Contact vitiligo: etiology and treatment.

Fifty patients of contact vitiligo were studied. Etiological agents of contact vitiligo were identified by clinical history, distribution of lesions and patch testing with suspected material. All patients were advised to avoid the suspected agent and treated with PUVASOL and topical steroid. Out of 50 patients (Male 8%, Female 92% age 14-60 years)., etiological agent of contact vitiligo was found to be sticking bindi alone in 24 (48%), while bindi along with other etiological agents were found to be purse, foot wear, plastic watch strap, lipstick and tooth paste in 14 (28%) cases. 14 (28%) patients also had disseminated lesions of vitiligo along with contact vitiligo. Positive reaction with patch testing was observed in 18 (36%) while depigmentation was seen in 4 (8%) cases. We observed that response of treatment was better in patients with shorter duration of disease while poor response was seen in patients with longer duration of disease.

Angiokeratoma of tongue.

An 8-year-old male child who presented with lesions of angiokeratoma on tongue is described.

Anti-lymphocyte globulin therapy in acquired aplastic anaemia.

Thirty five patients with acquired aplastic anaemia (AAA) were treated with anti-lymphocyte globulin (ALG). Fifteen (42.9%) had non-severe aplastic anaemia (NSAA), 14 (40%) severe aplastic anaemia (SAA) and 6 very severe aplastic anaemia (VSAA). There were 17 (48.6%) responders to the first course of ALG while 2 out of 5 (40%) responded to a second course, the overall response rate being 54.3%. Eleven out of 15 (73.3%) with NSAA responded, 8 out of 20 (40%) with SAA responded while none of VSAA responded. All the non-responders have died. Out of the responders, 1 died of non-A non-B hepatitis, and 1 with relapse of AA and sepsis. One has developed paroxysmal nocturnal haemoglobinuria (PNH) and one myelodysplasia. Another 2 needed infrequent red cell transfusion support. Remaining 13 (37.1%) are asymptomatic and without any external support since 18-78 months (35 +/- 21). We conclude that ALG is an effective modality of treatment for patients with AAA.

Glanzmann's thrombasthenia.

During January 1981 to June 1991, 20 patients from 16 unrelated families were detected to have Glanzmann's thrombasthenia (GT). Twelve families (75%) had history of consanguinity, with 6 first cousins and 3 uncle-niece marriages; of these 7 were Muslims, 6 Hindus and 3 Christians. There were 12 girls and 8 boys; the mean age at diagnosis was 7.05 +/- 6.03 yr (range 1 day-22 yr). All cases had initial bleeding prior to the age of 5 yr with the mean age at the initial episode of bleeding being 2.21 +/- 1.34 yr (range 1 day-5 yr). Common pattern of bleeding included epistaxis, gingival bleeding, post-traumatic bruises, menorrhagia, gastrointestinal (2 cases), post-operative (2 cases) and spontaneous bleeding (2 cases). No patient showed hemarthrosis, intracranial bleeding or hemoptysis. Menorrhagia was a serious problem necessitating repeated transfusions and hormonal therapy. Twelve cases (60%) required 1-120 units of blood transfusions while five received platelet concentrates.

Acquired haemoglobin H disease in a case of myelodysplastic syndrome.

A case of acquired haemoglobin H (HbH) disease with underlying myelodysplastic syndrome in the form of acquired idiopathic sideroblastic anaemia is reported. Family studies and subsequent drop in HbH percentage strongly supported the acquired nature of the defect.

Lupus anticoagulant. A report of 8 cases.

Eight cases with lupus anticoagulants (LA) were diagnosed over the last five years (1984-88). Of these, three were established cases of systemic lupus erythematosus (SLE), where bad obstetric history (2 cases) and recurrent deep venous thrombosis (DVT--1 case) prompted execution of laboratory tests for LA. In the remaining 5 cases, there was no clinical evidence of SLE. However, one case developed laboratory findings suggestive of SLE at a later date. One of these 5 patients was referred for unexplained abnormality in partial thromboplastin time (K). Three had recurrent abortions (one with additional history of DVT) while one had DVT with raised PTT (K). The clinical findings and laboratory tests by which lupus anticoagulants can be diagnosed have been discussed.

Hypopigmented lesions in early leprosy--a clinical and histological study.

26 Patients of leprosy presenting with hypopigmented lesions were divided on morphological grounds into 3 Sub groups, Group I (9 patients) with well-defined single patch with moderate to complete sensory loss; Group II (8 patients) with single ill-defined lesion having partial sensory loss; and Group III (9 patients) having multiple hypo-pigmented patches with mild to moderate sensory loss. Epidermal atrophy was a conspicuous histological finding in all groups. Only patients in Group I showed epitheloid cells in dermal infiltrate with erosion of epidermis in one case. This group may be labelled as maculoanesthetic leprosy. Patients in Group II and III showed mononuclear cell infiltrate in dermis, around neurovascular bundles and appendages. They were histologically consistent with indeterminate leprosy. Follow-up biopsy after six to eight months of treatment showed healing of the lesion of reduction in the infiltrate in most cases.

Ultrastructural study of epidermal Langherhans cells in leprosy.

ATPase staining and ultrastructural study of skin biopsies from six patients of leprosy (2TT, 4LL) and three normal subjects was carried out to study Langherhans Cells (LC). ATPase staining showed normal counts of LCs in tuberculoid patients, while significant reduction was observed in lepromatous cases. Electron microscopy revealed morphological changes in LL cases in the form of dense matrix and indistinct cristae of mitochondria; decreased number of lysosomes and rough endoplasmic reticulum; and numerous vacuoles in cytoplasm. TT cases showed normal morphology. Possible role of Langerhans Cells in pathogenesis of leprosy is discussed.