{"id":3708,"date":"2017-08-23T19:24:15","date_gmt":"2017-08-23T17:24:15","guid":{"rendered":""},"modified":"2025-05-27T21:29:29","modified_gmt":"2025-05-27T19:29:29","slug":"ulrike","status":"publish","type":"page","link":"https:\/\/aa-pnh.org\/en\/diseases\/patient-stories\/ulrike\/","title":{"rendered":"Patient story by Ulrike"},"content":{"rendered":"

Patient story by Ulrike<\/strong>
\n<\/em><\/span><\/h3>\n

 <\/p>\n

The first abnormalities in my blood count were found in March 1999 in the form of thrombocytopenia<\/a>, when I went to donate blood (irony of fate?). At that stage I hadn’t noticed any physical symptoms such as an increased bleeding tendency. But a few weeks later, the erythrocyte<\/a> and leukocyte<\/a> values had changed too; I became anaemic, and there were more lymphocytes<\/a> than usual among the leukocytes<\/a>. At first there was no clear diagnosis from the two bone marrow puncture<\/a>s, so that immunosuppressive<\/a> treatment was prescribed with little justification until October 1999, when another puncture supported the diagnosis of “very severe aplastic<\/a> anaemia (vSAA)”.<\/p>\n

By that time I was already dependent on transfusion<\/a>s, and was told to go to hospital as soon as the diagnosis was made, in order to receive the first ATG<\/a> and begin ciclosporin<\/a> therapy, which continued until the summer of 2007. The rabbit ATG<\/a> had no effect, but I continued to receive transfusion<\/a>s (platelets about every 6 days and red blood cells about every 14 days) as well as numerous preventive measures to support my weak immune system<\/a>. I could only wait and hope that the bone marrow would recover.<\/p>\n

In February 2000 I was diagnosed with PNH, but it didn’t play a role since treatment of aplastic<\/a> anaemia was still the focus. Two months later, I received the second treatment with ATG<\/a> (horse). In June 2000, two months after my therapy, the bone marrow started to show some platelet production. This was enough to discontinue the transfusion<\/a>s, and prophylaxis<\/a> against infection was gradually tapered off. I received my last foreign RBCs in January 2001, and the first visible PNH crisis occurred at the same time.<\/p>\n

By 2002, my blood levels had gradually stabilised, but the haemoglobin<\/a> levels already showed persistent PNH crises. The associated symptoms were mitigated by regular administration of packed RBCs<\/a> (since autumn 2005) and prednisolone, but they have significantly impaired my quality of life. I was particularly burdened by a pronounced feeling of weakness, which was often associated with the feeling that a rock was lying on my stomach. I therefore started therapy with the antibody<\/a> eculizumab in June 2010. Since then, the haemoglobinuria<\/a> has disappeared; this is a great relief, as I notice the PNH symptoms less often and less intensely. However, I still need transfusion<\/a>s and my stamina is very limited. My leukocyte<\/a> and platelet values are stable.<\/p>\n

I have been on an invalidity pension since 2000. I took advantage of the associated financial security and “leisure time”, and from 2001 to 2006 I studied history part-time at an English online university, which I had always wanted to do. I enjoyed my studies a lot, but the pressure on performance put me under considerable stress and showed me that I cannot really work in a concentrated way in the long term.<\/p>\n

My employer has supported me for the entire period of my illness and has employed me for two half days a week since 2001. This gives me the opportunity to take part in professional life and to maintain social contacts in addition to my voluntary commitment. I greatly appreciate this.<\/p>\n

The approval of ravulizumab in July 2019 made it possible for me to increase the intervals between attending a practice or clinic for infusion<\/a>s from every two weeks to every eight weeks. However, the fatigue<\/a> still makes things difficult, even though my RBC values have now stabilised and I hardly need any concentrates. I have high hopes for medications that are more effective than C5 inhibitors in reducing haemolysis<\/a>, and some of these are already undergoing clinical trials.<\/p>\n

You can contact me by email at ug-sh(at)web.de<\/a><\/p>\n

Berlin, August 2020<\/p>\n

 <\/p>\n","protected":false},"excerpt":{"rendered":"

Patient story by Ulrike   The first abnormalities in my blood count were found in March 1999 in the form of thrombocytopenia<\/a>, when I went to donate blood (irony of fate?). At that stage I hadn’t noticed any physical symptoms such as an increased bleeding…<\/p>\n","protected":false},"author":7,"featured_media":0,"parent":3704,"menu_order":67,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-3708","page","type-page","status-publish","hentry"],"_links":{"self":[{"href":"https:\/\/aa-pnh.org\/en\/wp-json\/wp\/v2\/pages\/3708","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/aa-pnh.org\/en\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/aa-pnh.org\/en\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/aa-pnh.org\/en\/wp-json\/wp\/v2\/users\/7"}],"replies":[{"embeddable":true,"href":"https:\/\/aa-pnh.org\/en\/wp-json\/wp\/v2\/comments?post=3708"}],"version-history":[{"count":1,"href":"https:\/\/aa-pnh.org\/en\/wp-json\/wp\/v2\/pages\/3708\/revisions"}],"predecessor-version":[{"id":8059,"href":"https:\/\/aa-pnh.org\/en\/wp-json\/wp\/v2\/pages\/3708\/revisions\/8059"}],"up":[{"embeddable":true,"href":"https:\/\/aa-pnh.org\/en\/wp-json\/wp\/v2\/pages\/3704"}],"wp:attachment":[{"href":"https:\/\/aa-pnh.org\/en\/wp-json\/wp\/v2\/media?parent=3708"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}