Indian Journal of Endocrinology and Metabolism

: 2012  |  Volume : 16  |  Issue : 2  |  Page : 321--322

Coexistence of pituitary macroadenoma with systemic lupus erythematosus and antiphospholipid syndrome

Neda Valizadeh, Sona Nury Vahed 
 Departments of Endocrinology and Rheumatologyy, Emam Khomeini Hospital, Urmia University of Medical Sciences, Urmia, Iran

Correspondence Address:
Neda Valizadeh
4th Floor, Ershad Street, Emam Khomeini Hospital, Urmia University of Medical Sciences, Urmia

How to cite this article:
Valizadeh N, Vahed SN. Coexistence of pituitary macroadenoma with systemic lupus erythematosus and antiphospholipid syndrome.Indian J Endocr Metab 2012;16:321-322

How to cite this URL:
Valizadeh N, Vahed SN. Coexistence of pituitary macroadenoma with systemic lupus erythematosus and antiphospholipid syndrome. Indian J Endocr Metab [serial online] 2012 [cited 2021 Jul 26 ];16:321-322
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Prolactin is a cytokine like hormone that is associated with autoimmune diseases such as systemic lupus erythematosus (SLE) and celiac disease. [1] It causes proliferation of immune cells and cytokine release. [1] Hyperprolactinemia is seen in 20-30% of SLE patients. [2] Some case reports of SLE associated with prolactinoma are found in the literature, but there is no cause and effect relationship between them. [2],[3] The degree of hyperprolactinemia may be associated with SLE activity and this finding may have a therapeutic role in the management of patients. [3],[4] Elevated prolactin levels in SLE may result from a nonfunctioning pituitary tumor.

A 35-year-old woman presented with hemiplegia of left upper limb and dysarthria. Dysarthria was resolved spontaneously after half an hour. Past medical history was positive for three spontaneous abortions, Bell's palsy, appendicectomy and one episode of seizure. Her menstrual cycle was regular. She had reduced force of proximal and distal muscles of left upper limb, increased deep tendon reflexes (DTR) of the same limb and right side Bell's palsy on examination. Vital signs were normal. Consciousness, sensation, Romberg, vibration, and cerebellar tests were all intact, but cognition was minimally impaired. Brain magnetic resonance imaging (MRI) revealed mild hydrocephaly with abnormal hyperintense lesions in periventricular white matter, centrum semioval, precentral and postcentral gyrus in T2-weighted images [Figure 1]. Cerebellar white matter was also involved and an abnormal mass in pituitary fossa was discovered. MRI of sella turcica in sagittal and coronal views demonstrated pituitary macroadenoma with chiasmatic compression [Figure 2]a and b. The findings on brain magnetic resonance angiography and magnetic resonance venography (MRA and MRV) were normal. Electromyography and nerve conduction velocity (EMG-NCV) showed upper motor lesion in left side upper extremity.{Figure 1}{Figure 2}

Laboratory results showed the following: WBC 3300/ μl [72% polymorphonuclear leukocytes (PMN) and 18.7% lymphocytes], lymphocytes 617/μl, hemoglobin (Hb) 8.9 g/dl, mean cell volume (MCV) 75, hematocrit (HCT) 26.4%, platelet (Plt) 46,000/μl, reticulocyte count (Ret C) 0.3%, erythrocyte sedimentation rate (ESR) 55 mm/ hour, C-reactive protein (CRP) +1, ferritin 64 ng/ml (normal level 7.4-73), fibrinogen degradation products (FDP) 0.18 mg/ dl (up to 0.2) and lactate dehydrogenase (LDH) 802 U/l (normal level <480). Blood sugar, calcium, magnesium, urine SG, renal and liver function tests and 24-hour urine protein level were all normal.

Endocrine and rheumatologic tests showed mild hyperprolactinemia [prolactin 31.6 ng/ml (normal level 4.8-23.3)], normal thyroid function, normal C3 and C4 levels, positive antinuclear antibody (ANA; 1.35 IU/ ml, normal level <1), positive anti-ds DNA (2.2 IU/ml, normal level <0.9), high anticardiolipin (IgG) level (78 GPL/ml, normal level <15), high titer of antiphospholipid Ab (IgG) (106 U/ml, normal level <10), positive lupus anticoagulant and negative antineutrophil cytoplasmic and perinuclear antibody (P-ANCA and C-ANCA).

The diagnosis of antiphospholipid syndrome (APS) secondary to SLE and nonfunctioning pituitary macroadenoma (NFPA) was made. The diagnosis of SLE was based on the presence of high titers of ANA, positive anti-ds DNA, leukopenia (lymphopenia) and CNS involvement. Because of mildly elevated prolactin level and on the basis of MRI finding, the diagnosis of NFPA was also made. Hyperprolactinemia in this patient originated from a nonfunctioning pituitary tumor. Hyperprolactinemia in SLE cannot be explained by the autoimmune nature of the disease or by its other known complications. We cannot confidently comment on the cause and effect relationship between hyperprolactinemia and the risk of SLE occurrence. We conclude that regardless of the autoimmune nature of SLE, pituitary imaging should be performed in all SLE patients with any degree of hyperprolactinemia to search for pituitary tumors.


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