Enrique Antón

Kaposi's sarcoma in an immunocompetent patient following corticosteroid therapy

A 55-year-old man presented with a several week history of multiple asymptomatic plaques on his left lower extremity. He had been taking prednisone, 30 mg daily, for 14 months for a cryptogenic organizing pneumonia. He had no other medical problems or sexual risk contacts. Physical examination showed multiple small, well-demarcated, rounded plaques and nodules longitudinally arranged on the left lower extremity. The lesions were firm, purplish-red, and non-blanchable. No lesions were seen in the oral mucosa. Cell-mediated and humoral immunity were normal and he was HIV-seronegative. Skin biopsy (punch) showed Kaposis sarcoma fusiform cells delineating abnormal, slit-like vascular spaces containing erythrocytes. A diagnosis of iatrogenic Kaposis sarcoma was made. The serum level of IgG antibody to HHV-8 was high (N640). HLA-typing showed the haplotypes DR3 and DR4, not predisposing to Kaposis sarcoma. The lesions improved after reducing the dose of steroids. After taking 5 mg daily of prednisone, the Kaposis sarcoma lesions spontaneously disappeared. Kaposis sarcoma (KS) is an angioproliferative neoplasia that was originally described in 1872. Iatrogenic KS, one of four described variants, was first reported in patients with high-dose immunosuppressive therapy (e.g., patients with transplants, autoimmune disorders, or cancer) [1]. Iatrogenic KS can also appears in patients receiving therapy with corticosteroids alone. In 1994, a novel herpesvirus, human herpesvirus 8 (HHV-8), was described from KS lesions in an HIV-positive patient [1]. HHV-8 has since been isolated from all clinical variants of KS. The development of KS post-transplantation seems to be related to the reactivation of latent HHV-8 infection by means of a chemokine-like, G-protein-coupled receptor that promotes the proliferation of endothelial cells through activation of the receptor F1k-1/KDR. Yet, steroid therapy can also lead to the appearance of KS in susceptible patients, stimulating tumor development and growth up-regulating glucocorticoid receptors on KS lesions [2].

SPONTANEOUS IDIOPATHIC BILATERAL MASSIVE ADRENAL HEMORRHAGE IN AN ELDERLY WOMAN

DISCUSSION This report highlights that the occurrence of acute abdominal symptoms during the course of a respiratory infection may suggest the presence of a spontaneous hematoma of the abdominal wall. The association between violent coughing with hematoma of the abdominal wall involving the rectus sheath muscle is well recognized (coughing causes intense contraction of the rectus muscle, with tearing and bleeding from the perforating branches of the inferior epigastric vessels within the muscle substance), but this report shows how a spontaneous hematoma involving the lateral muscles of the abdominal wall may also complicate coughing. In this case, the diagnosis may be difficult and frequently mistaken for other common intra-abdominal pathologies such as cholelitiasis, intestinal obstruction, paralitic ileus, neoplasm, perforated colon, diverticulitis, and acute appendicitis. In this patient, the spontaneous expanding abdominal hematoma was suspected only after development of the most typical symptom and signs (cutaneous ecchymoses and abdominal palpable mass). The patient’s history was negative for coagulation disorders, trauma, and drugs affecting coagulation. The most significant risk factor was the presence of acute cough related to pneumonia. It is clinically interesting that the pain developed 15 days before the clinical presentation of the hematoma, possibly due to slow intramuscular bleeding lasting for 2 weeks before the clear evidence of the hematoma. In conclusion, the occurrence in an elderly subject of sudden thoracic or abdominal pain after straining, for example coughing or sneezing, should alert the clinician to the possibility of the presence of a muscle abdominal hematoma even in the absence of overt clinical signs.

DYSPHAGIA AND ENLARGED THORACIC AORTIC ANEURYSM: IS THERE EVER A CAUSAL RELATIONSHIP?

To the Editor: I have read the interesting report by Ebihara et al. In my opinion, some debatable points appear in their article. Briefly, they have described an elderly man with progressive dysphagia attributed to enlargement of thoracic aortic aneurysm. His medical history included Alzheimer’s disease, cerebrovascular disease, and abdominal aortic aneurysm. Extrinsic compression of the esophagus due to an aneurysm of the atherosclerotic thoracic aorta may cause dysphagia in older people. This condition, known as dysphagia aortica, is uncommon and is usually associated with old age, women of short stature, hypertension, and kyphosis.

IS ESTABLISHING AN APPROPRIATE BLEEDING RISK PROFILE IN ELDERLY PATIENTS TREATED WITH LOW-MOLECULAR-WEIGHT HEPARINS NEEDED?

To the Editor: Lopez et al. report that ‘‘cholinesterase inhibitor (CEI) use had a clinically meaningful effect on the natural history of Alzheimer Disease (AD),’’ slowing disease progression and lowering risk of nursing home admission after 2 years. The design of the study is worrisome. Of 1,139 patients who enrolled in the AD Research Center over 7 years, 270 were selected; 135 began taking CEIs ‘‘immediately after enrollment, and continued to take them throughout the following 12 months,’’ and 135 never took the drug. How these individuals were selected is not otherwise described. They were matched on a few characteristics, such as age, Mini-Mental State Examination score, and education. This study resembles a study by Dr. Geldmacher et al. that showed that patients who took a CEI faithfully (80% of pills or more) had a significant delay in nursing home placement (NHP). Both of these nonrandomized studies failed to report important baseline characteristics of the groups being studied. In the Geldmacher article, for example, nonadherent patients were far less likely to have a spouse caregiver than faithful users, yet the authors, who claimed it was the donepezil that ‘‘resulted in significant delays in NHP,’’ omitted this fact. Both papers are easily distinguished from AD 2000, a properly randomized, controlled trial with the largest number of placebo-controlled patient-years of any cholinesterase study. In AD 2000, ‘‘no significant benefits were seen with donepezil compared with placebo in institutionalization or progression of disability . . . [or] in behavioral and psychological symptoms, carer psychopathology, formal care costs, unpaid caregiver time, adverse events, or death or between 5 mg and 10 mg of donepezil.’’ In the United Kingdom, the National Institute for Clinical Excellence Appraisal Committee has recently issued the following preliminary recommendation: ‘‘Donepezil, rivastigmine and galantamine are not recommended for use in the treatment of mild to moderate Alzheimer’s disease (AD).’’ Would Dr. Lopez modify the discussion of his paper, where he emphasizes the important benefits of donepezil, in view of the results from AD 2000, a larger, better-designed trial that failed to show any meaningful difference at all?

Transient ischemic attacks in elderly patients

Forty consecutive patients (7 men and 33 women) from this cohort had progressed to GDS 7 at the time the study results were analyzed and formed the study group. Of these, 28 progressed to end-stage dementia in a mean of 3.2 years and were determined to have a rapid course. The remaining 12 progressed more slowly to end-stage dementia, over a mean of 6.9 years. Patients whose decline was rapid had 6.0 MDCs at their baseline evaluation, which was significantly more than the 3.9 MDCs in patients whose course of dementia was slower. The patients in the rapid deterioration group suffered at baseline significantly more from peripheral vascular disease (36% vs 0%) and atherosclerotic heart disease (29% vs 8%) than those who progressed more slowly to end-stage AD. The incidence of diabetes mellitus and hypertension were significantly greater at baseline in the rapidly progressive group. Hip fractures, contractures, and decubiti were conditions that were not found at onset but had significantly higher incidence when end-stage AD was reached.