conclusion Platelet gel is an effective therapeutic alternative, provided compliance and effective metabolic control are ensured.

BackgroundRare pathogenic variants in either theITGA2BorITGB3genes have been linked to autosomal dominant macrothrombocytopenia associated with abnormal platelet production and function, deserving the designation of Glanzmann Thrombasthenia-Like Syndrome (GTLS) or ITGA2B/ITGB3-related thrombocytopenia.ObjectivesTo describe a series of patients with familial macrothrombocytopenia and decreased expression of αIIbβ3 integrin due to defects in theITGA2BorITGB3genes.MethodsWe reviewed the clinical and laboratory records of 10 Portuguese families with GTLS (33 patients and 11 unaffected relatives), including the functional and genetic defects.ResultsPatients had absent to moderate bleeding, macrothrombocytopenia, low αIIbβ3 expression, impaired platelet aggregation/ATP release to physiological agonists and low expression of activation-induced binding sites on αIIbβ3 (PAC-1) and receptor-induced binding sites on its ligand (bound fibrinogen), upon stimulation with TRAP-6 and ADP. Evidence for constitutive αIIbβ3 activation, occurred in 2 out of 9 patients from 8 families studied, but also in 2 out of 12 healthy controls. We identified 7 missense variants: 3 inITGA2B(5 families), and 4 inITGB3(5 families). Three variants (αIIb: p.Arg1026Trp and p.Arg1026Gln and β3: p.Asp749His) were previously reported. The remaining (αIIb: p.Gly1007Val and β3: p.Thr746Pro, p.His748Pro and p.Arg760Cys) are new, expanding the αIIbβ3 defects associated with GTLS. The integration of the clinical and laboratory data allowed the identification of two GTLS subgroups, with distinct disease severity.ConclusionsPreviously reportedITGA2BandITGB3variants related to thrombocytopenia were clustered in a confined region of the membrane-proximal cytoplasmic domains, the inner membrane clasp. For the first time, variants are reported at the outer membrane clasp, at the transmembrane domain of αIIb, and at the membrane distal cytoplasmic domains of β3. This is the largest single-center series of inherited macrothrombocytopenia associated with αIIbβ3 variants published to date.