854 Correspondence

Journal of the American Academy of

Dermatology

Table I. Final measurements

Pretreatment Posttreatmen~ Body part (era) (best values [cm])

Lower third of thigh 63 59 Knee 44 41 Calf 45.2 43.1 Distal gastrocnemius 39 37 Ankle 31.5 29.5 Instep 25.8 23.5 Metatarsal joint line 24 22

pressures approaching the patient's systolic blood pressure (100 mm Hg), she reported uncomfortable throbbing sensa- tions. Serum electrolyte concentrations were measured on days 2 and 3 of treatment, since compartment fluid shifts might be expected. All laboratory values were normal. Measurements of the treated lower extrern[ty were performed daily. After 3 days of treatment the tria[ was discontinued because the patient complained of a sharp pain in her right lower leg, which increased with standing. Physical examination revealed erythe- ma and increased warmth localized to the right ankle. Final measurements were obtained (Table I), and the patient was discharged and placed on 7 days of oral antibiotic therapy for possible early cellulitis. All symptoms resolved 5 days after discharge.

Discussion. A' number of compressive devices are availabIe for treatment of lymphedematous disorders, but many of these generate pressures of no greater than 60 mm Hg and/or do not generate sequential multicom- partmenta[ pressure changes that provide the "miLking" action inherent in the Lympha-Press design. This "milk- ing" action provided by the Lympha-Press is more efficient in preventing fluid backflow. A number of studies v3 have supported the efficacy of this treatment for lymphedema.

Unfortunately, in our patient with congenital lym- phedema (not truly Milroy's disease, as Milroy described hereditary lymphedema4), results were not good, and the cost/benefit ratio was believed to be too high to warrant further trials. In addition, although we could not be certain without cultures, we had concerns that the device may have triggered (perhaps by creating grossly undetected small breaks in the epidermal barri- er) an episode of cellulitis, so patients need to be monitored carefully. Also, to avoid causing any throb- bing discomfort or arterial occlusive problems while patients are using the device, we suggest that guidelines for use should include a precautionary note that pres- sures near or above the patient's own systolic pressure should be avoided or used with caution. Finally, before beginning therapy one must rule out evidence of decom- pensated heart failure, deep venous thrombosis, acute

infection, and arterial insufficiency of the affected limb.

Although devices such as Lympha-Press may be useful for treating some patients with lymphedema, this therapy is not always beneficial, and problems may arise as we have shown. We believe careful monitoring is necessary, and perhaps even hospitalization is indicated when starting therapy.

Michael R. Bastien, MD, Beth G. Goldstein, MD,

Jack L. Lesher, Jr., MD, and J. Graham Smith, Jr., AID,

Medical College of Georgia, Augusta, GA 30912-2900

REFERENCES 1. Zelikovski A, Manoach M, Giler SH, et al. Lympha-Press:

a new pneumatic device for the treatment of lymphedema of the limbs. Lymphology 1980;13:68-73.

2. Zelikovski A, Deutsch A, Reiss R. The sequential pneu- matic compression device in surgery for lymphedema of the limbs. J Cardiovasc Surg 1983;24:122-6.

3. Richmand DM, O'Donnell TF Jr, Zelikovski A. Sequential pneumatic compression for lymphedema: a controlled trial. Arch Surg 1985; 120: i 16-9.

4. Milroy WF. Chronic hereditary edema. Milroy's disease. JAMA 1928;91:1172-5.

Localized trichorrhexis nodosa

To the Editor: The two case reports by Dr. Camacho- Martinez (J AM ACAD DERMATOL 1989;20:696-7) underline the fact that trichorrhexis nodosa is caused by trauma. It can occur in any hair-bearing area affected by a pruritic dermatosis, where repeated excoriations have led to lichenified skin and fractured hair shafts.

Light microscopy of the affected hairs is advisable to distinguish trichorrhexis nodosa from piedra, trichomy- cosis, dermatophytosis, pediculosis, peripilar casts, deposits of extraneous material, and other abnormalities of the hair shaft.

David A. Whiting, MD Baylor Hair Research and Treatment Center

3600 Gaston Ave. Dallas, TX 75246

Disseminated paracoccidioidomycosis with skin lesions in a patient with acquired immunodeficiency syndrome

To the Editor: Patients with acquired immunodefieien- cy syndrome (AIDS) can have disseminated deep fungal

Volume 20 Number 5, Part 1 May 1989 Correspondence 855

Fig. 1. Ulcers with raised borders on the left side of the face.

]Fig, 2. Granuloma showing a round spore with doubly refractile capsule (arrow) in photomicrograph of skin biopsy specimen. (Hematoxylin-eosin stain; X400.)

infections with skin lesions. ~'3 We report a case of disseminated paracoccidioidomycosis with skin lesions in a patient with AIDS. To our knowledge, this is the first reported case.

Case report. A 31-year-old urban Brazilian transvestite homosexual man had a 2-week history of fever, headache, and painful ulcerations on the face and right thigh. At the time he was receiving treatment for oral and esophageal candidiasis with nystatin ointment and ketoconazole tablets and for intestinal and lymph node tuberculosis with rifampin, pyrazin- amide, and ethionamide. Previous diagnoses included cryptos- poridiosis and cytomegalovirus infection.

Examination revealed several small ulcers, surrounded by a red halo and slightly raised borders, on the face, mostly around the nose and mouth (Fig. 1). A similar ulcer on the right thigh was present for 5 months at the site of a silicone injection done for cosmetic purposes. A fungal infection of all toenails was also seen.

Chest x-ray examination revealed diffuse micronodules and

dense interstitial infiltration of both lungs. The biopsy speci- men of one of the skin ulcers on the face showed a granuloma with several round spores surrounded by a doubly refractile capsule (Fig. 2), typical of Paracoccidioides brasiliensis.

He was treated with intravenously administered amphoteri- ein B for 3 weeks (total dose 2 gin), with comptete healing of the pulmonary and cutaneous lesions.

Comment. This case, taken together with the experi- mental evidence in which dissemination of the disease is accompanied by lesions at the site of inoculation, 4 illustrates the importance of the immune system in the onset and course of the disease.

Lueio Bakos, MD, Mathias Kronfeld, AID,

Suzana Hampe, AID, In~s Castro, AID, and Marcia Zampese, AID

Hospital de Clinicas de Porto Alegre, Federal University of Rio Grande de Sul,

Porto Alegre, Brazil

REFERENCES 1. Penneys NS, Hicks B. Unusual cutaneous lesions associ-

ated with acquired immunodeficiency syndrome. J AM ACAD DERMA'rOE 1985;13:845-52.

2. Warner LC, Fisher BK. Cutaneous manifestations of the acquired immunodeficiency syndrome, lnt J Dermatol 1986;25:337-49.

3. Bibler MR, Luber H J, Glueck FI, Estes SA. Disseminated sporotrichosis in a patient with HIV infection after treat- ment for acquired factor VIIi inhibitor. JAMA 1986; 256:3125-6.

4. Kerr IB, Costa SCG, Alenear A. Experimental paracoccid- ioidomycosis in immunosuppressed mice. Immunol Lett 1982;5:151-4.

Urticarial dermatosis associated with Waldenstriim's macroglobulinemia

To the Editor: Dermatologic manifestations in Waiden- str6m's macroglobulinemia can be divided into specific (macroglobu[inemia cutis I and macroglobulinosis 2,3) and nonspccific, 4 such as cold injury or Raynaud's phenomenon, amyloidosis, purpura, pruritus, xanthoma- tosis, and urticaria.

We report a patient with WaldenstrSm's macroglob- ulinemia who had a chronic nonitching urticarial rash, associated with episodes of relapsing fever, arthralgias, and bone pain. This peculiar association has been reported previously 5"~2 and may constitute a peculiar, though nonspecific, manifestation of macroglobulinemia ( IgM paraproteinerrfia or Waldenstr6m's macroglobu- linemia).