Patricia Chang

ACQUIRED PERFORATING DISEASE: REPORT OF NINE CASES

Background. A study of nine Guatemalan patients with acquired perforating disease associated with chronic renal failure, diagnosed at the Guatemalan Social Security Institute, General Hospital, during the period of January 1990 to March 1993, is presented (Table 1).

MALIGNANT FIBROUS HISTIOCYTOMA OF THE SKIN

A 71-year-old Guatemalan man was seen in the General Disease Hospital of the Guatemalan Social Security Institute, because of a lesion on the anterior aspect of the right thigh. A lobulated mass of 10 x 7 cm, not fixed to deep tissues, was found with associated enlargement of the inguinal lymph nodes on the same side (Fig. 1). All laboratory tests performed were normal, including a radiograph of the right thigh. The patient was in good health until 3 months before admission, when he noted a small nodule on the right thigh that progressively increased in size. The physical examination was unremarkable, except for the lesion described on the thigh. The past history was noncontributory. An incisional biopsy of the skin lesion and the inguinal mass was done. The sections of the skin (Fig. 2) revealed numerous pleomorphic cells in the upper and lower dermis and in subcutaneous tissue with some multinucleated forms, prominent nucleolus, and variable amount of cytoplasm. The number of mitoses was remarkable. Associated with the neoplastic cells, there were many inflammatory cells, most of them mononuclear cells. In the sections of the lymph node the same type of neoplastic cells were seen with extensive changes in the normal architecture of the node. The patient was treated with prednisone, 50 mg/m^ per day, and vincristine, 2 mg intravenously for 6 weeks, with subsequent partial remission of the mass. The patient did not complete the treatment and 6 months later returned to the hospital with a large mass in the thigh. Chlorambucil, 8 mg/day and methotrexate, 50 mg i.m. per day were given. After 9 cycles of treatment the mass and the enlarged inguinal lymph nodes disappeared completely.

Mycotic Leukonychia in HIV Patients

Onychomycosis is the fungal infection of the nail, that can be caused by dermatophytes, Candida sp. or non-dermatophyte moulds (NDM). The term tinea unguium is a specific form of onychomycosis caused only by dermatophytes and thus, should not be regarded as synonymous. (Odds et al., 1992) On the other hand, the term leukonychia or white nails has a varied etiology, it can be congenital or acquired, infectious and non-infectious. In the case of onychomycosis, the diseased nail plate has an external origin, which is the fungal invasion that affects secondarily the normally formed nail. This is also known as fungal or mycotic leukonychia (Baran et al. 1994). Onychomycosis, with all the different clinical presentations, is responsible for about 50% of all dystrophic nails and has a prevalence of 3-10% in the general population. Frequency also depends, on geographic conditions and age groups, with an increase in the prevalence in the elderly. It is now becoming more evident that immunosuppressed patients, particularly those living with HIV infection, are at a higher risk of presenting this nail fungal infection, and any clinical presentation is higher compared to the same age group of the general population ( Denning et al. 1995; Moreno-Coutino et al., 2011; Winberg et al. 2003). The first classification of onychomycosis was proposed by Zaias, and is based on the clinical appearance of the nails (Zaias, 1972). He described four clinical types: [1] distal subungual onychomycosis (DSO), [2] white superficial onychomycosis (WSO), [3] proximal subungual onychomycosis (PSO) and [4] Candida sp. onychomycosis. Since the publication of this paper, some modifications have been added. In 1998, Baran et al. proposed [I] distal and lateral subungual onychomycosis (DLSO), [II] superficial onychomycosis, [III] proximal subungual onychomycosis (PSO), [IV] endonyx onychomycosis and [V] total dystrophic onychomycosis (TDO). The most used these days is the following: DLSO, white superficial onychomycosis (WSO), PSO, Candida onychomycosis (paronychia) and TDO (Table 1) , (Baran et al 1998). WSO and PSO are also known as mycotic leukonychia. Further subdivisions are included in almost all the categories, and will be discussed further when necessary (Gupta & Summerbell, 1999). In 1976, English described a classification based on etiology, instead of the clinical aspect of the fungal invasion. The categories are: (a) dermatophytes causing tinea unguium, (b) moulds (Non-dermatophyte moulds [NDM]) and (c) yeasts (Crozier et al. 1979). At this moment, the