Thrombocytopenia is a common finding in septic shock patients in the intensive care unit (ICU). Various mechanisms have been attributed to explain the occurrence of thrombocytopenia, including disseminated intravascular coagulation (DIC) 1-3 , cytokine-driven haemophagocytosis of platelets 4,5 , immune-mechanisms, such as elevated plateletassociated IgG 1,6 , invasive catheters, especially pulmonary artery catheters 7,8 , and medications, such as heparin and pencillin analogues. Thrombocytopenia in critically ill patients, including trauma patients and surgical patients, has been found to be an independent marker for poor prognosis, increased bleeding, longer ICU stay and increased mortality 7-11. Most studies so far have explored the risk factors and clinical outcomes in critically ill medical, surgical, trauma or cardiac patients with thrombocytopenia. In this study, we looked at thrombocytopenic septic shock patients in a medical ICU. The objectives of the study were to study, 1) incidence of various degrees of severity of thrombocytopenia in septic shock, 2) risk factors for its development and 3) the correlation of thrombocytopenia with organ dysfunction, length of ICU stay and clinical outcome including mortality.

Dyskeratosis congenita and Fanconi’s anemia share impressive features in common: primary refractory pancytopenia; bone marrow hyperplasia (curtailed phase) and megaloblastosis, eventuating in severe hypoplasia of the marrow; cutaneous melanotic dyschromia; lacrimal duct blockage and a host of other minor abnormalities, in addition to mental retardation and generalized impairment of growth. Evaluation of two brothers with dyskeratosis congenita, and review of previous reports, indicate the following to be more prominent in dyskeratosis congenita than in Fanconi’s anemia: cutaneous telangiectatic erythema and atrophy; exocrine, ungual, and dental dysplasias; mucosal leukoplakia, carcinomatosis, and stenosis; and esophageal diverticula. Prominent in Fanconi’s anemia but not dyskeratosis congenita are the renal and particular skeletal anomalies. Possible transition cases are discussed. The proband studied suffered from progressive refractory pancytopenia, fevers, abdominal pains, malabsorption syndrome, and finally subarachnoid hemorrhage. Cultured leukocytes had normal-appearing karyotypes. The proband’s brother had cutaneous alterations of dyskeratosis congenita, but a hemogram revealed only mild thrombocytopenia and macrocytosis. Both brothers had elevated levels of hemoglobin F, leukocyte alkaline phosphatase, serum IgG, and thyroglobulin antibody, and both had reduced levels of serum IgM and vitamin B12.

Although hypercalcemia is a frequent event during the course of many malignancies it has only rarely been described with patients with chronic lymphocytic leukemia. Review of the literature revealed only eleven such case reports. The mechanism of the hypercalcemia in these patients was generally unclear although one patient was found to have a parathyroid adenoma and in another patient tested the level of osteoclast activating factor was high. Two additional chronic lymphocytic leukemia patients with hypercalcemia are described in this report and in each a parathyroid adenoma was found. The patient in whom the diagnosis was made ante mortem had an excellent response to parathyroidectomy. Osteoclast activating factor level was measured in one patient and found to be within normal limits. Since three of the thirteen reported cases of chronic lymphocytic leukemia with hypercalcemia have demonstrated parathyroid adenomas, it is suggested that consideration be given to that possibility in such patients so that appropriate surgery may be done.