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Background: Although long-term management of psoriasis is paramount, this approach is challenging in clinical practice. In the recent PSO-LONG trial, a fixed-dose combination of betamethasone dipropionate (BD) and calcipotriol (Cal) foam applied twice a week on non-consecutive days for 52 weeks (proactive treatment) reduced the risk of relapse. However, the role of Cal/BD foam in the long-term management of psoriasis needs further clarifications. The ProActive Management (PAM) program, a nationwide Italian project, aims at reaching a consensus on the role of proactive management of psoriasis., Methods: A steering committee generated some statements through the nominal group technique (NGT). The statements were voted by an expert panel in an adapted Delphi voting process., Results: Eighteen statements were proposed, and the majority of them (14/18) reached a consensus during the Delphi voting. The need to provide long-term proactive topical treatment to reduce the risk of relapse for the treatment of challenging diseases sites or in patients where phototherapy or systemic therapies are contraindicated/ineffective was widely recognized. A consensus was reached about the possibility to associate the proactive treatment with systemic and biological therapies, without the need for dose intensification, thus favoring a prolonged remission. Moreover, the proactive treatment was recognized as more effective than weekend therapy in increasing time free from relapses. Approaches to improve adherence, on the other hand, need further investigation., Conclusions: The inclusion in guidelines of a proactive strategy among the effective treatment options will be a fundamental step in the evolution of a mild-moderate psoriasis therapeutic approach., (© 2022 The Authors. International Journal of Dermatology published by Wiley Periodicals LLC on behalf of the International Society of Dermatology.)

Background and Aim: Hashimoto's thyroiditis (HT) is a common endocrinopathy in children, particularly in females. Clinical overt presentation of hypothyroidism in HT includes mild to very severe forms, characterised by impairment of many body functions and organs, such as heart, brain, muscles, ovaries and liver., Case: we report the case of a 14-year-old girl, with severe hypothyroidism due to a late diagnosis of HT during the Covid-19 pandemic. Routine biochemical and hormonal exams were carried out at presentation. Moderate pericardial effusion was detected by echocardiography and polycystic ovarian morphology (PCOM) was found on the pelvic ultrasound. Furthermore, high levels of creatine phosphokinase (CPK), Lactic Acid Dehydrogenase (LDH) and hepatic liver enzymes, associated with muscular pseudohypertrophy and bilateral weakness of the lower limbs, were suggestive of a rare presentation of long-standing hypothyroidism defined Kocher-Debre-Semelaigne syndrome (KDSS). Levothyroxine replacement therapy was started immediately, leading to a rapid improvement of symptoms and a progressive normalization of the biochemical parameters. Due to persistent lower limb weakness, further neurological investigations were performed, showing bilateral peripheral polyneuropathy (PNP), ascribable to the longstanding and severe hypothyroidism. A pelvic ultrasound, performed after thyroid hormones had normalised and menses had turned to be regular, showed normal ovarian features supporting the hypothesis of the Van Wyk and Grumbach syndrome in a post-menarcheal girl., Conclusions: although clinical manifestation of hypothyroidism are usually mild, more severe and rare presentations such as ovarian dysfunction and myopathy are possible, particularly if the diagnosis is delayed and replacement therapy is not promptly administered.

In patients with liver cirrhosis, especially in the advanced stage, the coexistence of low clotting factor levels, hypofibrinogenemia, thrombocytopenia and elevated fibrin(ogen) degradation product (FDP) and D-dimer levels may suggest the presence of disseminated intravascular coagulation (DIC). In this study we evaluated, in 21 patients with decompensated liver cirrhosis and elevated FDP and D-dimer levels, the time sequence of their coagulation data during a follow-up period of 15 days after the first observation; our aim was to clarify if these patients tend to develop during this time interval a severe consumption coagulopathy as an expression of overt DIC. We evaluated serum fibrinogen, platelet count, prothrombin activity, serum FDP and plasma D-dimer levels at days 1, 3, 6, 10 and 15. The coagulation data were fairly stable during the study period in all patients, even in the two patients who had upper digestive tract bleeding during the study time. Only two patients affected by infectious diseases showed a decrease of D-dimer and FDP levels after healing. Our data suggest that in decompensated liver cirrhosis the detection of elevated FDP and D-dimer levels is seldom related to the occurrence of an overt DIC, at least during a short time interval; in this condition heparin therapy seems therefore not advisable and even potentially dangerous.

Laboratory diagnosis of disseminated intravascular coagulation (DIC) in liver cirrhosis (LC) could be complicated by the presence of the usual decrement of the hemocoagulative parameters and of an increase of the fibrinogen/fibrin degradation products (FDP). The D-dimer test, more sensible than the one for FDP and specific for the cross-linked fibrin degradation products is now available. A significant difference between the two tests, assayed simultaneously has been demonstrated in 217 LC patients, without any recent or present hemorrhagic signs. The D-dimer was increased in only 60 of the 108 patients with high values of FDP; therefore this test has a screening value higher than FDP. If only the D-dimer is elevated, the FDP assay is indicated: if FDP are normal a thrombosis may be present and, finally, if the FDP are also increased with a concomitant decrement of fibrinogenemia, the laboratory diagnosis of DIC is reasonably certain.

A morphological, cytochemical, genetic and autoradiographic examination of the myeloblasts observed in the terminal phase of a patient with Hodgkin's disease is reported. Comparison is made with the literature data in an assessment of the possible aetiopathogenesis of this association, which has become increasingly frequent in recent years in coincidence with the more widespread employment of more radical radio- and polychemotherapeutical management.

The aetiology, pathogenesis, clinical forms and therapeutic attempts carried out in connection with the central nervous system localizations in acute lymphoblastic leukaemia, on the basis of an extensive review of the literature and of personal experience are examined. The particular role which central nervous system leukaemia plays on the subsequent clinical course of the disease is stressed and the efforts made, both prophylactically and therapeutically, in order to decrease the incidence of this complication, which invariably has a deteriorating influence of the progress of the disease are described.