#1
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Àãðàíóëîöèòîç? Ëåéêîïåíèÿ íåÿñíîãî ãåíåçà
Äîáðûé äåíü,ïîìîãèòå ðàçîáðàòüñÿ.Ìóæ÷èíà 50 ëåò ,âåñ 88 êã.Èç àíàìíåçà ïñîðèàòè÷åñêèé àðòðèò â ïîñëåäíåé ñòàäèè(áîëåí áîëåå 20 ëåò).Ïðèíèìàåò òàáëåòêó ìåòèïðåäà. òå÷åíèè ãîäà ïàäàþò ëåéêîöèòû è íåéòðîôèëû âñ¸ íà÷àëîñü ñ íåèçâåñòíîãî èíôåêöèîííîãî çàáîëåâàíèÿ,ïðîâåäåíû âñå âîçìîæíûå îáñëåäîâàíèÿ ïöð ê covid,ãåðïåñ.ÖÌ G (1000 òèòðîâ ïðè íîðìå äî 12).Ìðò ìàëîãî òàçà (íîðìà),ìðò áðþøíûõ îðãàíîâ(íîðìà).Óçè ïå÷åíè è ñåëåçåíêè íåçíà÷èòåëüíîå óâåëè÷åíèå ñåë¸çåíêè è ïå÷åíè.Ñèìïòîìû îòñóñòâóþò ,áåñïîêîèò åäèíîðàçîâàÿ òåìïåðàòóðà ïåèîäè÷íîñòüþ 1 ðàç â 3 ìåñÿöà(38 ãðàäóñîâ),íå ïîòååò,íå õóäååò,àïïåòèò íå èçìåí¸í.Ñäåëàíà ïóíêöèÿ êîñòíîãî ìîçãà è òðåïàíîáèîïñèÿ.Ìû æèâ¸ì â Êèðîâå âðà÷è ðàçâîäÿò ðóêàìè,îòïðàâëÿþò â äåðìàòîëîãèþ â Ìîñêâó ,ñ÷èòàþò ,÷òî ýòî èç-çà ïñîðèàòè÷åñêèõ áëÿøåê ïîäàâëÿþòñÿ ëåéêîöèòû.
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#2
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äà, íóæíà òåëå-êîíñóëüòàöèÿ ãåìàòîëîãîâ èç Ìîñêâû, íå èñêëþ÷àþ äåáþò îäíîé èç ôîðì ìîíîöèòàðíûõ ëåéêåìèé, ïîäðîáíåå ïîçæå
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Èñêðåííå, Âàäèì Âàëåðüåâè÷. |
#3
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Ó ìóæ÷èíû ñ âûñîêîé ñòåïåíüþ âåðîÿòíîñòè õðîíè÷åñêàÿ ìèåëîìîíîöèòàðíàÿ ëåéêåìèÿ íà ñòàäèè íîëü èëè îëèãî-ìîíîöèòàðíàÿ ôîðìà áîëåçíè, íèæå èíôà íà àíãëèéñêîì äëÿ î÷íûõ ãåìàòîëîãîâ ñïåöèàëèñòîâ, ó êîòîðûõ áóäåò êîíñ. ìóæ÷èíà äëÿ îïðåäåëåíèÿ äàëüí. òàêòèêè äèàãíîñòèêè/ëå÷åíèÿ
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Èñêðåííå, Âàäèì Âàëåðüåâè÷. |
#4
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Âñå ïîä÷åðêíóòîå ìíîé äëÿ àêöåíòà ÷òî åñòü ó íåãî:
Diagnostic criteria for CMML: Persistent monocyte increases in PB; ≥1×10/9/L and ≥10% of leukocytes. Blasts are <20% in PB and BM. Dysplasia in at least 1 myeloid lineage CMML-0 <2% blasts in PB and <5% blasts in BM; no Auer rods Some patients with cytopenia do not meet the diagnostic criteria of CMML but have relative monocytosis and dysplastic features of the bone marrow. They are younger and have a lower WBC count than those with classical CMML but share the characteristics of CMML, such as splenomegaly, anemia, thrombocytopenia, and a high frequency of TET2 and SRSF2 gene mutations Oligomonocytic CMML Over the past few years, more and more cases of cytopenic patients exhibiting relative monocytosis (≥10%) and moderately increased absolute blood monocytes not reaching the required threshold to diagnose classical CMML (1.0x109/L) have been described. These cases have recently been referred to as oligomonocytic CMML.30 According to the WHO classification most of these patients would be classified as having MDS (with monocytosis) or perhaps MPN/MDS-unclassifiable. However, most of these patients exhibit typical features of CMML, including a typical morphology of PB and BM cells, splenomegaly, and CMML-related molecular features (e.g. mutations in TET2 and SRSF2).30-32 Some of these patients have prominent BM monocytosis without diagnostic PB monocytosis at diagnosis.30,32 Whereas several of these cases remain stable without progression, the majority will develop ‘overt’ CMML or, eventually, secondary AML during follow-up. Therefore, oligomonocytic CMML may also be regarded as a potential pre-phase of classical CMML. Our faculty is of the opinion that the term oligomonocytic CMML should be used in clinical practice. Diagnostic pre-requisite criteria for oligomonocytic CMML are: (i) persistent (lasting at least 3 months) absolute peripheral monocytosis of 0.5-0.9×109/L and relative blood monocytosis (≥10% of blood leukocytes); (ii) exclusion of BCR-ABL1+ leukemia, classical MPN and all other myeloid neoplasms that can explain monocytosis; and (iii) a blast cell count of 0-19% in PB and/or BM smears and exclusion of all histopathological, morphological, phenotypic, molecular and cytogenetic signs that count as proof of AML. Diagnostic dysplasia in one or more of the three major BM lineages (≥10%) must also be documented. If dysplasia is lacking or ‘sub-diagnostic’ (<10%), the presence of cytogenetic or molecular lesions (mutations) typically found in CMML and/or the presence of CMML-related flow cytometry abnormalities, may also lead to the conclusion that the patient has oligomonocytic CMML provided that the other diagnostic criteria described above are fulfilled and all other myeloid neoplasms have been excluded... Patients with oligomonocytic CMML should be managed and followed clinically in the same way as patients with classical CMML.
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Èñêðåííå, Âàäèì Âàëåðüåâè÷. |
#5
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Ñïàñèáî îãðîìíîå çà îòâåò!Ïîäñêàæèòå ,ýòà áîëåçíü ïîääà¸òñÿ ëå÷åíèþ? Íàøè ãåìàòîëîãè ãîâîðèëè ïðî õð.ìîíîöèòàðíûé ëåéêîç ñêàçàëè íà ýòîì ýòàïå åãî íå ëå÷àò ,à íàáëþäàþò äàæå åñëè îí åñòü.Îíè îòïðàâèëè â Ìîñêâó â äåðàìòàîëîãèþ íà ëå÷åíèå,ò.ê ñ÷èòàþò,÷òî ýòî íå çàáîëåâàíèå êðîâè,à èç çà ïñîðèàòè÷åñêèõ áëÿøåê óìåíüøåíèå êîë-âà ëåéêîöèòîâ.Î÷åíü ñòðàííî ,÷òî îíî òàê ïðîÿâèëîñü åñëè ýòî õìë ,ò.ê. ìû 3 ðàçà â ãîä ñäàâàëè àíàëèçû è 20 ëåò âñå áûëî îòëè÷íî áåç ïàòîëîãèé,åäèñòâåííîå íåçíà÷èòåëüíîå óâåëè÷åíèå ìîíîöèòîâ â îòíîñèò.÷èñëàõ.
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#6
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#7
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äëÿ âàøåãî ìóæ÷èíû ñäåëàë èñêëþ÷åíèå è ïðîêîíñóëüòèðîâàë ÷åðåç âàñ â íàðóøåíèå ïðàâèë ôîðóìà òîëüêî èç-çà ñîîáðàøåíèÿ âàæíîñòè ñåãî ìîìåíòà; Âû êàê ëþáÿøèé ðîäñòâåííèê, ìîæåòå îïëàòèòü òåëå-êîíñóëüòèðîâàíèå â ãåì. öåíòðå Ìîñêâû, åñëè äåéñòâèòåëüíî âîëíóåòåñü çà åòîãî ÷åëîâåêà è ïåðåâåñòè íà ðóññêèé äàííûå ôðàãìåíòû âûøå, ÷òîáû àðãóìåíòèðîâàòü ñ âðà÷àìè. Íèêàêèõ äð. êîíñóëüòàöèé èëè êîíòàêòîâ ñî ìíîé ÷åðåç âàñ íå áóäåò.
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Èñêðåííå, Âàäèì Âàëåðüåâè÷. |